Recession of the yielding areas of the chest. Respiratory distress syndrome of the fetus and newborn: when the first breath is difficult

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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 is manifested 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 pulmonary 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 glucose solution of 5% or 10%, providing the minimum energy requirement in the first 2-3 days of life (with a body weight of 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.

IN AND. Kulakov, V.N. Serov

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 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 of the cardiovascular system occurs: 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 (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 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 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 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 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 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 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 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 most likely indicates ventilation with excess tidal volume 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 a gestation period of 26 weeks 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 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 a 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 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 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 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 PIP is selected so that the tidal volume 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 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. 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.

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I. FEATURES OF PATHOGENESIS

Respiratory distress syndrome is the most common pathological condition in newborns in the early neonatal period. Its occurrence is higher, the lower the gestational age and the more often pathological conditions associated with pathology of the respiratory, circulatory and central nervous systems occur. The disease is polyetiological.

The pathogenesis of RDS is based on deficiency or immaturity of surfactant, which leads to diffuse atelectasis. This, in turn, contributes to a decrease in pulmonary compliance, an increase in the work of breathing, and an increase in pulmonary hypertension, resulting in hypoxia, which increases pulmonary hypertension, resulting in a decrease in the synthesis of surfactant, i.e. a vicious circle arises.

Deficiency and immaturity of surfactant are present in the fetus at a gestational age of less than 35 weeks. Chronic intrauterine hypoxia enhances and prolongs this process. Premature babies (especially very premature babies) constitute the first variant of the course of RDS. Even after going through the birth process without any deviations, they can develop a clinic for RDS in the future, because their type II pneumocytes synthesize immature surfactant and are very sensitive to any hypoxia.

Another, much more common variant of RDS, characteristic of newborns, is the reduced ability of pneumocytes to “avalanche-like” synthesize surfactant immediately after birth. Etiotropic factors here are those that disrupt the physiological course of labor. During normal childbirth through the natural birth canal, dosed stimulation of the sympatho-adrenal system occurs. Expansion of the lungs with an effective first breath helps to reduce pressure in the pulmonary circulation, improve the perfusion of pneumocytes and enhance their synthetic functions. Any deviation from the normal course of labor, even planned surgical delivery, can cause a process of insufficient synthesis of surfactant with the subsequent development of RDS.

The most common cause of the development of this variant of RDS is acute asphyxia of newborns. RDS accompanies this pathology, probably in all cases. RDS also occurs with aspiration syndromes, severe birth trauma, diaphragmatic hernia, often during delivery by cesarean section.

The third option for the development of RDS, characteristic of newborns, is a combination of previous types of RDS, which occurs quite often in premature infants.

One can think of acute respiratory distress syndrome (ARDS) in cases where the child underwent the birth process without abnormalities, and subsequently developed a picture of some disease that contributed to the development of hypoxia of any origin, centralization of blood circulation, and endotoxicosis.

It should also be taken into account that the period of acute adaptation in newborns born prematurely or sick increases. It is believed that the period of maximum risk of manifestations of breathing disorders in such children is: for those born from healthy mothers - 24 hours, and for those born from sick mothers it lasts, on average, until the end of 2 days. With persistent high pulmonary hypertension in newborns, fatal shunts persist for a long time, which contribute to the development of acute heart failure and pulmonary hypertension, which are an important component in the formation of RDS in newborns.

Thus, in the first variant of the development of RDS, the trigger point is the deficiency and immaturity of surfactant, in the second - persistent high pulmonary hypertension and the resulting unrealized process of surfactant synthesis. In the third option ("mixed"), these two points are combined. The variant of ARDS formation is due to the development of “shock” lung.

All these variants of RDS are aggravated in the early neonatal period by the limited hemodynamic capabilities of the newborn.

This contributes to the existence of the term “cardiorespiratory distress syndrome” (CRDS).

For more effective and rational treatment of critical conditions in newborns, it is necessary to distinguish between the options for the formation of RDS.

Currently, the main method of intensive therapy for RDS is respiratory support. Most often, mechanical ventilation for this pathology has to start with “hard” parameters, under which, in addition to the danger of barotrauma, hemodynamics are also significantly inhibited. To avoid “hard” parameters of mechanical ventilation with high average pressure in the respiratory tract, it is recommended to start mechanical ventilation preventively, without waiting for the development of interstitial pulmonary edema and severe hypoxia, i.e., those conditions when ARDS develops.

In the case of the expected development of RDS, immediately after birth, one should either “simulate” an effective “first breath”, or prolong effective breathing (in premature infants) with surfactant replacement therapy. In these cases, mechanical ventilation will not be so “hard” and long-lasting. A number of children will have the opportunity, after short-term mechanical ventilation, to carry out SDPPDV through binasal cannulas until the pneumocytes are able to “produce” a sufficient amount of mature surfactant.

Preventive initiation of mechanical ventilation with the elimination of hypoxia without the use of “hard” mechanical ventilation will allow for more effective use of drugs that reduce pressure in the pulmonary circulation.

