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 of 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 causes of the development of respiratory distress syndrome in newborns are:
- impaired synthesis and excretion of surfactant by type 2 alveolocytes, associated with functional and structural immaturity of 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 of the cardiovascular system occurs: secondary pulmonary hypertension with 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 (to a perinatal center) (C).

Pregnant women at 23-34 weeks' gestation who are at risk of preterm labor 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 to women at 35-36 weeks of gestation in the case of a planned cesarean section when the woman is not in labor. 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 a full therapeutic effect (B). 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 of membranes (premature rupture of amniotic fluid), as 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 mellitus in the mother;
- severe form of hemolytic disease of the 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.
Recession of the chest during 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 for diagnostic purposes, but to assess the effectiveness of respiratory therapy or as an indication for its initiation. Along with assessing the newborn's need for supplemental 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 carrying out a 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. Characterized by a rapid decrease in 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. The presence of meconium amniotic fluid and respiratory disorders since birth, their progression, the absence of laboratory signs of infection, as well as characteristic changes on the chest x-ray (infiltrative shadows interspersed with emphysematous changes, atelectasis, possible pneumomediastinum and pneumothorax) speak in favor of 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 translocation of abdominal organs into the thoracic cavity support the diagnosis of “congenital diaphragmatic hernia.” Features of the provision of primary and resuscitation care to newborns at high risk for 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 of caring for critically ill and very premature infants. 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 years of life as part of the initial measures of primary care for the 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 the 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 mechanical 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 artificial ventilation. Constant positive pressure in the respiratory tract helps 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 infants. This technique is performed once. The maneuver can be performed using a manual device with a T-connector or an automatic ventilator, which has the ability to maintain the required inspiratory pressure 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 an 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 a premature infant, 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 in the absence of spontaneous breathing for a long time (more than 5 minutes).

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 most likely indicates ventilation with excess tidal volume and a high risk of volume injury.

Invasive artificial ventilation of the lungs 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 lung 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 preparation for transporting the child in the mode of artificial pulmonary ventilation 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 (via 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 mechanical ventilation-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 artificial pulmonary 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 the best results in the 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 on 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 more than 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, as a starting method of non-invasive respiratory support, preference is given to the method of spontaneous breathing under constant positive pressure in the airways through nasal cannulas. 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 artificial pulmonary ventilation with continuous positive pressure.
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 larger cannulas 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 mechanical ventilation/continuous positive pressure mechanical 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 duration of 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, which prevents 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 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 over 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 inhalation 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. Constant determination of 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 due to 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 an acceptable blood gas composition it is necessary:
- 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 of 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 lung 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 to continuously drip the introduction of sterile distilled water into the humidifier chamber. Due to the high flow rate, 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 chest x-rays than children on conventional 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 of differential diagnosis of 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 with its subsequent 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 penicillin antibiotics 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 the intestinal wall in premature infants.

14149 0

Respiratory distress syndrome (RDS) of newborns (respiratory distress syndrome, hyaline membrane disease) is a disease of newborns, manifested by the development of respiratory failure (RF) immediately after birth or within a few hours after birth, increasing in severity up to 2-4 th day of life, followed by gradual improvement.

RDS is caused by the immaturity of the surfactant system and is characteristic mainly of premature infants.

Epidemiology

According to the literature, RDS is observed in 1% of all children born alive and in 14% of children born weighing less than 2500 g.

Classification

RDS in premature infants is distinguished by clinical polymorphism and is divided into 2 main variants:

■ RDS caused by primary deficiency of the surfactant system;

■ RDS in premature infants with a mature surfactant system, associated with secondary surfactant deficiency due to intrauterine infection.

Etiology

The main etiological factor in RDS is the primary immaturity of the surfactant system. In addition, a secondary disruption of the surfactant system is of great importance, leading to a decrease in the synthesis or increased breakdown of phosphatidylcholines. Secondary disorders are caused by intrauterine or postnatal hypoxia, birth asphyxia, hypoventilation, acidosis, and infectious diseases. In addition, the presence of diabetes mellitus in the mother, birth by cesarean section, male gender, birth as the second of twins, and incompatibility of maternal and fetal blood predispose to the development of RDS.

