Respiratory distress syndrome in children. Neonatal respiratory distress syndrome (RDS)

Neonatal respiratory distress syndrome (RDS)

ICD 10: P22.0

Year of approval (revision frequency): 2016 (reviewed every 3 years)

ID: KR340

Professional associations:

• Russian Association of Perinatal Medicine Specialists
• Russian Society of Neonatologists

Approved

Russian Association specialists in perinatal medicine __ __________201_

Agreed

Russian Society of Neonatologists __ __________201_ Scientific Council of the Ministry of Health of the Russian Federation __ __________201_

Keywords

• respiratory distress syndrome
• respiratory distress syndrome
• prematurity
• surfactant
• artificial pulmonary ventilation (ALV)
• non-invasive artificial ventilation
• extended breath

List of abbreviations

BPD – bronchopulmonary dysplasia

IVH - intraventricular hemorrhage

IVL - artificial lung ventilation

Ministry of Health of the Russian Federation – Ministry of Health of the Russian Federation

mg/kg – amount of drug in milligrams per kilogram of newborn’s body weight

VLBW - very low body weight

NICU - neonatal intensive care unit

RDS - respiratory distress syndrome

RCT - randomized controlled trial

RDS – respiratory distress syndrome

beats/min – number of beats in one minute

HR – heart rate

ELBM - extremely low body weight

EET – endotracheal tube

CO 2 – partial tension of carbon dioxide

Fi fraction of oxygen in the inhaled gas mixture

Peep – peak end-expiratory pressure

Pip – peak inspiratory pressure

SpO 2 – saturation, oxygen saturation of the blood, measured by pulse oximetry

CPAP – continuous positive airway pressure / method of respiratory therapy – continuous positive pressure in the respiratory tract

Terms and Definitions

Respiratory distress syndrome or “respiratory distress syndrome” (RDS) newborn - respiratory distress in children in the first days of life, caused by a primary deficiency of surfactant and immaturity of the lungs.

Surfacta?nt(translated from English - surfactant) - a mixture of surfactants lining the pulmonary alveoli from the inside (that is, located at the air-liquid interface).

CPAP - therapy from English Continuous Positive Airways Pressure (CPAP) is a method of creating constant positive pressure in the airways.

Extended inhalation maneuver- extended artificial inspiration, carried out at the end of primary measures, in the absence of spontaneous breathing, in case of irregular breathing or when breathing like “gasping” with a pressure of 20 cm H 2 O for 15-20 seconds, for the effective formation of residual lung capacity in premature infants.

INSURE – In tubation- sur factant- uh kstubation is a method of rapid administration of surfactant on non-invasive respiratory support with short-term tracheal intubation, which reduces the need for invasive mechanical ventilation

Minimally invasive surfactant administration – a method of administering surfactant to a patient on non-invasive respiratory support without tracheal intubation with an endotracheal tube. The surfactant is administered through a thin catheter inserted into the trachea while the patient breathes spontaneously under constant positive pressure. Allows to significantly reduce the need for invasive ventilation.

1. Brief information

1.1 Definition

Respiratory distress syndrome or “respiratory distress syndrome” (RDS) of the newborn is a respiratory disorder in children in the first days of life, caused by a primary deficiency of surfactant and immature lungs.

RDS is the most common cause of respiratory failure in the early neonatal period in newborns. Its occurrence is higher, the lower the gestational age and body weight of the child at birth.

1.2 Etiology and pathogenesis

The main reasons for the development of RDS in newborns are:

• disruption of the synthesis and excretion of surfactant by type 2 alveolocytes associated with functional and structural immaturity of lung tissue;
• a congenital qualitative defect in the structure of the surfactant, which is an extremely rare cause.

1.3 Epidemiology

1.4 ICD code - 10

P22.0 - Respiratory distress syndrome in a newborn.

1.5 Classification

1.6 Clinical picture

• Shortness of breath that occurs in the first minutes - the first hours of life;
• Expiratory noises (“moaning breathing”) caused by the development of compensatory spasm of the glottis during exhalation;
• Retraction 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.

2. Diagnostics

2.1 Complaints and anamnesis

Risk factors

Predisposing factors for the development of RDS, which can be identified before the birth of a child or in the first minutes of life, are:

• Development of RDS in siblings;
• Gestational diabetes and type 1 diabetes in the mother;
• 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 newborn.

2.2 Physical examination

• It is recommended to assess respiratory failure using scales.

Comments:Clinical assessment severity of respiratory disorders according to the Silverman scale (Appendix D1) is carried out not so much with diagnostic purpose, how much to assess the effectiveness of respiratory therapy or as an indication for its initiation. Along with assessing the newborn's need for supplemental oxygenation, it may be a criterion for switching from one level of respiratory support to another.

2.3 Laboratory diagnostics

• It is recommended 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.
• 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).

Comments : When carrying out a differential diagnosis with severe early neonatal 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 procalcitonin 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 RDS on the first day of the child’s life. RDS is characterized by negative inflammatory markers and a negative microbiological blood test result.

2.4 Instrumental diagnostics

• An X-ray examination is recommended for all newborns with respiratory disorders in the first day of life.

Comments : The X-ray picture of RDS 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 area lung root(air bronchogram). However, these changes are nonspecific and can be detected in early neonatal sepsis and congenital pneumonia.

2.5 Other diagnostics

Differential diagnosis

• Transient tachypnea of ​​newborns;
• Early neonatal sepsis, congenital pneumonia;
• Meconium aspiration syndrome;
• Air leak syndrome, pneumothorax;
• Persistent pulmonary hypertension of newborns;
• Aplasia/hypoplasia of the lungs;
• Congenital diaphragmatic hernia.

3. Treatment

3.1 Conservative treatment

3.1.1 Prevention of hypothermia in the delivery room in preterm infants

• Prevention of hypothermia in the delivery room in premature newborns is recommended.

Comments: The main measures to ensure thermal protection are carried out in the first 30 seconds of life as part of the initial measures of primary care for the newborn. The scope of measures to prevent hypothermia differs in premature infants weighing more than 1000 g (gestational age 28 weeks or more) and in children weighing less than 1000 g (gestational age less than 28 weeks).

3.1.2 Delayed cord clamping and cutting and cord expression

• Delayed clamping and cutting of the umbilical cord is recommended.

Comments: Clamping and intersection of the umbilical cord 60 seconds after birth in premature newborns with VLBW and ELBW leads to a significant reduction in the incidence of necrotizing enterocolitis, IVH, sepsis, and a reduction in the need for blood transfusions. The decision to carry out this manipulation is made collectively by obstetricians-gynecologists and neonatologists. During vaginal delivery, the newborn is placed on the mother's stomach or on warm diapers next to the mother. If pulsation of the umbilical cord persists and there is no need for urgent assistance to the mother (decided by obstetricians), it is carried out. delayed umbilical cord clamping while maintaining the thermal chain. When delivering a baby by Caesarean section, the first to make a decision are obstetrician-gynecologists who assess the woman’s condition, the situation in the surgical wound, and the presence or absence of bleeding. If there is no need to provide emergency assistance mother, persistent pulsation of the umbilical cord, the child is placed in a specially heated sterile diaper at the woman’s feet and covered with it to prevent excess heat loss. The time of birth in this situation is the complete separation of the child from the mother, regardless of the time of intersection of the umbilical cord, therefore, the Apgar timer is turned on immediately after the child is removed from the uterine cavity during a cesarean section or from the birth canal during a vaginal birth. An alternative to delayed clamping and cutting of the umbilical cord may be expressing the umbilical cord in cases where delayed clamping is not possible due to the condition of the mother or child.

3.1.3 Non-invasive respiratory therapy in the delivery room

• It is recommended to begin non-invasive respiratory therapy in the delivery room.

Comments: For premature babies born at 32 weeks of gestation or less with spontaneous breathing, including the presence of respiratory disorders, initial CPAP therapy with a pressure of 6-8 cm H2O is considered preferable. Prematures born at more than 32 weeks' gestation should receive CPAP if there are respiratory problems.

Extended inhalation can only be used when there is no breathing or gasping breathing or when breathing is irregular. If a child has been screaming since birth or breathing regularly, then even if there are respiratory disorders, an extended inhalation should not be carried out. Using an extended inhalation in premature infants with intact spontaneous breathing can lead to negative consequences associated with damage to the lungs from excess pressure. A prerequisite for performing the “extended inhalation” maneuver of the lungs is the registration of heart rate (HR) and SpO2 using pulse oximetry, which allows you to evaluate the effectiveness of the maneuver and predict further actions.

Further traditional tactics, described in the methodological letter of the Ministry of Health of Russia, provide for the beginning of artificial pulmonary ventilation (ALV) with a mask in the absence of spontaneous breathing in the child and/or with persistent bradycardia, followed by a transition to CPAP when breathing/heart rate is restored or to intubation in the absence of breathing and/ or persistent bradycardia. At the same time, upon completion of an extended inhalation, a different sequence of actions than in the methodological letter may be recommended, presented in Appendix B (patient management algorithm)

CPAP in the delivery room can be carried out by a ventilator with a CPAP function, a manual ventilator with a T-connector, or various CPAP systems. The CPAP technique can be performed 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 CPAP method is not significant.

The use of CPAP in the delivery room is contraindicated for children: choanal atresia or other congenital malformations of the maxillofacial region that prevent the correct application of nasal cannulas, masks, nasopharyngeal tubes; with diagnosed pneumothorax; with congenital diaphragmatic hernia; with congenital malformations incompatible with life (anencephaly, etc.); with bleeding (pulmonary, gastric, bleeding of the skin).

3.1.4 Invasive respiratory therapy in the delivery room.

• Tracheal intubation and mechanical ventilation are recommended if CPAP and mask ventilation are ineffective.

Comments: Artificial ventilation of the lungs in premature infants is carried out when bradycardia persists against the background of CPAP and/or in the absence of spontaneous breathing for a long time (more than 5 minutes). Necessary conditions for effective mechanical ventilation in very premature newborns are: control of pressure in the respiratory tract; mandatory maintenance of Reer +5-6 cm H 2 O; possibility of smooth adjustment of oxygen concentration from 21 to 100%; continuous monitoring of heart rate and SpO 2.

Starting parameters of mechanical ventilation: Pip – 20-22 cm H2O, Peep – 5 cm H2O, frequency 40-60 breaths per minute. The main indicator of the effectiveness of mechanical ventilation is an increase in heart rate>100 beats/min.

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. Verification of the position of the endotracheal tube by auscultation in children with extremely low body weight can present certain difficulties due to the low intensity of respiratory sounds and their significant irradiation. The use of devices to indicate CO2 in exhaled air makes it possible to confirm the correct placement of the endotracheal tube faster and more reliably than other methods.

3.1.5 Oxygen therapy and pulse oximetry

• It is recommended to monitor heart rate and SpO2 parameters in the delivery room when providing primary and resuscitation care to premature newborns using pulse oximetry.