With this option of starting mechanical ventilation, conditions are created for earlier closure of fetal shunts, which will help improve central and intrapulmonary hemodynamics.

II. DIAGNOSTICS.

A. Clinical signs

1. Symptoms of respiratory failure, tachypnea, chest swelling, nasal flaring, difficulty breathing and cyanosis.
2. Other symptoms, for example, hypotension, oliguria, muscle hypotonia, temperature instability, intestinal paresis, peripheral edema.
3. Prematurity at gestational age assessment.

During the first hours of life, the child undergoes a clinical assessment every hour using the modified Downes scale, on the basis of which a conclusion is made about the presence and dynamics of the course of RDS and the required amount of respiratory assistance.

RDS severity assessment (modified Downes scale)

Points Frequency Cyanosis of breathing per 1 min.	Retraction	Expiratory grunt	Breathing pattern during auscultation
0 < 60 нет при 21%	No	No	puerile
1 60-80 yes, disappears at 40% O2	moderate	listens- stethoscope	changed weakened
2 > 80 disappears or apnea with	significant	audible distance	Badly held

A score of 2-3 points corresponds to mild RDS

A score of 4-6 points corresponds to moderate RDS

A score of more than 6 points corresponds to severe RDS

B. CHEST X-RAY. Characteristic nodular or round opacities and an air bronchogram indicate diffuse atelectasis.

B. LABORATORY SIGNS.

1. Lecithin/Sphyringomyelin ratio in amniotic fluid less than 2.0 and negative shake test results in amniotic fluid and gastric aspirate. In newborns from mothers with diabetes mellitus, RDS can develop when L/S is more than 2.0.
2. Lack of phosphatildiglycerol in amniotic fluid.

In addition, when the first signs of RDS appear, Hb/Ht, glucose and leukocyte levels, and, if possible, CBS and blood gases should be examined.

III. COURSE OF THE DISEASE.

A. RESPIRATORY FAILURE, increasing over 24-48 hours and then stabilizing.

B. RESOLUTION is often preceded by an increase in the rate of urine output between 60 and 90 hours of life.

IV. PREVENTION

In case of premature birth at 28-34 weeks, an attempt should be made to slow down labor by using beta-mimetics, antispasmodics or magnesium sulfate, followed by glucocorticoid therapy according to one of the following regimens:

• - betamethasone 12 mg IM - after 12 hours - twice;
• - dexamethasone 5 mg IM - every 12 hours - 4 injections;
• - hydrocortisone 500 mg IM - every 6 hours - 4 injections. The effect occurs within 24 hours and lasts for 7 days.

In case of prolonged pregnancy, beta or dexamethasone 12 mg intramuscularly should be administered weekly. A contraindication for the use of glucocorticoids is the presence of a viral or bacterial infection in a pregnant woman, as well as a peptic ulcer.

When using glucocorticoids, blood sugar should be monitored.

If delivery by cesarean section is expected, if conditions exist, delivery should begin with an amniotomy performed 5-6 hours before surgery in order to stimulate the fetal sympathetic-adrenal system, which stimulates its surfactant system. In case of critical condition of the mother and fetus, amniotomy is not performed!

Prevention is facilitated by careful extraction of the fetal head during cesarean section, and in very premature infants, extraction of the fetal head in the amniotic sac.

V. TREATMENT.

The goal of RDS therapy is to support the newborn until the disease resolves. Oxygen consumption and carbon dioxide production can be reduced by maintaining optimal temperature conditions. Since renal function may be impaired during this period and perspiration losses increase, it is very important to carefully maintain fluid and electrolyte balance.

A. Maintaining airway patency

1. Lay the newborn down with the head slightly extended. Turn the baby. This improves drainage of the tracheobronchial tree.
2. Suction from the trachea is required to sanitize the tracheobronchial tree from thick sputum that appears during the exudative phase, which begins at approximately 48 hours of life.

B. Oxygen therapy.

1. The warmed, moistened and oxygenated mixture is given to the newborn in a tent or through an endotracheal tube.
2. Oxygenation should be maintained between 50 and 80 mmHg, and saturation between 85% and 95%.

B. Vascular access

1. An umbilical venous catheter, the tip of which is located above the diaphragm, can be useful in providing venous access and measuring central venous pressure.

D. Correction of hypovolemia and anemia

1. Monitor central hematocrit and blood pressure starting after birth.
2. During the acute phase, maintain hematocrit between 45-50% with transfusions. In the resolution phase, it is sufficient to maintain a hematocrit greater than 35%.

D. Acidosis

1. Metabolic acidosis (ME)<-6 мЭкв/л) требует выявления возможной причины.
2. Base deficiencies less than -8 mEq/L usually require correction to maintain a pH greater than 7.25.
3. If the pH drops below 7.25 due to respiratory acidosis, then artificial or assisted ventilation is indicated.

E. Feeding

1. If the hemodynamics of the newborn are stable and you manage to relieve respiratory failure, then feeding should begin at 48-72 hours of life.
2. Avoid pacifier feeding if shortness of breath exceeds 70 breaths per minute because... high risk of aspiration.
3. If enteral feeding is not possible, consider parenteral nutrition.
4. Vitamin A parenterally, 2000 units every other day, until enteral feeding is started, reduces the incidence of chronic lung diseases.