Pathogenesis

Insufficient synthesis and rapid inactivation of surfactant lead to a decrease in lung compliance, which, combined with impaired chest compliance in premature newborns, causes the development of hypoventilation and insufficient oxygenation. Hypercapnia, hypoxia, and respiratory acidosis occur. This in turn contributes to an increase in resistance in the pulmonary vessels with subsequent intrapulmonary and extrapulmonary shunting of blood. Increased surface tension in the alveoli causes their expiratory collapse with the development of atelectasis and hypoventilation zones. There is further disruption of gas exchange in the lungs, and the number of shunts increases. A decrease in pulmonary blood flow leads to ischemia of alveolocytes and vascular endothelium, which causes changes in the alveolar-capillary barrier with the release of plasma proteins into the interstitial space and the lumen of the alveoli.

Clinical signs and symptoms

RDS manifests itself primarily by symptoms of respiratory failure, which usually develops at birth or 2-8 hours after birth. Increased breathing, flaring of the wings of the nose, retraction of the compliant areas of the chest, participation of auxiliary respiratory muscles in the act of breathing, and cyanosis are noted. On auscultation, weakened breathing and crepitating rales are heard in the lungs. As the disease progresses, the signs of DN are accompanied by symptoms of circulatory disorders (decreased blood pressure, microcirculation disorder, tachycardia, the liver may increase in size). Hypovolemia often develops due to hypoxic damage to the capillary endothelium, which often leads to the development of peripheral edema and fluid retention.

RDS is characterized by a triad of radiological signs that appears in the first 6 hours after birth: diffuse foci of reduced transparency, air bronchogram, decreased airiness of the pulmonary fields.

These common changes are most clearly detected in the lower parts and at the apices of the lungs. In addition, a decrease in lung volume and cardiomegaly of varying severity are noticeable. Nodose-reticular changes observed during X-ray examination, according to most authors, represent diffuse atelectasis.

For edematous-hemorrhagic syndrome, a “blurred” x-ray picture and a decrease in the size of the lung fields are typical, and clinically - the release of foamy fluid mixed with blood from the mouth.

If these signs are not detected by X-ray examination 8 hours after birth, then the diagnosis of RDS seems doubtful.

Despite the non-specificity of radiological signs, examination is necessary to exclude conditions that sometimes require surgical intervention. Radiological signs of RDS disappear after 1-4 weeks, depending on the severity of the disease.

■ chest x-ray;

■ determination of CBS indicators and blood gases;

■ general blood test with determination of platelet count and calculation of the leukocyte intoxication index;

■ determination of hematocrit;

■ biochemical blood test;

■ Ultrasound of the brain and internal organs;

■ Doppler examination of blood flow in the cavities of the heart, vessels of the brain and kidneys (indicated for patients on mechanical ventilation);

■ bacteriological examination (smear from the throat, trachea, stool examination, etc.).

Differential diagnosis

Based only on the clinical picture in the first days of life, it is difficult to distinguish RDS from congenital pneumonia and other diseases of the respiratory system.

Differential diagnosis of RDS is carried out with respiratory disorders (both pulmonary - congenital pneumonia, lung malformations, and extrapulmonary - congenital heart defects, birth injury of the spinal cord, diaphragmatic hernia, tracheoesophageal fistulas, polycythemia, transient tachypnea, metabolic disorders).

When treating RDS, it is extremely important to provide optimal patient care. The main principle of treatment for RDS is the “minimal touch” method. The child should receive only the procedures and manipulations he needs, and the medical and protective regime should be observed in the ward. It is important to maintain optimal temperature conditions, and when treating children with very low body weight, to provide high humidity to reduce fluid loss through the skin.

It is necessary to strive to ensure that a newborn in need of mechanical ventilation is in conditions of neutral temperature (at the same time, oxygen consumption by tissues is minimal).