Comments: Registration of heart rate and SpO2 by 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 initial measures. Pulse oximetry in the delivery room has 3 main points of application: continuous monitoring of heart rate, starting from the first minutes of life; prevention of hyperoxia (SpO2 no more than 95% at any stage of the procedure resuscitation measures, if the child receives additional oxygen) prevention of hypoxia (SpO2 is not less than 80% by the 5th minute of life and not less than 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 the 1st minute of life, you should focus on the pulse oximeter readings (see Appendix D2) and follow the algorithm for changing the oxygen concentration described below. If the indicators determined in the child are outside the specified values, the concentration of additional O2 should be changed (increase/decrease) in steps of 10-20% every subsequent minute until the target indicators are achieved. The exception is children who require chest compressions during mechanical ventilation. In these cases, simultaneously with the start of chest compressions, the O2 concentration should be increased to 100%.

During further treatment of premature newborns receiving supplemental oxygenation, SpO2 levels should be maintained between 90-94%.

3.1.6 Surfactant therapy.

• It is recommended to administer surfactant according to indications, regardless of birth weight, to premature infants with RDS.

Comments: Prophylactically, in the first 20 minutes of life, for all children born at a gestational age of 26 weeks or less, unless their mothers have undergone a full course of antenatal steroid prophylaxis. All gestational age babies? 30 weeks, requiring tracheal intubation in the delivery room. Most effective time administration during the first 20 minutes of life.

Premature infants of gestational age > 30 weeks who required tracheal intubation in the delivery room with continued dependence on FiO2 > 0.3-04. The most effective time of administration is the first two hours of life.

Premature babies undergoing initial respiratory therapy using the CPAP method in the delivery room when they need FiO2? 0.5 or more to achieve SpO2 = 85% by 10 minutes of life and the absence of regression of respiratory disorders, as well as improvement of oxygenation in the next 10-15 minutes.

By 20-25 minutes of life, a decision must be made to administer surfactant or prepare to transport the child to the NICU on CPAP.

For children born at a gestational age of 28 weeks, on initial therapy with the CPAP method, if there are indications in the delivery room, surfactant can be administered using a minimally invasive method. For children of greater gestational age, on initial therapy with the CPAP method, if there are indications in the delivery room, surfactant can be entered using the traditional method.

In the intensive care unit for children born at term? 35 weeks, on respiratory therapy using CPAP/non-invasive mechanical ventilation with Silverman score >3 points in the first day of life and/or FiO2 requirements up to 0.35 in patients<1000 г и до 0,4 у детей >1000 g of surfactant can be administered using both the minimally invasive method and the INSURE method.

Repeated administration of surfactant is recommended: for children of gestational age? 35 weeks on CPAP who have already received the first dose of surfactant, when transferring them to mechanical ventilation due to an increase in respiratory disorders (FiO2 up to 0.3 in patients<1000г и до 0,4 у детей >1000g) on ​​the first day of life; children of gestational age? 35 weeks on mechanical ventilation who have already received the first dose of surfactant, with tightening ventilation parameters: MAP up to 7 cm H 2 O and FiO2 up to 0.3 in patients<1000 г и до 0,4 у детей >1000g on the first day of life. Repeated administration is recommended only after a chest x-ray. A third administration may be indicated for ventilated children with severe RDS. Intervals between injections are 6 hours. However, the interval may shorten as children’s need for FiO2 increases to 0.4. Surfactant can be re-introduced using both the minimally invasive method and the INSURE method.

Currently, the Pharmaceutical Committee of the Russian Federation has approved for use in our country. the following drugs natural surfactants: Poractant alpha, Bovactant, Beractant, Surfactant BL. According to the literature, surfactant preparations are not identical in their effectiveness. The most effective is poractant alpha at a starting dosage of 200 mg/kg. This dosage of poractant alfa is more effective than 100 mg/kg and leads to best results treatment of premature infants with RDS compared with beractant and bovactant. There are no large randomized comparative studies in the literature on the effectiveness of Surfactant-BL. Surfactant may be used in the treatment of congenital pneumonia in premature newborns

3.1.7 Non-invasive respiratory therapy in the NICU

• It is recommended to carry out non-invasive respiratory therapy in combination with surfactant therapy as indicated in premature infants with respiratory disorders.

Comments: Non-invasive respiratory therapy includes CPAP, different kinds non-invasive ventilation through nasal cannulas or a mask, high-flow cannulas. Non-invasive ventilation through nasal cannulas or a nasal mask is currently used as the optimal starting 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 CPAP, as well as after the administration of surfactant, leads to a lower need for reintubation and a lower incidence of apnea.

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 using the INSURE method); the occurrence of apnea resistant to CPAP and caffeine therapy; an increase in respiratory disorders to 3 or more points on the Silverman scale and/or an increase in the need for Fio2 > 0.4 in premature infants on CPAP.

Contraindications: Shock, convulsions, pulmonary hemorrhage, air leak syndrome, Starting parameters for open circuit devices (variable flow systems): Pip 8-10cm H2O; Peep 5-6 cm H2O; Frequency 20-30 per minute; Inhalation time 0.7-1.0 second;

Starting parameters for semi-closed loop devices (constant flow systems): Pip 12-18 cm H2O; Peep 5 cm H2O; Frequency 40-60 per minute; Inhalation time 0.3-0.5 seconds;

Reducing parameters: When using non-invasive ventilation for the treatment of apnea, the frequency of artificial breaths is reduced. When using non-invasive ventilation to correct respiratory disorders, Pip is reduced.

In both cases, a transfer is made from non-invasive ventilation to CPAP with further transfer to breathing without respiratory support.

Indications for transfer from non-invasive mechanical ventilation to traditional mechanical ventilation:

PaCO2 > 60 mmHg

FiO2 ? 0.4

Silverman scale score of 3 or more points.

Apnea, repeating more than 4 times within an hour.

Air leak syndrome, convulsions, shock, pulmonary hemorrhage.

In the absence of a non-invasive ventilator in the hospital as a starting method of non-invasive respiratory care? For support, preference is given to the method of spontaneous breathing under constant positive pressure in the airways through nasal cannulas. In very preterm infants, the use of variable flow CPAP devices has some advantage over constant flow systems, as they provide the least work of breathing in such patients. Cannulas for CPAP should be as wide and short as possible.

Indications for support of spontaneous breathing with nasal CPAP in newborns with RDS:

Prophylactically in the delivery room for premature infants with a gestational age of 32 weeks or less.

Silverman score of more than 3 points in children of gestational age over 32 weeks with spontaneous breathing.

Contraindications include:

Shock, convulsions, pulmonary hemorrhage, air leak syndrome.

Starting parameters for CPAP: 5-6 cm. H2O, FiO2 0.21-0.3. An increase in the need for FiO2 of more than 0.3 in children less than 1000 g and more than 0.35-0.4 in children more than 1000 g in the first day of life is an indication for the administration of surfactant using the INSURE method or a minimally invasive method. CPAP is discontinued when airway pressure decreases to 2 cmH2O or less and there is no need for additional oxygenation.

The use of high-flow cannulas may be recommended as an alternative to the CPAP method in some children when weaning them from respiratory therapy. A flow of 4-8 l/minute is used.

3.1.8 Mechanical ventilation in premature infants with RDS

• It is recommended to perform mechanical ventilation through an endotracheal tube in those patients in whom other methods of respiratory support have been ineffective.

Comments: Indications for transferring children with RDS to artificial ventilation are the ineffectiveness of non-invasive methods of respiratory support, as well as severe concomitant conditions: shock, convulsive status, pulmonary hemorrhage. The duration of mechanical ventilation in children with RDS should be minimal. If possible, mechanical ventilation should be performed with tidal volume control, which shortens its duration and minimizes the incidence of complications such as BPD and IVH.

Hypocarbia and severe hypercarbia should be avoided as factors that contribute to brain damage. When weaning off a respirator, moderate hypercarbia is acceptable while maintaining the arterial blood pH level above 7.22. Caffeine should be used during weaning from mechanical ventilation. Caffeine should be prescribed from birth to all children weighing less than 1500 g who require respiratory therapy as a proven means of reducing the incidence of BPD.

A short course of low-dose dexamethasone may be prescribed to facilitate weaning from mechanical ventilation if the patient continues to require mechanical ventilation after 1-2 weeks of life.

The technique of performing mechanical ventilation in newborns is described in the relevant medical guidelines. A prerequisite for the successful use of this type of respiratory therapy in newborns is the ability to regularly monitor the blood gas composition. Routine sedation and analgesia is not recommended for all ventilated children.

The need for additional oxygenation up to 45-50%, as well as high pressure at the end of inspiration up to 25 cm H2O and higher in premature newborns is an indication for transfer to high-frequency oscillatory (HFO) mechanical ventilation.

With high-frequency ventilation, due to the stabilization of the alveolar volume, atelectasis decreases, the gas exchange area increases, and pulmonary blood flow improves. As a result of properly administered therapy, a decrease in the ventilation-perfusion ratio, a decrease in intrapulmonary shunting, and a reduction in exposure to high oxygen concentrations are achieved. At the same time, tidal volume decreases, overextension of the lungs decreases, and the risk of baro- and volutrauma decreases.

3.1.9 Antibacterial therapy

• Antibacterial therapy is not recommended for newborns with RDS.

Comments: During the period differential diagnosis RDS with congenital pneumonia or with early neonatal sepsis, carried out in the first 48-72 hours of life, it is advisable to prescribe antibacterial therapy followed by its rapid cancellation in case of negative inflammatory markers and negative result microbiological blood test. 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 a single antibiotic wide range from the group of protected penicillins.

• It is not recommended to prescribe amoxicillin + clavulonic acid due to the possible adverse effects of clavulonic acid on the intestinal wall in premature infants.

3.2 Surgical treatment

There is no surgical treatment.

4. Rehabilitation

5. Prevention and clinical observation

• If there is a threat of premature birth, it is recommended to transport pregnant women to obstetric hospitals of level II - III, where there are neonatal intensive care units. If there is a threat of premature birth at 32 weeks of gestation or less, it is recommended to transport pregnant women to a level III hospital (to a perinatal center).

Comments:In areas where perinatal centers are located at a remote distance and transportation of women to level III institutions is difficult, it is recommended to promptly organize conditions for caring for premature newborns in those medical institutions where premature births occur.

• For pregnant women at 23-34 weeks of gestation with a threat of premature birth, a course of corticosteroids is recommended to prevent RDS of prematurity and reduce the risk of possible adverse complications such as IVH and NEC.

• Two alternative regimens for prenatal prevention of RDS are recommended:
• 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.

Comments:The maximum effect of therapy develops 24 hours after the start of therapy and lasts a week. By the end of the second week, the effect of steroid therapy is significantly reduced.

• A second course of RDS prophylaxis is recommended only 2-3 weeks after the first in case of repeated risk of premature birth at a gestation period of less than 33 weeks.

• It is recommended to prescribe corticosteroid therapy for women with a gestational age of 35-36 weeks in case of planned caesarean section when a woman is not in labor.