G. Chest X-ray

1. To make a diagnosis and assess the course of the disease.
2. To confirm the placement of the endotracheal tube, chest tube and umbilical catheter.
3. For the diagnosis of complications such as pneumothorax, pneumopericardium and necrotizing enterocolitis.

H. Excitement

1. Deviations of PaO2 and PaCO2 can and are caused by excitation. Such children should be handled very carefully and touched only when indicated.
2. If the newborn is not synchronized with the ventilator, sedation or muscle relaxation may be necessary to synchronize with the device and prevent complications.

I. Infection

1. In most newborns with respiratory failure, sepsis and pneumonia should be excluded, so it is advisable to prescribe empirical antibiotic therapy with broad-spectrum bactericidal antibiotics until culture results are confirmed.
2. Group B hemolytic streptococcus infection may clinically and radiologically resemble RDS.

K. Therapy of acute respiratory failure

1. The decision to use respiratory support techniques should be based on the medical history.
2. In newborns weighing less than 1500 g, the use of CPAP techniques may lead to unnecessary energy expenditure.
3. You should initially try to adjust the ventilation parameters to reduce FiO2 to 0.6-0.8. Typically, this requires maintaining an average pressure within 12-14 cmH2O.

• A. When PaO2 exceeds 100 mmHg, or there are no signs of hypoxia, FiO2 should be gradually reduced by no more than 5% to 60%-65%.
• b. The effect of reducing ventilation parameters is assessed after 15-20 minutes using blood gas analysis or a pulse oximeter.
• V. At low oxygen concentrations (less than 40%), a reduction in FiO2 of 2%-3% is sufficient.

5. In the acute phase of RDS, carbon dioxide retention may occur.

• A. Maintain pCO2 less than 60 mmHg by varying ventilation rates or peak pressures.
• b. If your attempts to stop hypercapnia lead to impaired oxygenation, consult with more experienced colleagues.

L. Reasons for the deterioration of the patient’s condition

1. Rupture of the alveoli and the development of interstitial pulmonary emphysema, pneumothorax or pneumopericardium.
2. Violation of the tightness of the breathing circuit.

• A. Check the connection points of the equipment to the source of oxygen and compressed air.
• b. Rule out endotracheal tube obstruction, extubation, or tube advancement into the right main bronchus.
• V. If endotracheal tube obstruction or self-extubation is detected, remove the old endotracheal tube and ventilate the child with a bag and mask. Reintubation is best done after the patient's condition has stabilized.

3. In very severe RDS, shunting of blood from right to left through the ductus arteriosus may occur.

4. When the function of external respiration improves, the resistance of the pulmonary vessels can sharply decrease, causing shunting through the ductus arteriosus from left to right.

5. Much less often, deterioration of the condition of newborns is caused by intracranial hemorrhage, septic shock, hypoglycemia, kernicterus, transient hyperammonemia, or inborn defects of metabolism.

Scale for selecting some parameters of mechanical ventilation in newborns with RDS

Body weight, g		< 1500	> 1500
	PEEP, see H2O	PIP, see H2O	PIP, see H2O

Note: This diagram is a guide only. Ventilator parameters can be changed based on the clinical picture of the disease, blood gases and CBS and pulse oximetry data.

Criteria for the use of respiratory therapy measures

	FiO2 required to maintain pO2 > 50 mmHg.
<24 часов	0,65	Non-invasive methods (O2 therapy, SDPPDV) Tracheal intubation (IVL, VIVL)
>24 hours	0,80	Non-invasive methods Tracheal intubation

M. Surfactant therapy

• A. Human, synthetic and animal surfactants are currently being tested. In Russia, the surfactant EXOSURF NEONATAL, from Glaxo Wellcome, is approved for clinical use.
• b. It is prescribed prophylactically in the delivery room or later, within a period of 2 to 24 hours. Prophylactic use of surfactant is indicated for: premature newborns with a birth weight of less than 1350 g with a high risk of developing RDS; newborns weighing more than 1350 g with lung immaturity confirmed by objective methods. For therapeutic purposes, surfactant is used in newborns with a clinically and radiologically confirmed diagnosis of RDS who are on mechanical ventilation through an endotracheal tube.
• V. It is administered into the respiratory tract in the form of a suspension in fiera solution. For preventive purposes, Exosurf is administered 1 to 3 times, for therapeutic purposes - 2 times. A single dose of Exosurf in all cases is 5 ml/kg. and is administered as a bolus in two half doses over a period of time from 5 to 30 minutes, depending on the child’s reaction. It is safer to administer the solution micro-jet at a rate of 15-16 ml/hour. A repeat dose of Exosurf is administered 12 hours after the initial dose.
• d. Reduces the severity of RDS, but the need for mechanical ventilation remains and the incidence of chronic lung diseases does not decrease.

VI. TACTICAL EVENTS

The team of specialists for the treatment of RDS is headed by a neonatologist. trained in resuscitation and intensive care or a qualified resuscitator.