In children with extreme prematurity, it is recommended to use additional plastic covering for the entire body (internal screen) and special foil to reduce heat loss.

Oxygen therapy

They are carried out to ensure the proper level of tissue oxygenation with minimal risk of oxygen intoxication. Depending on the clinical picture, it is carried out using an oxygen tent or by spontaneous breathing with the creation of constant positive pressure in the respiratory tract, traditional mechanical ventilation, high-frequency oscillatory ventilation.

Oxygen therapy must be administered with caution, as excessive amounts of oxygen can cause damage to the eyes and lungs. Oxygen therapy should be carried out under the control of blood gas composition, avoiding hyperoxia.

Infusion therapy

Correction of hypovolemia is carried out with non-protein and protein colloidal solutions:

Hydroxyethyl starch, 6% solution, iv 10-20 ml/kg/day, until a clinical effect is obtained or

Isotonic solution of sodium chloride intravenously 10-20 ml/kg/day, until a clinical effect is obtained or

Isotonic solution of sodium chloride/calcium chloride/monocarbonate

sodium/glucose IV 10-20 ml/kg/day, until clinical effect is obtained

Albumin, 5-10% solution, iv 10-20 ml/kg/day, until clinical effect is obtained or

Fresh frozen blood plasma IV 10-20 ml/kg/day until clinical effect is obtained. For parenteral nutrition use:

■ from the 1st day of life: a 5% or 10% glucose solution, providing the minimum energy requirement in the first 2-3 days of life (for body weight less than 1000 g, it is advisable to start with a 5% glucose solution, and when introducing a 10% solution, the speed does not must exceed 0.55 g/kg/h);

■ from the 2nd day of life: solutions of amino acids (AA) up to 2.5-3 g/kg/day (it is necessary that per 1 g of administered AA there should be about 30 kcal from non-protein substances; this ratio ensures the plastic function of AA) . If renal function is impaired (increased levels of creatinine and urea in the blood, oliguria), it is advisable to limit the dose of AA to 0.5 g/kg/day;

■ from the 3rd day of life: fat emulsions, starting from 0.5 g/kg/day, with a gradual increase in dose to 2 g/kg/day. In case of impaired liver function and hyperbilirubinemia (more than 100-130 µmol/l), the dose is reduced to 0.5 g/kg/day, and in case of hyperbilirubinemia more than 170 µmol/l, the administration of fat emulsions is not indicated.

Replacement therapy with exogenous surfactants

Exogenous surfactants include:

■ natural - isolated from human amniotic fluid, as well as from the lungs of piglets or calves;

■ semi-synthetic - obtained by mixing crushed cattle lungs with surface phospholipids;

■ synthetic.

Most neonatologists prefer to use natural surfactants. Their use provides faster results, reduces the incidence of complications and reduces the duration of mechanical ventilation:

Colfosceryl palmitate endotracheally 5 ml/kg every 6-12 hours, but not more than 3 times or

Poractant alpha endotracheally 200 mg/kg once,

then 100 mg/kg once (12-24 hours after the first administration), no more than 3 times or

Surfactant BL endotracheally

75 mg/kg (dissolve in 2.5 ml of isotonic sodium chloride solution) every 6-12 hours, but not more than 3 times.

BL surfactant can be administered through the side hole of a special endotracheal tube adapter without depressurizing the respiratory circuit and interrupting mechanical ventilation. The total duration of administration should be no less than 30 and no more than 90 minutes (in the latter case, the drug is administered using a syringe pump, drip-wise). Another method is to use an inhalation solution nebulizer built into the ventilator; in this case, the duration of administration should be 1-2 hours. Within 6 hours after administration, tracheal sanitation should not be carried out. In the future, the drug is administered under the condition of a continuing need for mechanical ventilation with an oxygen concentration in the air-oxygen mixture of more than 40%; the interval between administrations should be at least 6 hours.

Errors and unreasonable assignments

For RDS in newborns weighing less than 1250 g, spontaneous breathing with continuous positive expiratory pressure should not be used during initial therapy.