Comments: Prescribing a course of corticosteroid hormones (betamethasone, dexamethasone) to women in this category does not affect outcomes in newborns, but reduces the risk of developing respiratory disorders in children and, as a result, admission to the neonatal intensive care unit.

• If there is a threat of premature birth in the early stages, a short course of tocolytics is recommended 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 RDS with corticosteroids and the onset of the full therapeutic effect.

• Antibacterial therapy is recommended for women with premature rupture of membranes (premature rupture amniotic fluid), since it reduces the risk of premature birth.

Criteria for assessing the quality of medical care

Group name: RDS

ICD codes: R 22.0

Type of medical care: specialized, including high-tech

Age group: children

Conditions for providing medical care: stationary

Form of medical care: emergency

Quality criteria

Level of evidence

The severity of respiratory disorders was assessed using the Silverman scale

Pulse oximetry was performed with heart rate monitoring no later than 1 minute from the moment respiratory disorders were detected

A subsidy of air-oxygen mixture and/or non-invasive artificial ventilation and/or mechanical ventilation was provided (depending on medical indications)

Monitoring of vital functions (respiration, oxygen saturation level in the blood, pulse, blood pressure)

Poractant alpha was administered (if indicated and without medical contraindications)

A study of the acid-base state of the blood (pH, PaCO 2, PaO 2, BE, lactate) was performed no later than 3 hours from the moment of detection of respiratory disorders

A general (clinical) blood test, CRP and microbiological blood test were performed no later than 24 hours from the moment of detection of respiratory disorders

A chest x-ray was performed no later than 24 hours from the moment respiratory disorders were detected

Bibliography

1. McCall EM, Alderdice F, Halliday HL, Jenkins JG, Vohra S: Interventions to prevent hypothermia at birth in preterm and/or low birthweight infants. Cochrane Database Syst Rev 2010:CD004210.

2. Committee on Obstetric Practice, American College of Obstetricians and Gynecologists: Committee Opinion No. 543. Timing of umbilical cord clamping after birth. Obstet Gynecol 2012; 120:1522–1526.

3. Rabe H, Diaz-Rossello JL, Duley L, Dowswell T: Effect of timing of umbilical cord clamping and other strategies to influence placental transfusion at preterm birth on maternal and infant outcomes. Cochrane Database Syst Rev 2012:CD003248.

4. Lista G, Castoldi F, Cavigioli F, Bianchi S, Fontana P: Alveolar recruitment in the delivery room. J Matern Fetal Neonatal Med 2012; (suppl 1): 39–40.

5. Methodological letter of the Ministry of Health of Russia “Primary and resuscitation care for newborn children” dated April 21, 2010 N 15-4/10/2-3204.

6. Soll R, Ozek E: Prophylactic protein free synthetic surfactant for preventing morbidity and mortality in preterm infants. Cochrane Database Syst Rev 2010:CD001079.

7. Verlato G, Cogo PE, Benetti E, Gomirato S, Gucciardi A, Carnielli VP: Kinetics of surface-tant in respiratory diseases of the newborn infant. J Matern Fetal Neonatal Med 2004; 16(suppl 2):21–24.

8. Cogo PE, Facco M, Simonato M, Verlato G, Rondina C, Baritussio A, Toffolo GM, Carnielli VP: Dosing of porcine surfactant: effect on kinetics and gas exchange in respiratory distress syndrome. Pediatrics 2009; 124:e950–957.

9. Singh N, Halliday HL, Stevens TP, Suresh G, Soll R, Rojas-Reyes MX Comparison of animal-derived surfactants for the prevention and treatment of respiratory distress syndrome in preterm infants Cochrane Database Syst Rev. 2015 Dec 21;(12):CD010249.

10. Speer CP, Gefeller O, Groneck P, Laufk?tter E, Roll C, Hanssler L, Harms K, Herting E, Boenisch H, Windeler J, et al: Randomized clinical trial of two treatment regimens of natural surfactant preparations in neonatal respiratory distress syndrome. Arch Dis Child Fetal Neonatal Ed 1995; 72:F8–F13.

11. Sandri F, Plavka R, Ancora G, Simeoni U, Stranak Z, Martinelli S, Mosca F, Nona J, Thomson M, Verder H, Fabbri L, Halliday HL, CURPAP Study Group: Prophylactic or early selective surfactant combined with nCPAP in very preterm infants. Pediatrics 2010;125:e1402-e1409.

12. Rojas-Reyes MX, Morley CJ, Soll R: Prophylactic versus selective use of surfactant in preventing morbidity and mortality in preterm infants. Cochrane Database Syst Rev 2012:CD000510.

13. Rich W, Finer NN, Gantz MG, Newman NS, Hensman AM, Hale EC, Auten KJ, Schibler K, Faix RG, Laptook AR, Yoder BA, Das A, Shankaran S, SUPPORT and Generic Database Subcommittees of the Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network: Enrollment of extremely low birth weight infants in a clinical research study may not be representative. Pediatrics 2012;129:480–484.

14. Prof Wolfgang G?pel, Angela Kribs, Andreas Ziegler Reinhard Laux, Thomas Hoehn Christian Wieg, Jens Siegel, Stefan Avenarius, Axel von der Wense, Matthias Vochem, MDb MDa, Avoidance of mechanical ventilation by surfactant treatment of spontaneously breathing preterm infants (AMV): an open-label, randomized, controlled trial. THE LANCET Volume 378, Issue 9803, 5–11 November 2011, Pages 1627–1634.

15. Egbert Herting Less Invasive Surfactant Administration (LISA) - Ways to deliver surfactant in spontaneously breathing infants. Early Human Development Volume 89, Issue 11, November 2013, Pages 875–880.

16. Stevens TP, Harrington EW, Blennow M, Soll RF: Early surfactant administration with brief ventilation vs. selective surfactant and continued mechanical ventilation for preterm infants with or at risk for respiratory distress syndrome. Cochrane Database Syst Rev 2007:CD003063.

17. Rautava L, Eskelinen J, H?kkinen U, Lehtonen L, PERFECT Preterm Infant Study Group: 5-year morbidity among very preterm infants in relation to level of hospital care. Arch Pediatr Adolesc Med 2013; 167:40–46.

18. Roberts D, Dalziel S: Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database Syst Rev 2006:CD004454.

19. Sotiriadis A, Makrydimas G, PapatheodorouS, Ioannidis JP: Corticosteroids for preventing neonatal respiratory morbidity after elective caesarean section at term. Cochrane Database Syst Rev 2009:CD006614.

20. Kenyon S, Boulvain M, Neilson JP: Antibiotics for preterm rupture of membranes. Cochrane Database Syst Rev 2010:CD001058.

21 Neetu Singh, Kristy L. Hawley and Kristin Viswanathan Efficacy of Porcine Versus Bovine Surfactants for Preterm Newborns With Respiratory Distress Syndrome: Systematic Review and Meta-analysis Pediatrics 2011;128;e1588

22 Tan K, Lai NM, Sharma A: Surfactant for bacterial pneumonia in late preterm and term infants. Cochrane Database Syst Rev 2012; 2:CD008155

23 Bancalari E, Claure N: The evidence for noninvasive ventilation in the preterm infant. Arch Dis Child Fetal Neonatal Ed 2013; 98:F98–F102.

24. De Paoli AG, Davis PG, Faber B, Morley CJ: Devices and pressure sources for administration of nasal continuous positive airway pressure (NCPAP) in preterm neonates. Cochrane Database Syst Rev 2002; 3:CD002977.

25. Reynolds P, Leontiadi S, Lawson T, Otunla T, Ejiwumi O, Holland N: Stabilization of premature infants in the delivery room with nasal high flow. Arch Dis Child Fetal Neonatal Ed 2016; 101:F284–F287.

26. Wilkinson D, Andersen C, O'Donnell CP, de Paoli AG, Manley BJ: High flow nasal cannula for respiratory support in preterm infants. Cochrane Database Syst Rev 2016; 2: CD006405.

27. Erickson SJ, Grauaug A, Gurrin L, Swaminathan M: Hypocarbia in the ventilated preterm infant and its effect on intraventricular haemorrhage and bronchopulmonary dysplasia. J Paediatr Child Health 2002; 38:560–562.

28. Ambalavanan N, Carlo WA, Wrage LA, Das A, Laughon M, Cotten CM, et al; SUPPORT Study Group of the NICHD Neonatal Research Network: Pa CO 2 in surfactant, positive pressure, and oxygenation randomized trial (SUPPORT). Arch Dis Child Fetal Neonatal Ed 2015; 100:F145–F149

29. Woodgate PG, Davies MW: Permissive hypercapnia for the prevention of morbidity and mortality in mechanically ventilated newborn infants. Cochrane Database Syst Rev 2001; 2:CD002061

30. Dobson NR, Patel RM, Smith PB, KuehnDR, Clark J, Vyas-Read S, et al: Trends in clinical use and association between clinical outcomes and timing of therapy in very low birth weight infants. J Pediatr 2014; 164:992–998.

31. Taha D, Kirkby S, Nawab U, Dysart KC, Genen L, Greenspan JS, Aghai ZH: Early caffeine therapy for prevention of bronchopulmonary dysplasia in preterm infants. J Matern Fetal Neonatal Med 2014; 27:1698–1702.

32. Lodha A, Seshia M, McMillan DD, Barrington K, Yang J, Lee SK, Shah PS; Canadian Neonatal Network: Association of early caffeine administration and neonatal outcomes in very preterm neonates. JAMA Pediatr 2015; 169: 33–38.

33. Jefferies AL: Postnatal corticosteroids to treat or prevent chronic lung disease in preterm infants. Paediatr Child Health 2012; 17:573–574

34. Bell? R, de Waal K, Zanini R: Opioids for neonates receiving mechanical ventilation: a systematic review and meta-analysis. Arch Dis Child Fetal Neonatal Ed 2010; 95:F241–F251.