From LU with URNP 1 - 3, it is mandatory to contact the RCCN and face-to-face consultation on the 1st day. Rehospitalization to a specialized center for resuscitation and intensive care of newborns after stabilization of the patient’s condition after 24-48 hours by the RCBN.

It occurs in 6.7% of newborns.

Respiratory distress is characterized by several main clinical signs:

• cyanosis;
• tachypnea;
• retraction of the pliable areas of the chest;
• noisy exhalation;
• flaring of the wings of the nose.

To assess the severity of respiratory distress, the Silverman and Anderson scale is sometimes used, which evaluates the synchrony of movements of the chest and abdominal wall, retraction of the intercostal spaces, retraction of the xiphoid process of the sternum, expiratory “grunting,” and flaring of the wings of the nose.

A wide range of causes of respiratory distress in the neonatal period are represented by acquired diseases, immaturity, genetic mutations, chromosomal abnormalities, and birth injuries.

Respiratory distress after birth occurs in 30% of preterm infants, 21% of postterm infants, and only 4% of full-term infants.

CHDs occur in 0.5-0.8% of live births. The incidence is higher in stillbirths (3-4%), spontaneous miscarriages (10-25%) and preterm neonates (about 2%), excluding PDA.

Epidemiology: Primary (idiopathic) RDS occurs:

• Approximately 60% of premature babies< 30 недель гестации.
• Approximately 50-80% of preterm infants< 28 недель гестации или весом < 1000 г.
• Almost never in preterm infants >35 weeks gestation.

Causes of respiratory distress syndrome (RDS) in newborns

• Surfactant deficiency.
• Primary (I RDS): idiopathic RDS of prematurity.
• Secondary (ARDS): surfactant consumption (ARDS). Possible reasons:
  • Perinatal asphyxia, hypovolemic shock, acidosis
  • Infections such as sepsis, pneumonia (eg, group B streptococci).
  • Meconium aspiration syndrome (MAS).
  • Pneumothorax, pulmonary hemorrhage, pulmonary edema, atelectasis.

Pathogenesis: a disease of morphologically and functionally immature lungs caused by surfactant deficiency. Surfactant deficiency leads to collapse of the alveoli and, thereby, to a decrease in compliance and functional residual capacity of the lungs (FRC).

Risk factors for respiratory distress syndrome (RDS) in newborns

Increased risk in preterm birth, in boys, family predisposition, primary cesarean section, asphyxia, chorioamnionitis, hydrops, maternal diabetes.

Reduced risk with intrauterine “stress”, premature rupture of membranes without chorioamnionitis, maternal hypertension, drug use, low weight for gestational age, use of corticosteroids, tocolysis, thyroid medication.

Symptoms and signs of respiratory distress syndrome (RDS) in newborns

Onset - immediately after birth or (secondary) hours later:

• Respiratory failure with retractions (intercostal space, hypochondrium, jugular zones, xiphoid process).
• Dyspnea, tachypnea > 60/min, groan on exhalation, retraction of the wings of the nose.
• Hypoxemia. hypercapnia, increased oxygen demand.

To determine the cause of respiratory distress in a newborn, look for:

• Paleness of the skin. Causes: anemia, bleeding, hypoxia, birth asphyxia, metabolic acidosis, hypoglycemia, sepsis, shock, adrenal insufficiency. Pale skin in children with low cardiac output occurs due to shunting of blood from the surface to vital organs.
• Arterial hypotension. Causes: hypovolemic shock (bleeding, dehydration), sepsis, intrauterine infection, dysfunction of the cardiovascular system (CHD, myocarditis, myocardial ischemia), air leak syndromes (ALS), effusion in the pleural cavity, hypoglycemia, adrenal insufficiency.
• Cramps. Causes: HIE, cerebral edema, intracranial hemorrhage, central nervous system abnormalities, meningitis, hypocalcemia, hypoglycemia, benign familial seizures, hypo- and hypernatremia, inborn errors of metabolism, withdrawal syndrome, in rare cases, pyridoxine dependence.
• Tachycardia. Causes: arrhythmia, hyperthermia, pain, hyperthyroidism, administration of catecholamines, shock, sepsis, heart failure. Basically, any stress.
• Heart murmur. A murmur that persists after 24-48 hours or in the presence of other symptoms of heart disease requires identification of the cause.
• Lethargy (stupor). Causes: infection, DIE, hypoglycemia, hypoxemia, sedation/anesthesia/analgesia, inborn errors of metabolism, congenital pathology of the central nervous system.
• CNS excitation syndrome. Causes: pain, central nervous system pathology, withdrawal syndrome, congenital glaucoma, infections. Basically, any feeling of discomfort. Hyperactivity in premature newborns can be a sign of hypoxia, pneumothorax, hypoglycemia, hypocalcemia, neonatal thyrotoxicosis, bronchospasm.
• Hyperthermia. Reasons: high ambient temperature, dehydration, infections, central nervous system pathology.
• Hypothermia. Causes: infection, shock, sepsis, central nervous system pathology.
• Apnea. Causes: prematurity, infections, DIE, intracranial hemorrhage, metabolic disorders, drug-induced depression of the central nervous system.
• Jaundice in the first 24 hours of life. Causes: hemolysis, sepsis, intrauterine infections.
• Vomiting in the first 24 hours of life. Causes: gastrointestinal (GIT) obstruction, high intracranial pressure (ICP), sepsis, pyloric stenosis, milk allergy, stress ulcers, duodenal ulcer, adrenal insufficiency. Vomiting of dark blood is usually a sign of serious illness; if the condition is satisfactory, ingestion of maternal blood can be assumed.
• Bloating. Causes: obstruction or perforation of the gastrointestinal tract, enteritis, intra-abdominal tumors, necrotizing enterocolitis (NEC), sepsis, peritonitis, ascites, hypokalemia.
• Muscular hypotonia. Causes: immaturity, sepsis, HIE, metabolic disorders, withdrawal syndrome.
• Sclerema. Causes: hypothermia, sepsis, shock.
• Stridor. It is a symptom of airway obstruction and can be of three types: inspiratory, expiratory and biphasic. The most common cause of inspiratory stridor is laryngomalacia, expiratory stridor is tracheo- or bronchomalacia, and biphasic stridor is vocal cord paralysis and subglottic stenosis.