Forecast

With careful adherence to protocols for antenatal prevention and treatment of RDS and in the absence of complications in children with a gestational age of more than 32 weeks, cure can reach 100%. The younger the gestational age, the lower the likelihood of a favorable outcome.

V.I. Kulakov, V.N. Serov

A pathological condition of newborns that occurs in the first hours and days after birth due to morphofunctional immaturity of the lung tissue and surfactant deficiency. The syndrome of respiratory disorders is characterized by respiratory failure of varying severity (tachypnea, cyanosis, retraction of the compliant areas of the chest, participation of auxiliary muscles in the act of breathing), signs of central nervous system depression and circulatory disorders. Respiratory distress syndrome is diagnosed on the basis of clinical and radiological data, and assessment of surfactant maturity indicators. Treatment of respiratory distress syndrome includes oxygen therapy, infusion therapy, antibiotic therapy, and endotracheal instillation of surfactant.

General information

Respiratory distress syndrome (RDS) is a pathology of the early neonatal period, caused by the structural and functional immaturity of the lungs and the associated disruption of surfactant formation. In foreign neonatology and pediatrics, the term “respiratory distress syndrome” is identical to the concepts of “respiratory distress syndrome”, “hyaline membrane disease”, “pneumopathy”. Respiratory distress syndrome develops in approximately 20% of premature infants (in children born before 27 weeks of gestation - in 82-88% of cases) and 1-2% of full-term newborns. Among the causes of perinatal mortality, respiratory distress syndrome accounts for, according to various sources, from 35 to 75%, which indicates the relevance and largely unresolved problem of caring for children with RDS.

Causes of respiratory distress syndrome

As already indicated, the pathogenesis of respiratory distress syndrome in newborns is associated with the immaturity of the lung tissue and the resulting insufficiency of the anti-atelectatic factor - surfactant, its inferiority, inhibition or increased destruction.

Surfactant is a surface-active lipoprotein layer that covers the alveolar cells and reduces the surface tension of the lungs, i.e., preventing the collapse of the alveolar walls. Surfactant begins to be synthesized by alveolocytes from 25-26 weeks of fetal development, but its most active formation occurs from 32-34 weeks of gestation. Under the influence of many factors, including hormonal regulation by glucocorticoids (cortisol), catecholamines (adrenaline and norepinephrine), estrogens, and thyroid hormones, the maturation of the surfactant system is completed by the 35-36th week of gestation.

Therefore, the lower the gestational age of the newborn, the lower the amount of surfactant in the lungs. In turn, this leads to collapse of the walls of the alveoli during exhalation, atelectasis, a sharp decrease in the area of ​​gas exchange in the lungs, the development of hypoxemia, hypercapnia and respiratory acidosis. Violation of alveolocapillary permeability leads to sweating of plasma from the capillaries and subsequent precipitation of hyaline-like substances onto the surface of bronchioles and alveoli, which further reduces the synthesis of surfactant and contributes to the development of pulmonary atelectasis (hyaline membrane disease). Acidosis and pulmonary hypertension support the preservation of fetal communications (patent foramen ovale and ductus arteriosus) - this also aggravates hypoxia, leading to the development of disseminated intravascular coagulation syndrome, edematous hemorrhagic syndrome, and further disruption of surfactant formation.

The risk of developing respiratory distress syndrome increases with prematurity, morpho-functional immaturity in relation to gestational age, intrauterine infections, fetal hypoxia and asphyxia of the newborn, congenital heart disease, lung malformations, intracranial birth injuries, multiple pregnancy, aspiration of meconium and amniotic fluid, congenital hypothyroidism, etc. Maternal risk factors for the development of respiratory distress syndrome in a newborn include diabetes mellitus, anemia, labor hemorrhage, and delivery by cesarean section.

Classification of respiratory distress syndrome

Based on the etiological principle, respiratory distress syndromes are distinguished: hypoxic, infectious, infectious-hypoxic, endotoxic, genetic (with a genetically determined surfactant pathology) genesis.

Based on developing pathological changes, 3 degrees of severity of respiratory distress syndrome are distinguished.