Appendix A1. Composition of the working group

Averin Andrey Petrovich- senior resident of the intensive care unit for newborns and premature infants, Municipal Budgetary Healthcare Institution "City" clinical Hospital No. 8", Chelyabinsk

Antonov Albert Grigorievich– Doctor of Medical Sciences, Professor, Honored Scientist, Chief Researcher of the Department of Resuscitation and Intensive Care of the Department of Neonatology and Pediatrics of the Federal State Budgetary Institution "Scientific Center for Obstetrics, Gynecology and Perinatology named after V.I. Kulakov" of the Ministry of Health of the Russian Federation, Professor of the Department Neonatology FSBEI HE Perm State Medical University named after. M.I. Sechenov Ministry of Health of the Russian Federation, Moscow

Baibarina Elena Nikolaevna- Doctor of Medical Sciences, Professor, Chief Researcher of the Federal State Budgetary Institution "Scientific Center of Obstetrics, Gynecology and Perinatology named after V.I. Kulakov" of the Ministry of Health of the Russian Federation, Moscow

Grebennikov Vladimir Alekseevich– Doctor of Medical Sciences, Professor, Professor of the Department of Pediatric Anesthesiology and Intensive Care of the Federal Institution of Higher Education of the Russian National Research Medical University named after. N.I. Pirogov, Moscow

Degtyarev Dmitry Nikolaevich- Doctor of Medical Sciences, Professor, Deputy Director of the Federal State Budgetary Institution "Scientific Center of Obstetrics, Gynecology and Perinatology named after V.I. Kulakov" of the Ministry of Health of the Russian Federation, Head of the Department of Neonatology of the Federal State Budgetary Educational Institution of Higher Education First Moscow State Medical University named after. M.I. Sechenov Ministry of Health of the Russian Federation, Moscow

Degtyareva Marina Vasilievna- Doctor of Medical Sciences, Professor, Head of the Department of Neonatology, Federal Faculty of Postgraduate Education, Russian National Research Medical University named after. N.I. Pirogov Ministry of Health of the Russian Federation, Moscow

Ivanov Dmitry Olegovich- Doctor of Medical Sciences, Chief Neonatologist of the Ministry of Health of the Russian Federation, acting. Rector of the St. Petersburg State Pediatric Medical University, St. Petersburg

Ionov Oleg Vadimovich- Candidate of Medical Sciences, Head of the Department of Reanimation and Intensive Care of the Department of Neonatology and Pediatrics of the Federal State Budgetary Institution "Scientific Center of Obstetrics, Gynecology and Perinatology named after V.I. Kulakov" of the Ministry of Health of the Russian Federation, Associate Professor of the Department of Neonatology of the Federal State Budgetary Educational Institution of Higher Education First Moscow State Medical University named after. THEM. Sechenov Ministry of Health of the Russian Federation, Moscow

Kirtbaya Anna Revazievna- Candidate of Medical Sciences, Head of Clinical Work of the Department of Resuscitation and Intensive Care of the Department of Neonatology and Pediatrics of the Federal State Budgetary Institution "Scientific Center of Obstetrics, Gynecology and Perinatology named after V.I. Kulakov" of the Ministry of Health of the Russian Federation, Associate Professor of the Department of Neonatology of the Federal State Budgetary Educational Institution of Higher Education Perinatal Moscow State Medical University named after . THEM. Sechenov Ministry of Health of the Russian Federation, Moscow

Lenyushkina Anna Alekseevna- Candidate of Medical Sciences, Head of Clinical Work, Department of Reanimation and Intensive Care, Department of Neonatology and Pediatrics, Federal State Budgetary Institution "Scientific Center for Obstetrics, Gynecology and Perinatology named after V.I. Kulakov" of the Ministry of Health of the Russian Federation, Moscow

Mostovoy Alexey Valerievich- Candidate of Medical Sciences, Head of the NICU, Kaluga Regional Clinical Hospital, chief neonatologist of the Ministry of Health of the Russian Federation in the North Caucasus Federal District, Kaluga

Mukhametshin Farid Galimovich- Candidate of Medical Sciences, Head of the NICU and ND No. 2 of the State Budgetary Institution of Healthcare of the Collective Clinical Hospital No. 1, assistant of the Department of Anesthesiology and Reanimatology of the Faculty of Pedagogical Training and PP of the USMU, expert of Roszdravnadzor in the specialty “Neonatology”, Ekaterinburg

Pankratov Leonid Gennadievich– Candidate of Medical Sciences, resuscitator-neonatologist at the Center for Resuscitation and Intensive Care of Children's City Hospital No. 1, assistant at the Department of Neonatology and Neonatal Reanimatology of the Faculty of Training and Faculty of St. Petersburg State Pediatric Medical Academy, St. Petersburg

Petrenko Yuri Valentinovich- Ph.D., acting Vice-Rector for Medical Work, St. Petersburg State Pediatric Medical University, St. Petersburg

Prutkin Mark Evgenievich- Head of the Department of AR and ITN and ND No. 1 of the State Budgetary Institution of Healthcare of the CSTO No. 1, Yekaterinburg

Romanenko Konstantin Vladislavovich- Candidate of Medical Sciences, Head of NICU and ND MBUZ "Children's City Clinical Hospital No. 8", chief neonatologist of the Chelyabinsk region, Chelyabinsk

Ryndin Andrey Yurievich– Candidate of Medical Sciences, Senior Researcher of the Department of Reanimation and Intensive Care of the Department of Neonatology and Pediatrics of the Federal State Budgetary Institution "Scientific Center of Obstetrics, Gynecology and Perinatology named after V.I. Kulakov" of the Ministry of Health of the Russian Federation, Moscow, Associate Professor of the Department of Neonatology of the Federal State Budgetary Educational Institution IN PMSMU im. THEM. Sechenov Ministry of Health of the Russian Federation, Moscow

Soldatova Irina Gennadievna- Doctor of Medical Sciences, Professor, Deputy Minister of Health of the Moscow Region, Moscow

Starring:

Babak Olga Alekseevna– Candidate of Medical Sciences, Head of ICU 2, City Clinical Hospital No. 24 "Perinatal Center", Moscow

Vereshchinsky Andrey Mironovich- Head of the department of resuscitation and intensive care of the Khanty-Mansiysk Autonomous Okrug-Yugra “Nizhnevartovsk District Clinical Perinatal Center”, Nizhnevartovsk

Vorontsova Yulia Nikolaevna- Candidate of Medical Sciences, anesthesiologist-resuscitator of the intensive care unit for newborns and premature infants of the Center for Pregnancy and Resuscitation, Moscow

Gorelik Konstantin Davidovich- anesthesiologist-resuscitator, NICU, Children's City Hospital No. 1, St. Petersburg

Efimov Mikhail Sergeevich– Doctor of Medical Sciences, Professor, Head of the Department of Neonatology of the Federal State Budgetary Educational Institution of Further Professional Education RMPO of the Ministry of Health of the Russian Federation, Moscow

Ivanov Sergei Lvovich- doctor anesthesiologist-resuscitator of the intensive care unit of neonatal children's hospital No. 1 of St. Petersburg, assistant of the department of anesthesiology, resuscitation and emergency pediatrics of the Faculty of Pediatrics and Pediatrics of the St. Petersburg State Pediatric Medical Academy, St. Petersburg

Karpova Anna Lvovna- Candidate of Medical Sciences, Deputy Chief Physician for Children, Kaluga Regional Clinical Hospital Perinatal Center, Chief Neonatologist of the Kaluga Region

Lyubimenko Vyacheslav Andreevich- Candidate of Medical Sciences, Associate Professor, Honored Doctor of the Russian Federation, Deputy. Ch. doctor for resuscitation and anesthesiology, Children's City Hospital No. 1, St. Petersburg

Obelchak Elena Vadimovna- Head of the Department of Reanimation and Intensive Care of Newborns Branch No. 1 Maternity Hospital City Clinical Hospital No. 64, Moscow

Pankratieva Lyudmila Leonidovna- Candidate of Medical Sciences, neonatologist, Federal State Budgetary Institution Federal Scientific Center for Children's Orthopedic Orthopedics named after. Dmitry Rogachev, Moscow

Romanenko Vladislav Alexandrovich- Doctor of Medical Sciences, Professor, Honored Doctor of the Russian Federation, Head of the Department of Emergency Pediatrics and Neonatology, Physiotherapology and Additional Professional Education, South Ural State Budgetary Educational Institution of Higher Professional Education medical University» Ministry of Health of Russia, Chelyabinsk

Rusanov Sergei Yurievich- Candidate of Medical Sciences, Head of the Department of Reanimation and Intensive Care of Newborns, Federal State Budgetary Institution "Ural Research Institute of Maternal and Infant Care" of the Ministry of Health of Russia, Yekaterinburg

Shvedov Konstantin Stanislavovich- Head of the Department of Reanimation and Intensive Care of Newborns No. 1, State Budgetary Healthcare Institution of the Tyumen Region “Perinatal Center”, Tyumen

Everstova Tatyana Nikolaevna– Candidate of Medical Sciences, Head of the Department of Resuscitation and Intensive Care of Children's City Clinical Hospital No. 13 named after. N.F. Filatova, Moscow

Conflict of interest: All members Working group have confirmed that they have no financial support/conflicts of interest to report.

Methods used to collect/select evidence:

search in electronic databases, library resources.

Description of methods used to collect/select evidence: evidence base for recommendations are publications included in the Cochrane Library, EMBASE and MEDLINE databases, as well as monographs and articles in leading specialized peer-reviewed domestic medical journals on this topic. The search depth was 10 years.

Methods used to assess the quality and strength of evidence: expert consensus, assessment of significance according to a rating scheme.

1. Neonatology;
2. Pediatrics;
3. Obstetrics and gynecology.

Table A.1

Levels of evidence according to international criteria

Table A.2 – Levels of Recommendation Strength

The mechanism for updating clinical recommendations provides for their systematic updating - at least once every three years or when new information about the tactics of managing patients with this disease becomes available. The decision to update is made by the Ministry of Health of the Russian Federation based on proposals submitted by medical non-profit professional organizations. Formed proposals must take into account the results comprehensive assessment medicines, medical devices, as well as the results of clinical testing.

Appendix A3. Related documents

1. Methodological letter of the Ministry of Health and Social Development of the Russian Federation dated April 21, 2010 N 15-4/10/2-3204 “Primary and resuscitation care for newborn children.”
2. The procedure for providing medical care in the field of “Obstetrics and gynecology (except for the use of assisted reproductive technologies)” (Order of the Ministry of Health of the Russian Federation dated November 1, 2012 No. 572n).
3. The procedure for providing medical care in the specialty “neonatology” (Order of the Ministry of Health of the Russian Federation of November 15, 2012 N 921n).

1. International Classification of Diseases, Injuries and Conditions Affecting Health, 10th Revision (ICD-10) (World Health Organization) 1994.
2. Federal Law “On the fundamentals of protecting the health of citizens in the Russian Federation” dated November 21, 2011 No. 323 F3.
3. List of vital and essential drugs for 2016 (Order of the Government of the Russian Federation dated December 26, 2015 No. 2724-r.
4. nomenclature medical services(Ministry of Health and Social Development of the Russian Federation) 2011.

Appendix B. Patient management algorithms

Appendix B: Patient Information

An insufficient amount of surfactant in the lungs of a premature baby leads to the fact that when exhaling, the lungs seem to slam shut (collapse) and the baby has to re-inflate them with each breath. This requires a lot of energy; as a result, the newborn’s strength is depleted and severe respiratory failure develops. In 1959, American scientists M.E. Avery and J. Mead discovered pulmonary surfactant deficiency in premature newborns suffering from respiratory distress syndrome, thus identifying the main cause of RDS. The frequency of development of RDS is higher, the shorter the period at which the child was born. Thus, it affects on average 60 percent of children born at a gestational age of less than 28 weeks, 15-20 percent - at a period of 32-36 weeks, and only 5 percent - at a period of 37 weeks or more. It is difficult to predict whether a given person will develop specific child RDS or not, scientists were able to identify a certain risk group. Predisposes to the development of the syndrome are diabetes mellitus, infections and maternal smoking during pregnancy, birth by cesarean section, birth of the second of twins, asphyxia during childbirth. In addition, it has been found that boys suffer from RDS more often than girls. Prevention of the development of RDS comes down to the prevention of premature birth.