Cyanosis

The presence of cyanosis indicates a high concentration of oxygen-unsaturated hemoglobin due to deterioration of the ventilation-perfusion ratio, right-to-left shunting, hypoventilation or impaired oxygen diffusion (structural immaturity of the lungs, etc.) at the level of the alveoli. It is believed that cyanosis of the skin appears when saturation, SaO 2<85% (или если концентрация деоксигенированного гемоглобина превышает 3 г в 100 мл крови). У новорожденных концентрация гемоглобина высокая, а периферическая циркуляция часто снижена, и цианоз у них может наблюдаться при SaO 2 90%. SaO 2 90% и более при рождении не может полностью исключить ВПС «синего» типа вследствие возможного временного постнатального функционирования сообщений между правыми и левыми отделами сердца. Следует различать периферический и центральный цианоз. Причиной центрального цианоза является истинное снижение насыщения артериальной крови кислородом (т.е. гипоксемия). Клинически видимый цианоз при нормальной сатурации (или нормальном PaO 2) называется периферическим цианозом. Периферический цианоз отражает снижение сатурации в локальных областях. Центральный цианоз имеет респираторные, сердечные, неврологические, гематологические и метаболические причины. Осмотр кончика языка может помочь в диагностике цианоза, поскольку на его цвет не влияет тип человеческой расы и кровоток там не снижается, как на периферических участках тела. При периферическом цианозе язык будет розовым, при центральном - синим. Наиболее частыми патологическими причинами периферического цианоза являются гипотермия, полицитемия, в редких случаях сепсис, гипогликемия, гипоплазия левых отделов сердца. Иногда верхняя часть тела может быть цианотичной, а нижняя розовой. Состояния, вызывающие этот феномен: транспозиция магистральных сосудов с легочной гипертензией и шунтом через ОАП, тотальный аномальный дренаж легочных вен выше диафрагмы с ОАП. Встречается и противоположная ситуация, когда верхняя часть тела розовая, а нижняя синяя.

Acrocyanosis of a healthy newborn in the first 48 hours of life is not a sign of disease, but indicates vasomotor instability, blood sludge (especially with some hypothermia) and does not require examination and treatment of the child. Measuring and monitoring oxygen saturation in the delivery room is useful in identifying hypoxemia before the onset of clinically obvious cyanosis.

With pronounced anatomical changes, cardiopulmonary distress can be caused by coarctation of the aorta, hypoplasia of the right heart, tetralogy of Fallot, and large septal defects. Since cyanosis is one of the leading symptoms of congenital heart disease, it is proposed to conduct pulse oximetry screening for all newborns before discharge from the maternity hospital.

Tachypnea

Tachypnea in newborns is defined as a RR greater than 60 per minute. Tachypnea can be a symptom of a wide range of diseases of both pulmonary and non-pulmonary etiology. The main reasons leading to tachypnea: hypoxemia, hypercapnia, acidosis or an attempt to reduce the work of breathing in restrictive lung diseases (in obstructive diseases, the opposite pattern is “beneficial” - rare and deep breathing). At high RR, expiratory time decreases, residual volume in the lungs increases, and oxygenation increases. MOB also increases, which reduces PaCO 2 and increases pH as a compensatory response to respiratory and/or metabolic acidosis and hypoxemia. The most common respiratory problems leading to tachypnea are RDS and TTN, but, in principle, this is typical for any lung disease with low compliance; non-pulmonary diseases - PPH, congenital heart disease, infections of newborns, metabolic disorders, pathology of the central nervous system, etc. Some newborns with tachypnea may be healthy (“happy tachypneic infants”). Periods of tachypnea during sleep are possible in healthy children.

In children with damage to the lung parenchyma, tachypnea is usually accompanied by cyanosis when breathing air and disturbances in the “mechanics” of breathing; in the absence of parenchymal lung disease, newborns often have only tachypnea and cyanosis (for example, with congenital heart disease).