I (mild degree)– occurs in relatively mature children who have a moderate condition at birth. Symptoms develop only during functional loads: feeding, swaddling, manipulation. RR less than 72/min; the blood gas composition is not changed. The newborn's condition returns to normal within 3-4 days.

II (moderate-severe degree)– the child is born in a serious condition, which often requires resuscitation measures. Signs of respiratory distress syndrome develop within 1-2 hours after birth and persist for up to 10 days. The need for oxygen supplementation usually disappears on the 7th-8th day of life. Against the background of respiratory distress syndrome, every second child develops pneumonia.

III (severe degree)– usually occurs in immature and very premature babies. Signs of respiratory distress syndrome (hypoxia, apnea, areflexia, cyanosis, severe depression of the central nervous system, impaired thermoregulation) appear from the moment of birth. From the cardiovascular system, tachycardia or bradycardia, arterial hypotension, and signs of myocardial hypoxia on the ECG are noted. There is a high probability of death.

Symptoms of respiratory distress syndrome

Clinical manifestations of respiratory distress syndrome usually develop on days 1-2 of a newborn’s life. Shortness of breath appears and intensively increases (respiratory rate up to 60–80 per minute) with the participation of auxiliary muscles in the respiratory act, retraction of the xiphoid process of the sternum and intercostal spaces, and inflation of the wings of the nose. Characteristic features include expiratory noises (“grunting exhalation”) caused by spasm of the glottis, attacks of apnea, cyanosis of the skin (first perioral and acrocyanosis, then general cyanosis), foamy discharge from the mouth, often mixed with blood.

In newborns with respiratory distress syndrome, there are signs of central nervous system depression caused by hypoxia, an increase in cerebral edema, and a tendency to intraventricular hemorrhages. DIC syndrome can manifest itself as bleeding from injection sites, pulmonary hemorrhage, etc. In severe forms of respiratory distress syndrome, acute heart failure with hepatomegaly and peripheral edema rapidly develops.

Other complications of respiratory distress syndrome may include pneumonia, pneumothorax, pulmonary emphysema, pulmonary edema, retinopathy of prematurity, necrotizing enterocolitis, renal failure, sepsis, etc. As a result of respiratory distress syndrome, the child may experience recovery, bronchial hyperreactivity, perinatal encephalopathy, immune disorders, COLD (bullous disease, pneumosclerosis, etc.).

Diagnosis of respiratory distress syndrome

In clinical practice, to assess the severity of respiratory distress syndrome, the I. Silverman scale is used, where the following criteria are assessed in points (from 0 to 2): excursion of the chest, retraction of the intercostal spaces during inspiration, retraction of the sternum, flaring of the nostrils, lowering of the chin during inspiration , expiratory noises. A total score below 5 points indicates a mild degree of respiratory distress syndrome; above 5 – moderate, 6-9 points – severe and from 10 points – extremely severe SDR.

In the diagnosis of respiratory distress syndrome, lung radiography is of decisive importance. The X-ray picture changes in different pathogenetic phases. With diffuse atelectasis, a mosaic pattern is revealed, caused by alternating areas of decreased pneumatization and swelling of the lung tissue. Hyaline membrane disease is characterized by an “air bronchogram” and a reticular-nadose mesh. At the stage of edematous-hemorrhagic syndrome, vagueness, blurring of the pulmonary pattern, massive atelectasis are determined, which determine the picture of the “white lung”.

To assess the degree of maturity of the lung tissue and surfactant system in respiratory distress syndrome, a test is used that determines the ratio of lecithin to sphingomyelin in amniotic fluid, tracheal or gastric aspirate; “foam” test with the addition of ethanol to the analyzed biological fluid, etc. It is possible to use the same tests when conducting invasive prenatal diagnostics - amniocentesis, carried out after 32 weeks of gestation, by a pediatric pulmonologist, pediatric cardiologist, etc.