Appendix D

Note:

• A score of 0 points indicates the absence of respiratory distress syndrome (RDS);
• Score from 1 to 3 points - initial signs HAPPY BIRTHDAY;
• Score 4-5 points - moderate severity of SDR (indication for transition to the next level of respiratory support)
• With a total score of 6 points or more, newborns are diagnosed with severe RDS.

Currently, due to changes in the concept of managing children with respiratory distress, assessment of the severity of respiratory disorders in newborns using the Silverman scales is carried out not so much for diagnostic purposes, but to determine indications for early start respiratory therapy, as well as to assess its effectiveness

A score of 1-3 points indicates a compensated condition of the child against the background of ongoing therapeutic measures. A score of 4 or more points indicates the ineffectiveness of respiratory support and requires increasing the intensity of respiratory therapy (switching from high-flow cannulas to CPAP, from CPAP to non-invasive mechanical ventilation, and if non-invasive mechanical ventilation is insufficiently effective, switching to traditional mechanical ventilation). In addition, an increase in the severity of respiratory distress, as assessed by the Silverman scale, along with an increase in the child's need for supplemental oxygen, may be an indication for surfactant replacement therapy.

Miscarriage and premature birth at the present stage are a pressing social issue, since it is directly related to the level of public health.

Miscarriage is a spontaneous termination of pregnancy at various stages of pregnancy up to 38 weeks. Habitual miscarriage- termination of pregnancy two or more times. Prematurity is the termination of pregnancy between 28 and 37 weeks (less than 259 days).

Despite modern advances in obstetrics and pharmacotherapy, the incidence of premature birth, according to the literature, ranges from 6 to 15% and has not shown a downward trend over the past 5 years. The frequency of premature births in the Russian Federation remains significant, reaching an average of 14%, and primarily determines high rates of perinatal morbidity and mortality. According to statistics from the Moscow Health Committee for 2000-2001, with a prematurity rate of 6.9%, more than 70% of children who died from perinatal causes were premature babies. The highest mortality rate is observed among very premature infants with a gestational age of less than 32 weeks and a body weight of less than 1500 g, the main cause of death of which is respiratory distress syndrome.

That is why the main obstetric task, along with prolonging pregnancy, is to reduce the role of respiratory distress syndrome in the structure of mortality. This task has two directions: maximum prolongation of pregnancy and prevention of respiratory distress syndrome.

Premature birth - termination of pregnancy at 22-37 weeks. In connection with the peculiarities of obstetric tactics and nursing of children, it is advisable to distinguish the following gestational intervals:

Premature birth at 22-27 weeks;

Premature birth at 28-33 weeks;

Premature birth at 34-37 weeks.

Risk factors for preterm birth

Among the causes of premature birth, about 28% are cases of induced delivery due to severe forms of gestosis, fetal hypoxia, placental abruption and antenatal fetal death.

72% are spontaneous preterm labor, of which about 40% are induced by premature rupture of membranes.

Predisposing factors for preterm birth

Social and behavioral: low socio-economic status of the mother, malnutrition, smoking, age of the first-time mother less than 16 or more than 30 years, psychosocial stress.

Pathology of pregnancy: placental abruption and previa, antiphospholipid syndrome, isthmic-cervical insufficiency, infection of amniotic fluid and chorioamnial infection, premature rupture of membranes, preeclampsia, uterine developmental abnormalities, uterine fibroids, multiple pregnancies, polyhydramnios.

Genetic factors: family members and history of premature birth.

Extragenital diseases: arterial hypertension, bronchial asthma, hyperthyroidism, drug addiction, diabetes mellitus, Rh isoimmunization.

Features of the course and complications of premature birth.

Premature rupture of amniotic fluid.

Incorrect position and presentation of the fetus.

Anomalies of labor.

Placental abruption.

Bleeding in the afterbirth and early postpartum periods.

Infectious complications during childbirth and the postpartum period.

Fetal hypoxia.

Respiratory distress syndrome of the newborn.

The high level of ineffectiveness of treatment for preterm birth is associated, on the one hand, with their polygenic nature and the frequent impossibility of timely identification of etiological factors and specific treatment; and on the other hand, with the ineffectiveness of tocolytic therapy, as a rule, due to inadequate selection of the administration regimen.

Clinical picture of threatened premature birth.

Pain in the lower back and lower abdomen.

The excitability and tone of the uterus are increased.

The cervix is ​​preserved, its external os is closed.

Clinical picture of the onset of premature labor.

Regular labor.

Dynamics of cervical dilatation (more than 2-4 cm).

Today in our country the main official guideline regulating the management of threatened preterm birth is the Appendix? 1 to the Order of the Ministry of Health of the Russian Federation? 318 of December 4, 1992

Morbidity structure of premature newborns.

Congenital infection.

Pneumopathy.

Birth injury.

Developmental defects.

Respiratory distress syndrome

This syndrome is the leading cause of death in premature infants in developed countries.

The fetal lungs are filled with fluid secreted by the epithelium of potential air spaces. In the first minutes after birth, absorption of this fluid occurs, probably stimulated by an increase in the concentration of catecholamines in the circulating blood of the fetus, and the lungs are usually quickly cleared of fluid. Pulmonary surfactant forms an insoluble film at the air-liquid interface in the alveoli, displacing water molecules in the surface layer and reducing surface tension. The main component of surfactant is phospholipid-dipalmitoyl-phosphatidylcholine.

The synthesis of phosphatidylcholine is enhanced by thyroid hormones, estrogens, prolactin, epidermal growth factor, and the secretion of surfactant phospholipids from type 2 alveolocytes is significantly stimulated by corticosteroids. In general, adrenergic agonists increase surfactant secretion into potential air spaces and maternal treatment β - adrenergic agents can reduce the severity of respiratory distress syndrome in newborns -

nogo. However, it is also possible that the administration of high doses or long courses of adrenergic agonists may lead to depletion of intracellular surfactant stores if the rate of surfactant synthesis is low.

Chemical composition of surfactant

Phospholipids 80%

Phosphatidylcholine 65%

Phosphatidylglycerol 5%

Phosphatidylethanolamine 5%

Sphingomyelin 3%

Other components 2%

Neutral lipids 10%

Proteins 10%

Prenatal diagnosis

Assessment of fetal lung maturity by analysis of amniotic fluid

Clements ethanol foam test.

Determination of the optical density of fetal fluid using a spectrophotometer or photoelectric calorimeter (wavelength 650 nm).

Lecithin/sphingomyelin concentration ratio (L/S >2.0).

Presence of phosphatidylglycerol (>2 µg/ml).

Determination of the number of lamellar bodies: ratio of phospholipids of lamellar bodies to total phospholipids >0.35.

It is known that it is advisable to determine fetal maturity by the sum of the following parameters: calendar dates of pregnancy, ultrasound data, biochemical parameters of amniotic fluid. The simplest tests to assess fetal lung maturity are listed below.

1. Clements ethanol “foam” test.

To 3-5 ml of fetal fluid obtained by amniocentesis, add 1 ml of 95% ethyl alcohol solution. The test tube is shaken for 15 s twice with an interval of 5 min. The test is considered positive if there are bubbles covering the surface of the liquid, questionable if there are bubbles around the circumference of the tube, negative if there are no bubbles.

2. Determination of the optical density of water with a spectrophotometer or photoelectric calorimeter (at a wavelength of 650 nm after centrifugation for 10 minutes at a speed of 2000 rpm).

3. The most common and diagnostically valuable criteria for the synthesis and secretion of the surfactant system are obtained by determining the lipid component of the amniotic fluid.

The level of total lipids in amniotic fluid is quite significant and averages 0.5 g/l. A special role is played by phospholipids, the identification of the content of which is of primary diagnostic importance for assessing the maturity of the fetal lungs.

By the end of the third trimester of pregnancy, phospholipids are most abundantly represented by phosphatidylcholine (synonym: lecithin) and sphingomyelin; minor fractions are phosphatidylserine and phosphatidylinositol.

The increase in the amount of phospholipids during pregnancy occurs mainly due to an increase in the concentration of lecithin. During the period from 24 to 40 weeks of pregnancy, a 6-fold increase in its level is observed (from 0.62±0.05 to 3.84±0.17 mg%), and the share in the total phospholipid fraction increases from 43.9 to 71. 2%.

At the same time, the content of sphingomyelin, which exceeds that of lecithin at 22-24 weeks, on the contrary, decreases during pregnancy and after 35 weeks becomes significantly lower than the level of lecithin.

These changes in phospholipid composition are reflected by the lecithin/sphingomyelin (L/S) concentration ratio, which is widely used to determine the degree of maturity of the fetal lungs, since it reflects the presence of pulmonary surfactant in the amniotic fluid 1 .

In the second trimester of pregnancy this figure is approximately 1.5; at 35-36 weeks - 1.8-2.0; at 37-38 weeks - 2.5-2.7. As a rule, when L/S is 2 or more, the maturity of the fetal lungs is noted, and the risk of developing SDR in newborns is minimized.

The second criterion for fetal lung maturity is the concentration of phosphatidylglycerol.

During the initial period of fetal development, the main surfactant phospholipid is phosphatidylinositol (sphingomyelin), and the level of phosphatidylglycerol remains low. High level sphingomyelia-

1 A study of the relationship between the content of these phospholipids in amniotic fluid and fetal urine led to the conclusion that urine cannot be a significant source of phospholipids in amniotic fluid and, therefore, the importance of pulmonary surfactant in the formation of amniotic phosphatidylcholine and sphingomyelin is predominant.

in the blood of the fetus decreases in periods close to the end of pregnancy, and as its concentration decreases, the production of phosphatidylglycerol increases, which underlies the clinical use of its level in amniotic fluid as an indicator of fetal lung maturity. The presence of phosphatidylglycerol in amniotic fluid is a reliable sign of the maturity of the surfactant system.

Phosphatidylglycerol is detected in amniotic fluid at 35-36 weeks of pregnancy. The criterion for lung maturity is considered to be a level of 2 μg/ml or higher.

4. The next diagnostic criterion for fetal lung maturity is determined by assessing the lamellar bodies.

As already mentioned, surfactant is synthesized by type 2 alveolar epithelium. The lamellar bodies of this epithelium serve as a site of accumulation of pulmonary surfactant and the main components of the lamellar bodies are part of the surfactant system.

It should be emphasized that the phospholipid content of lamellar bodies correlates with the level of total phospholipids, and the ratio between the first and second, equal to 0.35, is equivalent to an L/S ratio of 2.

Treatment of threatened preterm birth.

Bed rest.

Non-medicinal means:

Psychotherapy;

Electrorelaxation of the uterus;

Acupuncture;

Electroanalgesia;

Electrophoresis of magnesium.