Retraction of the pliable areas of the chest

Recession of the pliable areas of the chest is a common symptom of lung diseases. The lower the pulmonary compliance, the more pronounced this symptom is. A decrease in retractions over time, all other things being equal, indicates an increase in pulmonary compliance. There are two types of retractions. Obstruction of the upper respiratory tract is characterized by retraction of the suprasternal fossa, in the supraclavicular regions, and in the submandibular region. In diseases with reduced compliance of the lungs, retraction of the intercostal spaces and retraction of the sternum are observed.

Noisy exhalation

Lengthening expiration serves to increase lung FOB, stabilize alveolar volume, and improve oxygenation. A partially closed glottis produces a characteristic sound. Depending on the severity of the condition, noisy exhalation may occur periodically or be constant and loud. Endotracheal intubation without CPAP/PEEP eliminates the effect of a closed glottis and can lead to a drop in FRC and a decrease in PaO 2 . Equivalent to this mechanism, PEEP/CPAP should be maintained at 2-3 cmH2O. Noisy exhalation is more common with pulmonary causes of distress and is not usually seen in children with heart disease until the condition has become extremely deteriorating.

Nose flaring

The physiological basis of the symptom is a decrease in aerodynamic resistance.

Complications of respiratory distress syndrome (RDS) in newborns

• Patent ductus arteriosus, PFC syndrome = persistent pulmonary hypertension of the newborn.
• Necrotizing enterocolitis.
• Intracranial bleeding, periventricular leukomalacia.
• Without treatment - bradycardia, cardiac and respiratory arrest.

Diagnosis of respiratory distress syndrome (RDS) in newborns

Survey

At the initial stage, one should assume the most common causes of distress (lung immaturity and congenital infections), after excluding them, think about rarer causes (CHD, surgical diseases, etc.).

Mother's history. The following information will help make a diagnosis:

• gestational age;
• age;
• chronic diseases;
• blood group incompatibility;
• infectious diseases;
• fetal ultrasound data;
• fever;
• polyhydramnios/oligohydramnios;
• preeclampsia/eclampsia;
• taking medications/drugs;
• diabetes;
• multiple pregnancy;
• use of antenatal glucocorticoids (AGC);
• How did your previous pregnancy and childbirth end?

Course of labor:

• duration;
• anhydrous interval;
• bleeding;
• C-section;
• fetal heart rate (HR);
• breech presentation;
• the nature of the amniotic fluid;
• labor analgesia/anesthesia;
• mother's fever.

Newborn:

• assess the degree of prematurity and maturity at gestational age;
• assess the level of spontaneous activity;
• skin color;
• cyanosis (peripheral or central);
• muscle tone, symmetry;
• characteristics of a large fontanelle;
• measure body temperature in the armpit;
• RR (normal values ​​are 30-60 per minute), breathing pattern;
• Heart rate at rest (normal values ​​for full-term babies are 90-160 per minute, for premature babies - 140-170 per minute);
• the size and symmetry of chest excursions;
• when sanitation of the trachea, evaluate the quantity and quality of the secretion;
• insert a tube into the stomach and evaluate its contents;
• Auscultation of the lungs: the presence and nature of wheezing, their symmetry. Immediately after birth, wheezing may occur due to incomplete absorption of fetal lung fluid;
• Auscultation of the heart: heart murmur;
• "white spot" symptom:
• blood pressure (BP): if congenital heart disease is suspected, blood pressure should be measured in all 4 limbs. Normally, blood pressure in the lower extremities is slightly higher than blood pressure in the upper extremities;
• assess the pulsation of peripheral arteries;
• measure pulse pressure;
• palpation and auscultation of the abdomen.

Acid-base state

Acid-base status (ABS) is recommended to be determined in any newborn who requires oxygen for more than 20-30 minutes after birth. The absolute standard is the determination of CBS in arterial blood. Umbilical artery catheterization remains a popular technique in newborns: the insertion technique is relatively simple, the catheter is easy to fix, with proper monitoring there are few complications, and invasive blood pressure determination is also possible.

Respiratory distress can be accompanied by respiratory failure (RF), or it can develop without it. DN can be defined as a disruption in the ability of the respiratory system to maintain adequate homeostasis of oxygen and carbon dioxide.

X-ray of the chest organs

It is a necessary part of the assessment of all patients with respiratory distress.

Please pay attention to:

• location of the stomach, liver, heart;
• heart size and shape;
• pulmonary vascular pattern;
• transparency of the lung fields;
• diaphragm level;
• symmetry of the hemidiaphragm;
• PEF, pleural effusion;
• location of the endotracheal tube (ETT), central catheters, drainages;
• fractures of ribs, collarbones.