A child with respiratory distress syndrome needs continuous monitoring of emergency, respiratory rate, blood gas composition, CBS; monitoring indicators of general and biochemical blood tests, coagulograms, ECG. To maintain optimal body temperature, the child is placed in an incubator, where he is provided with maximum rest, mechanical ventilation or inhalation of humidified oxygen through a nasal catheter, and parenteral nutrition. The child periodically undergoes tracheal aspiration, vibration and percussion chest massage.

For respiratory distress syndrome, infusion therapy with a solution of glucose and sodium bicarbonate is carried out; transfusion of albumin and fresh frozen plasma; antibiotic therapy, vitamin therapy, diuretic therapy. An important component of the prevention and treatment of respiratory distress syndrome is endotracheal instillation of surfactant preparations.

Forecast and prevention of respiratory distress syndrome

The consequences of respiratory distress syndrome are determined by the date of delivery, the severity of respiratory failure, additional complications, and the adequacy of resuscitation and treatment measures.

In terms of preventing respiratory distress syndrome, the most important thing is to prevent premature birth. If there is a threat of premature birth, it is necessary to carry out therapy aimed at stimulating the maturation of lung tissue in the fetus (dexamethasone, betamethasone, thyroxine, aminophylline). Premature babies need early (in the first hours after birth) surfactant replacement therapy.

In the future, children who have suffered respiratory distress syndrome, in addition to the local pediatrician, should be observed by a pediatric neurologist, pediatric pulmonologist,

Stenosing laryngitis, croup syndrome

Croup is an acute respiratory disorder, usually accompanied by a low temperature (most often an infection with the parainfluenza virus). With croup, breathing is difficult (inspiratory dyspnea).

Signs of croup

Hoarseness of voice, barking, noisy breathing on inspiration (inspiratory stridor). Signs of severity are pronounced retraction of the jugular fossa and intercostal spaces, a decrease in the level of oxygen in the blood. Grade III croup requires emergency intubation, grade I-II croup is treated conservatively. Epiglottitis should be excluded (see below).

Examination for croup

Measuring blood oxygen saturation - pulse oximetry. The severity of croup is sometimes assessed using the Westley scale (Table 2.2).

Table 2.1. Westley Croup Severity Rating Scale

Symptom severity	Points*
Stridor (noisy breathing)
Absent	0
When excited	1
At rest	2
Retraction of the compliant areas of the chest
Absent	0
Lung	1
Moderately expressed	2
Sharply expressed	3
Airway patency
Normal	0
Moderately damaged	1
Significantly reduced	2
Cyanosis
Absent	0
During physical activity	4
At rest	5
Consciousness
No changes	0
Impaired consciousness	5
* less than 3 points - mild, 3-6 points - moderate, more than 6 points - severe.

Treatment of croup

Most cases of laryngitis and croup are caused by viruses and do not require antibiotics. Budesonide (Pulmicort) is prescribed in inhalation 500-1000 mcg per 1 inhalation (possibly together with bronchodilators salbutamol or the combined drug Berodual - ipratropium bromide + fenoterol), in more severe cases, in the absence of effect from inhalation or with re-development of croup, administered intramuscularly dexamethasone 0.6 mg/kg. In terms of effectiveness, inhaled and systemic glucocorticosteroids (GCS) are the same, but for children under 2 years of age it is better to start treatment with systemic drugs. If necessary, use moistened oxygen and vasoconstrictor nasal drops.

Important!!! Viral croup responds well to treatment with glucocorticoids and does not pose any major therapeutic problems. In a patient with laryngeal stenosis, it is important to immediately rule out epiglottitis.

Epiglottitis

Epiglottitis is an inflammation of the epiglottis. It is most often caused by N. influenzae type b, less commonly by pneumococcus, in 5% of cases - by S. aureus, and is characterized by high fever and intoxication. It is distinguished from viral croup by the absence of catarrh, cough, hoarseness, the presence of a sore throat, limited jaw mobility (trismus), the “tripod” position, increased salivation, as well as a wide open mouth, noisy breathing when inhaling, retraction of the epiglottis in the supine position , leukocytosis > 15x10 9 /l. Inhalation of Pulmicort, administration of prednisolone or dexamethasone do not bring significant relief.