Drug therapy:

Sedative (tinctures of motherwort, valerian);

Tocolytic therapy;

Prevention of fetal SDD;

Etiological: hormone therapy, antibiotic therapy.

Prevention of respiratory distress syndrome

Glucocorticoids increase the secretion of surfactant by second-order alveolocytes.

Contraindications: bacterial, viral infection, tuberculosis, herpes zoster.

Side effects: hyperglycemia, leukocytosis, immunosuppression, fluid retention - pulmonary edema, IVH, enterocolitis.

Regimen for the prevention of fetal respiratory distress syndrome

Dexamethasone - course dose 20 mg, 4 mg intramuscularly every 6 hours (? 5).

Betamethasone - course dose 24 mg, 12 mg intramuscularly every 12 hours (? 2).

Hydrocortisone 500 mg intramuscularly? 4 after 6 hours. Total dose = 2 g.

Usually the effect occurs within 24-48 hours.

Drug therapy

An analysis of the frequency of premature termination of pregnancy over the past 10 years shows no significant reduction. A large number of medications and other interventions are used to control preterm labor, but unfortunately no method is 100% effective (ACOG, 1995). Currently, in order to treat threatened labor and stop labor, tocolytic drugs with different mechanisms of action are used - β 2-adrenergic agonists, magnesium sulfate, non-steroidal anti-inflammatory drugs, calcium channel blockers, two new groups of tocolytic agents - nitric oxide donors such as nitroglycerin and glyceryl trinitrate, and competitive oxytocin agonists - the drug atosiban.

1. β 2-adrenergic agonists

The mechanism of action of this group is to stimulate the smooth muscle receptors of the uterus and increase the synthesis of cAMP, which plays an important role in the suppression of uterine contractions.

Adrenergic receptors, when bound by catecholamines, can stimulate or inhibit adenylate cyclase, and the latter in turn affects the level of cAMP in the cell. During the normal course of pregnancy, from the 28th week there is a gradual increase in cAMP levels. Before childbirth, its concentration decreases. The cAMP level during normal pregnancy is: 28-30 weeks - 15.79 nmol/l; at 31-36 weeks - 18.59 nmol/l; at 37-38 weeks - 17.16 nmol/l; at 40-41 weeks - 13.28 nmol/l. Increasing the contractile activity of the uterus can be done by

There is a decrease in cAMP in the blood plasma by 1.5-2 times compared to normal.

In our country, the most widely used drugs are fenoterol (partusisten), terbutaline (bricanil), ginipral (hexoprenaline) and the new domestic β 2-adrenergic agonist - salgim. The drug is a derivative of salbutamol hemisuccinate and succinic acid, which takes part in the Krebs cycle and gives an antihypoxic effect.

Partusisten. Massive tocolysis: intravenous drip 1 mg/day (2 ampoules of 500 mcg) per 400 ml of physiological solution at a rate of 3-4 mcg/min (25-30 drops per minute) Maintenance dose: enterally 2-3 mg (4-6 tablets ) per day.

Ginipral(hexoprenaline) - highly selective β 2-adrenergic agonist, selectively acting on the myometrium (selectivity index 5:1). Massive tocolysis: intravenous drip of 100-150 mcg (4-5 ampoules of 25 mcg each) per 400 ml of physiological solution at a rate of 0.3 mcg/min (15-20 drops per 1 min). Maintenance tocolysis: intravenous drip at a rate of 0.075 mcg/min (8-10 drops per 1 min), enterally 2-3 mg (4-6 tablets) per day.

Salgim. Massive tocolysis: intravenous drip of 10 mg (2 ampoules of 5 mg each) per 400 ml of physiological solution at a rate of 20-25 mcg/min (15-20 drops per 1 min). Maintenance tocolysis: enterally 16-24 mg (4-6 tablets) per day. Contraindications for use β 2-adrenomimetics: fever, infectious diseases in the mother and fetus, hypokalemia, cardiovascular diseases: car-

diomyopathy, conduction and heart rhythm disorders; thyrotoxicosis, glaucoma, bleeding during pregnancy, diabetes.

Potential complications caused by β 2-adrenergic agonists: hyperglycemia; hypotension; hypokalemia; pulmonary edema; arrhythmia; myocardial ischemia.

2. Magnesium sulfate

The effect of magnesium sulfate is associated with the competitive interaction of magnesium ions and the blocking of cell calcium channels, which in turn reduces the intracellular supply of calcium and the activity of myosin light chain kinases.

Magnesium ions in high concentrations can inhibit the contractility of the myometrium as in vitro, so and in vivo due to competition with free calcium ions. Magnesium tocolysis can be effective at therapeutic serum drug concentrations of at least 6 mEq/L (5.5-7.5 mg%). Extensive foreign and own experience shows that effective magnesium tocolysis is ensured by the following administration regimen - 6 g of dry matter for 1 hour and 3 g per hour in a daily dose of 24 g.

Literature data regarding the tocolytic effectiveness of magnesium sulfate are contradictory. Semchyshyn (1983) reported that unintentional (accidental) administration of 17.3 g of magnesium sulfate over 45 minutes did not stop uterine contractility. And yet, most authors note the lower effectiveness of magnesium sulfate compared to that β 2-adrenergic agonists. According to our data, the effectiveness of tocolysis for threatened preterm birth was comparable when using ginipral and magnesium sulfate and amounted to 94.7 and 90%, respectively. In the latent phase of the first stage of labor, the effectiveness of ginipral was 83.3%, and magnesium sulfate - 30%.

Effects of Magnesium Sulfate

Of course, hypermagnesemia has its negative consequences. Side effects in the form of hypotension, feelings of heat, facial hyperemia occur with massive magnesium tocolysis in almost half of the cases. Due to the curare-like effect of high doses of magnesium sulfate when its level in the serum exceeds 10 mEq/L (120 g/L), inhibition of reflex activity, including knee reflexes, is observed. At a concentration of more than 10 meq/l, magnesium has a toxic effect, and more than 12 meq/l causes paralysis of the respiratory muscles. Magnesium sulfate in toxic concentrations causes complications: pulmonary edema, respiratory depression, cardiac arrest, deep muscle paralysis, hypotension.

Therefore, magnesium tocolysis should be carried out taking into account potential complications under strict monitoring of diuresis (at least 30 ml/h), knee reflex activity or serum magnesium concentration.

Effect of tocolytics on fetal heart rate according to CTG data

Magnesium sulfate

Reduced variability.

No effect on basal rate.

Ginipral

Tachycardia.

Reducing the number of accelerations.

Reduced variability.

However, it has been shown that the administration of magnesium sulfate at a dose of 4.5 g per hour gives an effect equivalent to that of parthusistene, terbutaline, and isadrine. Moreover, magnesium sulfate in the case of a combination of premature birth and placental abruption is the only drug of choice for tocolysis, which distinguishes it favorably from drugs in the group β 2-adrenergic agonists.

3. Non-steroidal anti-inflammatory drugs The most common drug in this group is indomethacin, a prostaglandin synthetase inhibitor. However, caution is raised by data confirming the association of the use of the drug (especially before 32 weeks of pregnancy) with premature closure of the ductus arteriosus, IVH and necrotizing enterocolitis. Potential complications of long-term use of indomethacin include

drug-induced hepatitis, renal failure, gastrointestinal bleeding. Indomethacin infusion causes hemodynamic disturbances of cerebral circulation, namely: a significant decrease in the average blood flow velocity, peak systolic and end-diastolic blood flow velocity in the anterior and middle cerebral arteries.

Indomethacin is prescribed 50-100 mg every 8 hours for 2-3 days. Its prescription for polyhydramnios is justified, as it reduces urine production in the fetus.

Calcium antagonists reduce the contractile activity of the myometrium by impairing the penetration of calcium ions into the smooth muscle cell. Most studies have shown the low tocolytic effectiveness of this group of drugs. Side effects not expressed. Possible complications associated with the use of nifedipine are the following: transient hypotension, tachycardia, arrhythmia.

Oxytocin receptor antagonists (atosiban)

The effectiveness of oxytocin receptor antagonists has been shown when administered intravenously or long-term subcutaneously after 28 weeks of pregnancy with intact membranes.

The drug atosiban is a non-protein analogue of oxytocin that can suppress oxytocin-induced myometrial contractions. The use of the drug to stop labor is approved in the United States. However, there is insufficient data on the clinical use of atosiban to accurately assess its effectiveness and safety.

However, despite the large arsenal of modern tocolytic agents, the incidence of preterm birth does not have a significant downward trend. This is primarily due to late start treatment, inadequate choice of drug, its dose and mode of administration.

The next aspect of tocolytic therapy that deserves special attention is its use in the management of pregnant women with prenatal rupture of water. Obstetric tactics for prenatal rupture of water (the cause of at least 40% of all premature births) is the most difficult and not fully resolved obstetric problem.

Currently, when water breaks before 34 weeks of pregnancy, expectant management is officially adopted, and the duration of tocolysis is limited to the time of prevention of fetal respiratory distress syndrome - i.e. 2 days. Is this approach regulated in the Order? 318 Ministry of Health of the Russian Federation.

However, significant successes of neonatologists in caring for very premature newborns dictate the need to revise obstetric tactics during antenatal rupture of water in the direction of maximally prolonging pregnancy.

After 28 weeks of pregnancy, the survival rate of newborns progressively increases and the percentage of disability decreases. This means that maximum prolongation of pregnancy during these periods should be a strategic goal of perinatology.

Unfortunately, the high risk of purulent-septic complications of the mother makes us extremely cautious about prolonging pregnancy during prenatal rupture of water. However, strict implementation of preventive measures and the availability of a wide range of modern antimicrobials can significantly reduce the percentage of purulent-septic complications and provide the possibility of long-term tocolysis during prenatal rupture of water.

Prophylactic antibiotic regimens for antenatal rupture of water

1. Empirical prescription of antibacterial therapy immediately after taking material for culture.

2. Carrying out antibacterial therapy after receiving the results of laboratory tests (microscopy/culture of amniotic fluid, culture from the cervical canal).

3. Conducting antibacterial therapy when clinical signs of chorioamnionitis appear.

The most common scheme is the empirical prescription of antibiotic therapy, and since group B streptococcus is of primary importance among bacterial pathogens in the genesis of infectious lesions of the fetus, semisynthetic penicillins (ampicillin) are the antibiotics of choice.

In this regard, it is promising to carry out long-term tocolytic therapy up to 32-34 weeks of pregnancy in accordance with the level of equipment and qualifications of the neonatal service and against the background of the prevention of fetal respiratory distress syndrome, taking into account clearly limited contraindications.

Tactics for managing premature pregnancy (up to 34 weeks) with antenatal rupture of amniotic fluid.

1. Prevention of infection: compliance with hygienic principles and standards;

Exclusion of vaginal examinations;

Dynamic laboratory analysis microflora.

2. Monitoring the mother's condition:

Thermometry;

Clinical laboratory blood test;

Visual assessment of discharge (water) from the genital tract.