Hyperoxic test

The hyperoxic test can help differentiate a cardiac from a pulmonary cause of cyanosis. To carry it out, it is necessary to determine arterial blood gases in the umbilical and right radial arteries or carry out transcutaneous oxygen monitoring in the area of ​​the right subclavian fossa and on the abdomen or chest. Pulse oximetry is much less useful. Arterial oxygen and carbon dioxide are determined when breathing air and after 10-15 minutes of breathing with 100% oxygen to completely replace alveolar air with oxygen. It is believed that with “blue” type congenital heart disease there will not be a significant increase in oxygenation, with PPH without a powerful right-to-left shunt it will increase, and with pulmonary diseases it will increase significantly.

If the PaO 2 value in the preductal artery (right radial artery) is 10-15 mm Hg. more than in the postductal artery (umbilical artery), this indicates a right-to-left shunt through the AN. A significant difference in PaO 2 may occur with PPH or left heart obstruction with bypass through the AP. The response to breathing 100% oxygen should be interpreted depending on the overall clinical picture, especially the degree of pulmonary pathology on the radiograph.

To distinguish severe PLH from blue-type CHD, a hyperventilation test is sometimes performed to increase the pH to a level greater than 7.5. Mechanical ventilation begins at a rate of about 100 breaths per minute for 5-10 minutes. At high pH, ​​pressure in the pulmonary artery decreases, pulmonary blood flow and oxygenation increase with PLH and almost does not increase with blue-type congenital heart disease. Both tests (hyperoxic and hyperventilation) have rather low sensitivity and specificity.

Clinical blood test

You need to pay attention to the changes:

• Anemia.
• Neutropenia. Leukopenia/leukocytosis.
• Thrombocytopenia.
• The ratio of immature forms of neutrophils and their total number.
• Polycythemia. May cause cyanosis, respiratory distress, hypoglycemia, neurological disorders, cardiomegaly, heart failure, PLH. The diagnosis should be confirmed by central venous hematocrit.

C-reactive protein, procalcitonin

The level of C-reactive protein (CRP) usually increases in the first 4-9 hours after the onset of infection or injury, its concentration may increase over the next 2-3 days and remains elevated as long as the inflammatory response persists. The upper limit of normal values ​​in newborns is accepted by most researchers as 10 mg/l. The concentration of CRP increases not in all, but only in 50–90% of newborns with early systemic bacterial infections. However, other conditions - asphyxia, RDS, maternal fever, chorioamnionitis, prolonged anhydrous period, intraventricular hemorrhage (IVH), meconium aspiration, NEC, tissue necrosis, vaccination, surgery, intracranial hemorrhage, resuscitation with chest compressions - can cause similar changes .

Procalcitonin concentrations may increase within hours of infection becoming systemic, regardless of gestational age. The sensitivity of the method as a marker of early infections is reduced by the dynamics of this indicator in healthy newborns after birth. In them, the concentration of procalcitonin increases to a maximum at the end of the first - beginning of the second day of life and then decreases to less than 2 ng/ml by the end of the second day of life. A similar pattern was also found in premature newborns; the level of procalcitonin decreases to normal levels only after 4 days. life.

Blood and cerebrospinal fluid culture

If sepsis or meningitis is suspected, blood and cerebrospinal fluid (CSF) cultures should be obtained, preferably before antibiotics are prescribed.

Concentration of glucose and electrolytes (Na, K, Ca, Md) in blood serum

It is necessary to determine the levels of glucose and electrolytes (Na, K, Ca, Mg) in the blood serum.

Electrocardiography

Echocardiography

Echocardiography (EchoCG) is the standard examination method for suspected congenital heart disease and pulmonary hypertension. An important condition for obtaining valuable information will be to perform the study by a doctor with experience in performing cardiac ultrasound in newborns.

Treatment of respiratory distress syndrome (RDS) in newborns

For a child in extremely serious condition, the basic rules of resuscitation should certainly be followed:

• A - ensure airway patency;
• B - ensure breathing;
• C - ensure circulation.

The causes of respiratory distress must be quickly recognized and appropriate treatment instituted. You should:

• Conduct constant monitoring of blood pressure, heart rate, respiratory rate, temperature, continuous or periodic monitoring of oxygen and carbon dioxide.
• Determine the level of respiratory support (oxygen therapy, CPAP, mechanical ventilation). Hypoxemia is much more dangerous than hypercapnia and requires immediate correction.
• Depending on the severity of DN, it is recommended:
  • Spontaneous breathing with supplemental oxygen (oxygen tent, cannulas, mask) is usually used for mild DN, without apnea, with almost normal pH and PaCO 2, but low oxygenation (SaO 2 when breathing air less than 85-90%). If low oxygenation remains during oxygen therapy, with FiO 2 >0.4-0.5 the patient is transferred to CPAP through nasal catheters (nCPAP).
  • nCPAP - used for moderately severe DN, without severe or frequent episodes of apnea, with pH and PaCO 2 below normal, but within reasonable limits. Condition: stable hemodynamics.
  • Surfactant?
• Minimum number of manipulations.
• Insert a naso- or orogastric tube.
• Provide an axillary temperature of 36.5-36.8°C. Hypothermia can cause peripheral vasoconstriction and metabolic acidosis.
• Give intravenous fluid if it is impossible to absorb enteral nutrition. Maintaining normoglycemia.
• In case of low cardiac output, arterial hypotension, increasing acidosis, poor peripheral perfusion, low diuresis, you should consider intravenous administration of NaCl solution over 20-30 minutes. It is possible to administer dopamine, dobutamine, adrenaline, and glucocorticosteroids (GCS).
• For congestive heart failure: reduction of preload, inotropes, digoxin, diuretics.
• If a bacterial infection is suspected, antibiotics should be prescribed.
• If it is not possible to perform echocardiography and there is a suspicion of ductus-dependent congenital heart disease, prostaglandin E 1 should be prescribed with an initial injection rate of 0.025-0.01 mcg/kg/min and titrated to the lowest working dose. Prostaglandin E 1 maintains the AP open and increases pulmonary or systemic blood flow depending on the pressure difference in the aorta and pulmonary artery. The reasons for the ineffectiveness of prostaglandin E 1 may be incorrect diagnosis, large gestational age of the newborn, or the absence of AP. With some heart defects, there may be no effect or even worsening of the condition.
• After initial stabilization, the cause of respiratory distress should be identified and treated.