Important!!! Examination of the oropharynx is carried out only in the operating room under general anesthesia, in full readiness to intubate the child.

X-ray of the neck in the lateral projection, recommended by a number of authors, is justified only if there is uncertainty in the diagnosis, since in 30-50% of cases it does not reveal pathology. Determination of blood gases for diagnosis is not necessary: ​​if epiglottitis is suspected, any manipulations other than vital ones are undesirable. It is enough to do a blood test, determine CRP, and perform pulse oximetry.

For the differential diagnosis of viral croup and epilottitis, the following table is used. 2.3 set of features.

Table 2.3. Differential diagnostic criteria for epiglottitis and viral croup (according to DeSoto N., 1998, as amended)

	Epiglottitis	Croup
Age	Any	Most often from 6 months to 6 years
Start	Sudden	Gradual
Localization of stenosis	Above the larynx	Under the larynx
Body temperature	High	Most often low-grade fever
Intoxication	Expressed	Moderate or absent
Dysphagia	Heavy	Absent or mild
Sore throat	Expressed	Moderate or absent
Breathing problems	Eat	Eat
Cough	Rarely	Specific
Patient position	Sits upright with mouth open	Any
X-ray signs	Shadow of an enlarged epiglottis	Spire symptom

Treatment of epiglottitis

Intravenous cefotaxime 150 mg/kg per day (or ceftriaxone 100 mg/kg per day) + aminoglycoside. Cefotaxime should not be administered intramuscularly to children under 2.5 years of age due to pain. If ineffective (staphylococcus!) - intravenous clindamycin 30 mg/kg/day or vancomycin 40 mg/kg/day. Early intubation is indicated (prevention of sudden asphyxia). Extubation is safe after the temperature has normalized, consciousness has cleared and symptoms have subsided, usually after 24-72 hours (before extubation, examination through a flexible endoscope). Epiglottitis is often accompanied by bacteremia, which increases the duration of treatment.

Important!!! If you have epiglottitis, it is forbidden to: inhale, sedate, or provoke anxiety!

Structural approach to the treatment of critical illness in children

Learning Objective

In this section you will learn:

1. about how to recognize a child’s serious condition;
2. about a structural approach to assessing the condition of a child with a serious illness;
3. about a structural approach to resuscitation and intensive care in a child with a serious illness.

Introduction

The prognosis for life in children after cardiac arrest is usually poor. Early and treatment of respiratory, circulatory and cerebral failure helps reduce mortality and improve the outcome of the disease. This section presents symptoms that are used for a quick initial assessment of the condition of a seriously ill child.

Initial assessment of the airway and breathing

Diagnosis of respiratory failure

Breathing effort

The severity of respiratory pathology can be judged by the severity of respiratory effort. The following indicators need to be assessed.

Respiration rate

The normal respiratory rate in children is presented in Table 7.1. Newborns have the highest respiratory rate, and with age it gradually decreases. Single measurements of respiratory rate must be taken with caution: a newborn can breathe from 30 to 90 times per minute, and this depends on his activity.

Table 7.1. Respiratory frequency in children of different ages

According to WHO recommendations, a respiratory rate in infants and young children above 60 per minute, along with other symptoms, is regarded as a sign of pneumonia. In order to assess the dynamics of respiratory failure, it is more important to analyze trends in respiratory rate.

Thus, tachypnea is a reflection of the body’s increased need for hyperventilation due to pathology of the lungs and respiratory tract or due to metabolic acidosis. Bradypnea occurs when the respiratory muscles are tired, the central nervous system is depressed, and also in the preagonal stage of the dying process.

Retraction of the compliant areas of the chest

Retractions of the intercostal spaces, lower thoracic outlet and retraction of the sternum indicate increased work of breathing. These symptoms are more noticeable in newborns and infants because their chest wall is more pliable. The presence of retractions in older children (after 6-7 years) is possible only in the presence of severe breathing pathology. As fatigue develops, the degree of retraction decreases.