3. Fetal monitoring:

Dynamic assessment of amniotic fluid volume (amniotic fluid index).

4. Prevention of fetal respiratory distress syndrome.

5. Tocolytic therapy.

6. Antibiotic therapy.

Contraindications to tocolytic therapy for premature rupture of membranes

1. Gestational period is more than 34 weeks.

2. The appearance of signs of systemic inflammation (fever, leukocytosis with a shift in the leukocyte formula).

3. The appearance of clinical signs of chorioamnionitis and/or endometritis.

4. Intrauterine suffering and fetal death.

5. Complications of pregnancy and other pathologies for which termination of pregnancy is indicated, regardless of the presence of amniotic sac.

The lecture discusses the main aspects of the etiology, pathogenesis, clinical picture, diagnosis, therapy and prevention of respiratory distress syndrome.

Respiratory distress syndrome premature infants: modern tactics therapy and prevention

The lecture considers the main aspects of etiology, pathogenesis, clinical manifestations, diagnosis, therapy and prevention of respiratory distress syndrome.

Respiratory distress syndrome (RDS) of newborns is an independent nosological form (ICD-X code - R 22.0), clinically expressed in the form of respiratory failure as a result of the development of primary atelectasis, interstitial pulmonary edema and hyaline membranes, the appearance of which is based on surfactant deficiency, manifested in conditions of imbalance of oxygen and energy homeostasis.

Respiratory distress syndrome (synonyms: hyaline membrane disease, respiratory distress syndrome) is the most common cause of respiratory failure in the early neonatal period. Its occurrence is higher, the lower the gestational age and birth weight. RDS is one of the most common and severe diseases of the early neonatal period in premature infants, and it accounts for approximately 25% of all deaths, and in children born at 26-28 weeks of gestation, this figure reaches 80%.

Etiology and pathogenesis. The concept that the basis for the development of RDS in newborns is the structural and functional immaturity of the lungs and surfactant system currently remains leading, and its position was strengthened after data appeared on the successful use of exogenous surfactant.

Surfactant is a monomolecular layer at the interface between the alveoli and air, the main function of which is to reduce the surface tension of the alveoli. Surfactant is synthesized by type II alveolocytes. Human surfactant consists of approximately 90% lipids and 5-10% proteins. The main function - reducing surface tension and preventing the collapse of alveoli during exhalation - is performed by surface-active phospholipids. In addition, surfactant protects the alveolar epithelium from damage and promotes mucociliary clearance, has bactericidal activity against gram-positive microorganisms and stimulates the macrophage reaction in the lungs, participates in the regulation of microcirculation in the lungs and the permeability of the alveolar walls, and prevents the development of pulmonary edema.

Type II alveolocytes begin to produce surfactant in the fetus from the 20-24th week of intrauterine development. A particularly intense release of surfactant onto the surface of the alveoli occurs at the time of birth, which contributes to the primary expansion of the lungs. The surfactant system matures by the 35-36th week of intrauterine development.

Primary surfactant deficiency may be due to low activity of synthesis enzymes, energy deficiency, or increased degradation. The maturation of type II alveolocytes is delayed in the presence of hyperinsulinemia in the fetus and is accelerated under the influence of chronic intrauterine hypoxia caused by factors such as pregnancy hypertension and intrauterine growth retardation. Surfactant synthesis is stimulated by glucocorticoids, thyroid hormones, estrogens, adrenaline and norepinephrine.

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 of the lungs, tidal volume and vital capacity lungs. 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 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 fibrinous-based eosinophilic membranes. In newborns who died from RDS in the first hours of life, hyaline membranes are rarely found.

Clinical signs and symptoms. RDS most often develops in preterm infants with a gestational age of less than 34 weeks. Risk factors for the development of RDS among newborns born at a later date and full term are maternal diabetes mellitus, multiple pregnancy, isoserological incompatibility of maternal and fetal blood, intrauterine infections, bleeding due to abruption or placenta previa, cesarean section before the onset of labor, asphyxia of the fetus and newborn.

The classic picture of RDS is characterized by the staged development of clinical and radiological symptoms that appear 2-8 hours after birth: a gradual increase in breathing, flaring of the wings of the nose, “trumpeter’s breathing”, the appearance of a sonorous groaning exhalation, retraction of the sternum, cyanosis, depression of the central nervous system. The child moans to lengthen the exhalation, due to which there is a real improvement in alveolar ventilation. With inadequate treatment, blood pressure and body temperature decrease, muscle hypotension, cyanosis and pallor of the skin increase, and chest rigidity develops. With the development of irreversible changes in the lungs, general edema and oliguria may appear and increase. On auscultation, weakened breathing and crepitating rales are heard in the lungs. As a rule, signs of cardiovascular failure are observed.

Depending on the morphofunctional maturity of the child and the severity of respiratory disorders, clinical signs of respiratory disorders can occur in various combinations and have varying degrees of severity. Clinical manifestations of RDS in premature infants with a body weight of less than 1500 g and a gestational age of less than 32 weeks have their own characteristics: there is a more prolonged development of symptoms of respiratory failure, a peculiar sequence of symptoms. The earliest signs are diffuse cyanosis on a purple background, then swelling of the chest in the anterosuperior parts, later - retraction of the lower intercostal spaces and retraction of the sternum. Breathing rhythm disturbances most often manifest as apnea attacks, convulsive and paradoxical breathing is often observed. For children with extremely low body weight, such signs as flaring of the wings of the nose, sonorous exhalation, “trumpeter’s breathing,” and severe shortness of breath are uncharacteristic.

Clinical assessment of the severity of respiratory disorders is carried out using the Silverman and Downes scales. In accordance with the assessment, RDS is divided into a mild form of the disease (2-3 points), moderate (4-6 points) and severe (more than 6 points).

An X-ray examination of the chest organs reveals a characteristic triad of signs: a diffuse decrease in the transparency of the pulmonary fields, the borders of the heart are not differentiated, and an “air” bronchogram.

As complications of RDS, it is possible to develop air leak syndromes from the lungs, such as pneumothorax, pneumomediastinum, pneumopericardium and interstitial pulmonary emphysema. Chronic diseases and late complications of hyaline membrane disease include bronchopulmonary dysplasia and tracheal stenosis.

Principles of RDS therapy. A mandatory condition for the treatment of premature babies with RDS is the creation and maintenance of a protective regime: reducing light, sound and tactile effects on the child, local and general anesthesia before performing painful manipulations. Great importance has the creation of an optimal temperature regime, starting with the provision of primary and resuscitation care in the delivery room. When providing resuscitation care to premature infants with a gestational age of less than 28 weeks, it is advisable to additionally use a sterile plastic bag with a slit for the head or a disposable polyethylene-based diaper, which can prevent excessive heat loss. At the end of the complex of primary and resuscitation measures, the child is transferred from the delivery room to the intensive care post, where he is placed in an incubator or under a radiant heat source.

Antibacterial therapy is prescribed to all children with RDS. Infusion therapy is carried out under the control of diuresis. In children, as a rule, there is fluid retention in the first 24-48 hours of life, which requires limiting the volume of infusion therapy. Prevention of hypoglycemia is important.

In severe RDS and high oxygen dependence, parenteral nutrition is indicated. As the condition stabilizes on the 2-3rd day after the trial administration of water through a tube, enteral nutrition with breast milk or infant formula should be gradually added, which reduces the risk of necrotizing enterocolitis.

Respiratory therapy for RDS. Oxygen therapy used for mild forms of RDS using a mask, oxygen tent, nasal catheters.

CPAP- continuous positive airway pressure - constant (i.e. continuously maintained) positive pressure in the airways prevents the collapse of the 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. The use of binasal cannulas and variable flow devices (NCPAP) is preferred.

Prophylactic or early (within the first 30 minutes of life) administration of CPAP is used for all newborns of gestational age 27-32 weeks who are breathing spontaneously. In the absence of spontaneous breathing in a premature infant, mask ventilation is recommended; After spontaneous breathing is restored, CPAP is started.

The use of CPAP in the delivery room is contraindicated, despite the presence of spontaneous breathing in children: with choanal atresia or other congenital malformations of the maxillofacial region, diagnosed pneumothorax, with congenital diaphragmatic hernia, with congenital malformations incompatible with life, with bleeding (pulmonary, gastric, bleeding skin), with signs of shock.

Therapeutic uses of CPAP. Indicated in all cases when a child develops the first signs of respiratory disorders and becomes increasingly dependent on oxygen. In addition, CPAP is used as a method of respiratory support after extubation in newborns of any gestational age.

Mechanical ventilation is the main treatment for severe respiratory failure in newborns with RDS. It should be remembered that performing mechanical ventilation, even with the most advanced devices, inevitably leads to lung damage. Therefore, the main efforts should be aimed at preventing the development of severe respiratory failure. The introduction of surfactant replacement therapy and early use of CPAP helps to reduce the share of mechanical ventilation in the intensive care of newborns with RDS.

In modern neonatology, quite a lot of a large number of methods and modes of mechanical ventilation. In all cases where a child with RDS is not in critical condition, it is better to start with assisted synchronized (trigger) ventilation modes. This will allow the child to actively participate in maintaining the required volume of minute ventilation and will help reduce the duration and frequency of complications of mechanical ventilation. If traditional mechanical ventilation is ineffective, the high-frequency mechanical ventilation method is used. The choice of a specific mode depends on the severity of the patient’s respiratory efforts, the doctor’s experience and the capabilities of the ventilator used.

A necessary condition for effective and safe mechanical ventilation is monitoring the vital functions of the child’s body, blood gas composition and breathing parameters.

Surfactant replacement therapy. Surfactant replacement therapy is a pathogenetic method of treating RDS. This therapy is aimed at replenishing surfactant deficiency, and its effectiveness has been proven in numerous randomized controlled trials. It allows you to avoid high pressures and oxygen concentrations during mechanical ventilation, which helps to significantly reduce the risk of barotrauma and the toxic effect of oxygen on the lungs, reduces the incidence of bronchopulmonary dysplasia, and increases the survival rate of premature infants.

Of the surfactants registered in our country, the drug of choice is Kurosurf, a natural surfactant of pork origin. Available as a suspension in 1.5 ml bottles with a phospholipid concentration of 80 mg/ml. The drug is injected in a stream or slowly in a stream into the endotracheal tube (the latter is possible only if special double-lumen endotracheal tubes are used). Kurosurf must be warmed to 35-37ºC before use. Jet administration of the drug promotes homogeneous distribution of surfactant in the lungs and ensures optimal clinical effect. Exogenous surfactants are prescribed for both the prevention and treatment of neonatal respiratory distress syndrome.

Preventive It is considered that the use of surfactant before the development of clinical symptoms of respiratory distress syndrome in newborns with the highest risk of developing RDS: gestational age less than 27 weeks, absence of a course of antenatal steroid therapy in premature infants born at 27-29 weeks of gestation. The recommended dose of curosurf for prophylactic administration is 100-200 mg/kg.