Surfactant therapy

Indications:

• FiO 2 > 0.4 and/or
• PIP > 20 cm H20 (in premature infants< 1500 г >15 cm H 2 O) and/or
• PEEP > 4 and/or
• Ti > 0.4 sec.
• In premature babies< 28 недель гестации возможно введение сурфактанта еще в родзале, предусмотреть оптимальное наблюдение при транспортировке!

Practical approach:

• When administering surfactant, 2 people should always be present.
• It is good to sanitize the child and stabilize as much as possible (BP). Keep your head straight.
• Pre-install pO 2 / pCO 2 sensors to ensure stable measurements.
• If possible, attach the SpO 2 sensor to the right handle (preductal).
• A bolus of surfactant is administered through a sterile gastric tube shortened to the length of the endotracheal tube or an additional tube over a period of approximately 1 minute.
• Dosage: Alveofact 2.4 ml/kg = 100 mg/kg. Curosurf 1.3 ml/kg = 100 mg/kg. Survanta 4 ml/kg = 100 mg/kg.

Effects of using surfactant:

Increased tidal volume and FRC:

• PaCO 2 drop
• Increase in paO 2 .

Actions after administration: increase PIP by 2 cm H 2 O. Now the tense (and dangerous) phase begins. The child should be observed extremely carefully for at least one hour. Fast and continuous optimization of respirator settings.

Priorities:

• Reduce PIP while increasing tidal volume due to improved compliance.
• Reduce FiO 2 if SpO 2 increases.
• Then reduce PEEP.
• Finally, reduce Ti.
• Often ventilation improves dramatically only to deteriorate again 1-2 hours later.
• Sanitation of the endotracheal tube without rinsing is allowed! It makes sense to use TrachCare, since PEEP and MAP are preserved during rehabilitation.
• Repeat dose: The 2nd dose (calculated as for the first) can be used after 8-12 hours if ventilation parameters deteriorate again.

Attention: The 3rd or even 4th dose in most cases does not bring further success, and there may even be a deterioration in ventilation due to airway obstruction by large quantities of surfactant (usually more harm than good).

Attention: Reducing PIP and PEEP too slowly increases the risk of barotrauma!

Lack of response to surfactant therapy may indicate:

• ARDS (inhibition of surfactant proteins by plasma proteins).
• Severe infections (eg caused by group B streptococci).
• Meconium aspiration or pulmonary hypoplasia.
• Hypoxia, ischemia or acidosis.
• Hypothermia, peripheral hypotension. D Caution: Side effects."
• Blood pressure drop.
• Increased risk of IVH and PVL.
• Increased risk of pulmonary hemorrhage.
• Discussed: increased incidence of PDA.

Prevention of respiratory distress syndrome (RDS) in newborns

Prophylactic intratracheal surfactant therapy used in newborns.

Induction of lung maturation by administration of betamethasone to a pregnant woman in the last 48 hours before delivery of a premature pregnancy until the end of the 32nd week (possibly until the end of the 34th week of gestation).

Prevention of neonatal infection by peripartum antibacterial prophylaxis in pregnant women with suspected chorioamnionitis.

Optimal correction of diabetes mellitus in pregnant women.

Very careful management of childbirth.

Gentle but persistent resuscitation of premature and full-term infants.

Prognosis of respiratory distress syndrome (RDS) in newborns

Very variable, depending on the initial conditions.

Danger, for example, pneumothorax, BPD, retinopathy, secondary infection during mechanical ventilation.

Results of long-term studies:

• Lack of effect from using surfactant; on the incidence of retinopathy of prematurity, NEC, BPD or PDA.
• Beneficial effect of surfactan-1 administration on the development of pneumothorax, interstitial emphysema and mortality.
• Shortening the duration of ventilation (on a tracheal tube, CPAP) and reducing mortality.

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
Without 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. Most often caused by N. influenzae type b, less often by pneumococcus, in 5% of cases - by S. aureus, 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 during inspiration, 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
A 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 temperature normalizes, consciousness clears and symptoms subside, 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!