Inspiratory and expiratory sounds

Noisy inspiration or inspiratory stridor is a sign of obstruction at the level of the larynx or trachea. With severe obstruction, expiration may also be difficult, but, as a rule, the inspiratory component of stridor is more pronounced. Wheezing occurs due to obstruction of the lower respiratory tract and is best heard during exhalation. A prolonged exhalation also indicates narrowing of the lower airways. The volume of noisy breathing is not a reflection of the severity of the disease.

Granting

Grunting (expiratory grunting or groaning breathing) occurs when air is exhaled through partially closed vocal cords. This reflects an attempt to create positive end-expiratory pressure to prevent end-expiratory alveolar collapse in a patient with hard lungs. This is a sign of severe respiratory distress and is pathognomonic of pneumonia or pulmonary edema in young children. This symptom may also occur in patients with intracranial hypertension, abdominal distension, and peritonitis.

Use of accessory muscles

With increased work of breathing, children, like adults, use auxiliary muscles, primarily the sternocleidomastoid muscles. Infants may experience head nodding movements with each breath, which reduces breathing efficiency.

Nasal alar stretch

This symptom is especially common in infants with respiratory distress.

Gasping breath

This is a sign of severe hypoxia, appearing in the preagonal stage.

Exceptions

Signs of increased work of breathing may be absent or mild in three cases:

1. As fatigue develops in a child with severe respiratory pathology, the severity of symptoms of increased work of breathing decreases. Fatigue is a pregonal sign.
2. When consciousness is depressed in a child with intracranial hypertension, poisoning or encephalopathy, breathing is inadequate and there are no symptoms of increased work of breathing. Inadequate breathing in this case is due to central respiratory depression.
3. In children with neuromuscular diseases (such as spinal amyotrophy or muscular dystrophy), respiratory failure occurs without signs of increased work of breathing.

In children with the pathology described above, respiratory failure is diagnosed based on an assessment of breathing efficiency and other symptoms of inadequate breathing. These symptoms are discussed below.

Breathing efficiency

Assessing the excursion of the chest (or, in newborns, the movement of the anterior abdominal wall) allows us to judge the amount of air entering the lungs. The same information can be obtained by auscultation of the lungs. Attention should be paid to weakening, asymmetry or bronchial breathing. A “silent” chest is an extremely alarming symptom.

To assess arterial blood oxygen saturation (SaO2), the pulse oximetry method is used, the sensitivity of which, however, decreases with SaO2 less than 70%, shock and the presence of carboxyhemoglobin in the blood. The level of SaO2 when breathing air is a good indicator of breathing efficiency. Oxygen therapy masks this information unless hypoxia is very severe. The normal SaO2 level in infants and children is 97-100%.

Effect of respiratory failure on other organs

Heart rate

Hypoxia causes tachycardia in infants and children. Along with this, tachycardia can be a consequence of excitement and increased body temperature. Severe and prolonged hypoxia leads to bradycardia, which is a preagonal symptom.

Skin color

An early symptom of hypoxia is pallor of the skin, which is caused by vasospasm caused by the release of catecholamines. Cyanosis is a preagonal symptom of hypoxia. The progression of central cyanosis in acute respiratory pathology indicates that respiratory arrest may occur in the near future. In a child with anemia, cyanosis does not appear even with deep hypoxia. In some children, cyanosis may be a sign of blue heart disease. The severity of such cyanosis does not change during oxygen therapy.

Level of consciousness

With hypoxia and hypercapnia, the child may be agitated or drowsy. Gradually, the depression of consciousness progresses until it is completely lost. This particularly important and useful symptom is more difficult to identify in young children. Parents may note that the child is “not himself.” During examination, it is necessary to assess the level of consciousness, focusing on such signs as visual concentration, response to voice and, if necessary, response to a painful stimulus. With hypoxic depression of the brain, generalized muscle hypotonia is also observed.

Re-evaluation

Frequent reassessment of respiratory rate, degree of retraction, and other symptoms of respiratory failure is necessary to determine the patient's progress.