Early therapeutic use called the use of surfactant in children at risk for RDS due to increasing respiratory failure.

In premature infants with regular spontaneous breathing against the background of early use of CPAP, it is advisable to administer surfactant only when clinical signs of RDS increase. For children born at a gestational age of less than 32 weeks and requiring tracheal intubation for mechanical ventilation in the delivery room due to ineffective spontaneous breathing, surfactant administration is indicated within the next 15-20 minutes after birth. The recommended dose of Kurosurf for early therapeutic administration is at least 180 mg/kg (optimally 200 mg/kg).

Delayed therapeutic use of surfactants. If surfactant was not administered to the newborn for prophylactic or early therapeutic purposes, then after transferring a child with RDS to mechanical ventilation, replacement therapy with surfactant should be carried out as early as possible. The effectiveness of late therapeutic use of surfactant is significantly lower than preventive and early therapeutic use. If there is no or insufficient effect from the first dose, the surfactant is reintroduced. Typically, surfactant is re-administered 6-12 hours after the previous dose.

The use of surfactant for therapeutic treatment is contraindicated in cases of pulmonary hemorrhage, pulmonary edema, hypothermia, decompensated acidosis, arterial hypotension and shock. The patient's condition must be stabilized before administering surfactant. In case of complications of RDS by pulmonary hemorrhage, surfactant can be used no earlier than 6-8 hours after the bleeding has stopped.

Prevention of RDS. The following interventions can improve survival among newborns at risk of developing RDS:

1. Antenatal ultrasound diagnostics to more accurately determine gestational age and assess the condition of the fetus.

2. Continuous fetal monitoring to confirm satisfactory fetal condition during labor or detect fetal distress with subsequent changes in labor management.

3. Assessment of fetal lung maturity before birth - lecithin/sphingomyelin ratio, phosphatidylglycerol content in amniotic fluid.

4. Prevention of premature birth using tocolytics.

5. Antenatal corticosteroid therapy (ACT).

Corticosteroids stimulate the processes of cellular differentiation of numerous cells, including type II alveolocytes, increase the production of surfactant and the elasticity of lung tissue, and reduce the release of proteins from the pulmonary vessels into the airspace. Antenatal use of corticosteroids in women at risk of preterm birth at 28–34 weeks significantly reduces the incidence of RDS, neonatal mortality, and intraventricular hemorrhage (IVH).

Corticosteroid therapy is indicated for the following conditions:

— premature rupture of amniotic fluid;

- clinical signs of the onset of premature labor (regular labor, sharp shortening/smoothing of the cervix, opening up to 3-4 cm);

- bleeding during pregnancy;

- complications during pregnancy (including preeclampsia, intrauterine growth restriction, placenta previa), in which early termination of pregnancy is carried out on a planned or emergency basis.

Maternal diabetes mellitus, preeclampsia, prophylactically treated chorioamnionitis, treated tuberculosis are not contraindications to the use of ACT. In these cases, strict glycemic control and blood pressure monitoring are carried out. Corticosteroid therapy is prescribed under the guise of antidiabetic drugs, antihypertensive or antibacterial therapy.

Corticosteroid therapy is contraindicated in systemic infectious diseases (tuberculosis). Precautionary measures must be observed if chorioamnionitis is suspected (therapy is carried out under the guise of antibiotics).

The optimal interval between corticosteroid therapy and delivery is 24 hours to 7 days from the start of therapy.

Drugs used to prevent RDS:

Betamethasone- 2 doses of 12 mg intramuscularly every 24 hours.

Dexamethasone- 6 mg intramuscularly every 12 hours for 2 days. Since in our country the drug dexamethasone is distributed in ampoules of 4 mg, intramuscular administration of 4 mg 3 times a day for 2 days is recommended.

If there is a threat of premature birth, antenatal administration of betamethasone is preferable. It, as studies have shown, quickly stimulates lung maturation, helps reduce the incidence of IVH and periventricular leukomalacia in premature infants with a gestational age of more than 28 weeks, leading to a significant reduction in perinatal morbidity and mortality.

Doses of corticosteroids do not increase during multiple pregnancies.

A repeat course of ACT is carried out no earlier than 7 days after the decision of the council.

Respiratory distress syndrome (RDS) continues to be one of the most common and severe diseases of the early neonatal period in premature newborns. Antenatal prevention and adequate therapy for RDS can reduce mortality and reduce the incidence of complications in this disease.

O.A. Stepanova

Kazan State Medical Academy

Olga Aleksandrovna Stepanova – Candidate of Medical Sciences, Associate Professor of the Department of Pediatrics and Neonatology

Literature:

1. Grebennikov V.A., Milenin O.B., Ryumina I.I. Respiratory distress syndrome in newborns. - M., 1995. - 136 p.

2. Prematurity: Per. from English / ed. V.H.Yu. Victor, E.K. Vuda-M.: Medicine, 1995. - 368 p.

3. Neonatology: National Guide / ed. N.N. Volodina. - M.: GEOTAR-Media, 2007. - 848 p.

4. Neonatology: Transl. from English / ed. T.L. Gomella, M.D. Cunnigum. - M., 1995. - 640 p.

5. Perinatal audit for premature birth / V.I. Kulakov, E.M. Vikhlyaeva, E.N. Baibarina, Z.S. Khodzhaeva and others // Moscow, 2005. - 224 p.

6. Principles of management of newborns with respiratory distress syndrome / Guidelines edited by N.N. Volodina. - M., 2009. - 32 p.

7. Shabalov N.P. Neonatology. - In 2 volumes. - M.: MEDpress-inform, 2006.

8. Emmanouilidis G.K., Baylen B.G. Cardiopulmonary distress in newborns / Trans. from English - M., Medicine, 1994. - 400 p.

9. Crowley P., Chalmers I., Keirse M. The effects of corticosteroid administration before preterm delivery: an overview of the evidence from controlled trials // BJOG. - 1990. - Vol. 97. - P. 11-25.

10. Yost C.C., Soll R.F. Early versus delayed selective surfactant treatment for neonatal respiratory distress syndrome // Cochrane Library issue 4, 2004.

Respiratory distress syndrome (RDS)- one of the serious problems that doctors caring for premature babies have to face. RDS is a disease of newborns, manifested by the development of respiratory failure immediately or within a few hours after birth. The disease gradually gets worse. Usually, by 2-4 days of life, its outcome is determined: gradual recovery or the death of the baby.

Why do the child’s lungs refuse to perform their functions? Let's try to look into the very depths of this vital organ and figure out what's what.

Surfactant

Our lungs are made up of huge amount small sacs - alveoli. Their total surface is comparable to the area of ​​a football field. You can imagine how tightly all this is packed in the chest. But in order for the alveoli to perform their main function - gas exchange - they must be in a straightened state. A special “lubricant” prevents the alveoli from collapsing - surfactant. The name of the unique substance comes from the English words surface- surface and active- active, that is, surface active. It reduces the surface tension of the inner, air-facing surface of the alveoli, preventing them from collapsing during exhalation.

Surfactant is a unique complex consisting of proteins, carbohydrates and phospholipids. The synthesis of this substance is carried out by the epithelial cells lining the alveoli - alveolocytes. In addition, this “lubricant” has a number of remarkable properties - it is involved in the exchange of gases and liquids through the pulmonary barrier, in the removal of foreign particles from the surface of the alveoli, protecting the alveolar wall from oxidants and peroxides, and to some extent, from mechanical damage.

While the fetus is in the uterus, its lungs do not function, but, nevertheless, they are slowly preparing for future independent breathing - at the 23rd week of development, alveolocytes begin to synthesize surfactant. Its optimal amount is about 50 cubic millimeters per square meter surface of the lungs - accumulates only by the 36th week. However, not all babies “survive” to this date and various reasons appear on White light earlier than expected 38-42 weeks. And this is where the problems begin.

What's happening?

An insufficient amount of surfactant in the lungs of a premature baby leads to the fact that when exhaling, the lungs seem to slam shut (collapse) and the child has to re-inflate them with each breath. This requires a lot of energy; as a result, the newborn’s strength is depleted and severe respiratory failure develops. In 1959, American scientists M.E. Avery and J. Mead discovered pulmonary surfactant deficiency in premature newborns suffering from respiratory distress syndrome, thus identifying the main cause of RDS. The frequency of development of RDS is higher, the shorter the period at which the child was born. Thus, it affects on average 60 percent of children born at a gestational age of less than 28 weeks, 15-20 percent - at a period of 32-36 weeks, and only 5 percent - at a period of 37 weeks or more.

The clinical picture of the syndrome is manifested, first of all, by symptoms of respiratory failure, developing, as a rule, at birth, or 2-8 hours after birth - increased breathing, flaring of the wings of the nose, retraction of the intercostal spaces, participation of auxiliary respiratory muscles in the act of breathing, development of cyanosis (cyanosis). Due to insufficient ventilation of the lungs, a secondary infection often occurs, and pneumonia in such infants is by no means uncommon. The natural healing process begins after 48-72 hours of life, but not all children have this process quickly enough - due to the development of the infectious complications already mentioned.

With rational care and careful adherence to treatment protocols for children with RDS, up to 90 percent of small patients survive. The respiratory distress syndrome suffered in the future has virtually no impact on the health of children.

Risk factors

It is difficult to predict whether a given child will develop RDS or not, but scientists have been able to identify a certain risk group. Predisposes to the development of the syndrome are diabetes mellitus, infections and maternal smoking during pregnancy, birth by cesarean section, birth of the second of twins, asphyxia during childbirth. In addition, it has been found that boys suffer from RDS more often than girls. Prevention of the development of RDS comes down to the prevention of premature birth.

Treatment

Diagnosis of respiratory distress syndrome is carried out in a maternity hospital.

The basis of treatment for children with RDS is the “minimal touch” technique; the child should receive only absolutely necessary procedures and manipulations. One of the methods of treating the syndrome is intensive respiratory therapy, various types of artificial pulmonary ventilation (ALV).

It would be logical to assume that since RDS is caused by a lack of surfactant, then the syndrome should be treated by introducing this substance from the outside. However, this is associated with so many restrictions and difficulties that the active use of artificial surfactant preparations began only in the late 80s - early 90s of the last century. Surfactant therapy allows you to improve the child’s condition much faster. However, these drugs are very expensive, their effectiveness is high only if they are used in the first few hours after birth, and their use requires modern equipment and qualified medical personnel, since there is a high risk of developing severe complications.

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

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

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

Causes of occurrence and mechanism of development

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

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

The following factors may increase your risk of developing RDS:

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

The important role of surfactant

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

Surfactant is vital for maintaining normal breathing

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

Types and prevalence

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

There are:

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

Symptoms

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

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

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

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

Diagnostics

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

To make a correct diagnosis, consider the following information:

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

The following indicators are also used for diagnosis:

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

Treatment

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

Surfactant therapy

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

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

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

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

One of the surfactant preparations

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

CPAP therapy

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

mechanical ventilation

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

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

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

General principles of therapy

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

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

Prevention

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

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

Forecast

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

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