Prevention of respiratory distress syndrome (RDS) in preterm birth. Corticosteroid (glucocorticoid) therapy for threatened preterm labor

The newborn develops due to a lack of surfactant in the immature lungs. Prevention of RDS is carried out by prescribing pregnant therapy, under the influence of which there is a faster maturation of the lungs and accelerated surfactant synthesis.

Indications for the prevention of RDS:

- Threatened preterm labor with the risk of developing labor activity (3 courses from the 28th week of pregnancy);
- Premature rupture of membranes during premature pregnancy (up to 35 weeks) in the absence of labor;
- From the beginning of the first stage of labor, when it was possible to stop labor;
- Placenta previa or low attachment of the placenta with the risk of rebleeding (3 courses from the 28th week of pregnancy);
- Pregnancy is complicated by Rh-sensitization, which requires early delivery (3 courses from the 28th week of pregnancy).

With active labor, the prevention of RDS is carried out through a set of measures for the intranatal protection of the fetus.

Acceleration of the maturation of the lung tissue of the fetus contributes to the appointment of corticosteroids.

Dexamethasone is prescribed intramuscularly at 8-12 mg (4 mg 2-3 times a day for 2-3 days). In tablets (0.5 mg) 2 mg on the first day, 2 mg 3 times on the second day, 2 mg 3 times on the third day. The appointment of dexamethasone, in order to accelerate the maturation of the lungs of the fetus, is advisable in cases where saving therapy does not have a sufficient effect and there is a high risk of preterm birth. Due to the fact that it is not always possible to predict the success of maintenance therapy for threatened preterm labor, corticosteroids should be prescribed to all pregnant women undergoing tocolysis. In addition to dexamethasone, for the prevention of distress syndrome, prednisolone at a dose of 60 mg per day for 2 days, dexazone at a dose of 4 mg intramuscularly twice a day for 2 days can be used.

In addition to corticosteroids, other drugs may be used to stimulate surfactant maturation. If a pregnant woman has a hypertensive syndrome, for this purpose, a 2.4% solution of aminophylline is prescribed at a dose of 10 ml in 10 ml of a 20% glucose solution for 3 days. Despite the fact that the effectiveness of this method is low, with a combination of hypertension and the threat of preterm labor, this drug is almost the only one.

The acceleration of the maturation of the lungs of the fetus occurs under the influence of the appointment of small doses (2.5-5 thousand OD) folliculin daily for 5-7 days, methionine (1 tab. 3 times a day), Essentiale (2 capsules 3 times a day) introduction of an ethanol solution , partusist. Lazolvan (Ambraxol) is not inferior to cortecosteroids in terms of the effectiveness of the effect on the lungs of the fetus and has almost no contraindications. It is administered intravenously in a dose of 800-1000 mg per day for 5 days.

Lactin (the mechanism of action of the drug is based on the stimulation of prolactin, which stimulates the production of lung surfactant) is administered at 100 IU intramuscularly 2 times a day for 3 days.
Nicotinic acid is prescribed in a dose of 0.1 g for 10 days no more than a month before a possible premature delivery. Contraindications for this method of prevention of fetal SDR have not been clarified. Perhaps the combined appointment of nicotinic acid with corticosteroids, which contributes to the mutual potentiation of the action of drugs.

Prevention of fetal RDS makes sense at a gestational age of 28-34 weeks. The treatment is repeated after 7 days 2-3 times. In cases where prolongation of pregnancy is possible, after the birth of a child, alveofact is used as a replacement therapy. Alveofact is a purified natural surfactant from the lungs of livestock. The drug improves gas exchange and motor activity of the lungs, reduces the period of intensive care with mechanical ventilation, reduces the incidence of bronchopulmonary dysplasia. Alveofactoma treatment is carried out immediately after birth by intratracheal instillation. During the first hour after birth, the drug is administered at the rate of 1.2 ml per 1 kg of body weight. The total amount of the drug administered should not exceed 4 doses for 5 days. There are no contraindications for the use of Alfeofakt.

With water up to 35 weeks, conservative-expectant tactics are permissible only in the absence of infection, late toxicosis, polyhydramnios, fetal hypoxia, suspicion of fetal malformations, severe somatic diseases of the mother. In this case, antibiotics are used, means for the prevention of SDR and fetal hypoxia and a decrease in the contractive activity of the uterus. Diapers for women must be sterile. Every day, it is necessary to conduct a study of a blood test and discharge from a woman's vagina for the timely detection of possible infection of the amniotic fluid, as well as to monitor the heartbeat and condition of the fetus. In order to prevent intrauterine infection of the fetus, we have developed a method of intra-amniotic drip administration of ampicillin (0.5 g in 400 ml of saline), which contributed to the reduction of infectious complications in the early neonatal period. If there is a history of chronic diseases of the genitals, an increase in leukocytosis in the blood or in a vaginal smear, a deterioration in the condition of the fetus or mother, they switch to active tactics (incitation of labor).

With the discharge of amniotic fluid during pregnancy more than 35 weeks after the creation of an estrogen-vitamin-glucose-calcium background, labor induction is indicated by intravenous drip of enzaprost 5 mg per 500 ml of 5% glucose solution. Sometimes it is possible to simultaneously introduce enzaprost 2.5 mg and oxytocin 0.5 ml in a glucose solution 5%-400 ml intravenously.
Premature birth is carried out carefully, following the dynamics of cervical dilatation, labor activity, advancement of the presenting part of the fetus, the condition of the mother and fetus. In case of weakness of labor activity, a mixture of enzaprost 2.5 mg and oxytocin 0.5 ml and glucose solution 5% -500 ml is carefully injected intravenously at a rate of 8-10-15 drops per minute, monitoring the contractile activity of the uterus. In case of rapid or rapid preterm labor, drugs that inhibit the contractile activity of the uterus - b-agonists, magnesium sulfate should be prescribed.

Mandatory in the first period of preterm labor is the prevention or treatment of fetal hypoxia: glucose solution 40% 20 ml with 5 ml of 5% ascorbic acid solution, sigetin 1% solution - 2-4 ml every 4-5 hours, the introduction of curantyl 10-20 mg in 200 ml of 10% glucose solution or 200 ml of reopoliglyukin.

Premature birth in the II period is carried out without protection of the perineum and without "reins", with pudendal anesthesia 120-160 ml of 0.5% novocaine solution. In women who give birth for the first time and with a rigid perineum, an episio-or perineotomy is performed (dissection of the perineum towards the ischial tuberosity or anus). A neonatologist must be present at the birth. The newborn is taken in warm diapers. The prematurity of the child is evidenced by: body weight less than 2500 g, height does not exceed 45 cm, insufficient development of subcutaneous tissue, soft ear and nasal cartilage, the boy’s testicles are not lowered into the scrotum, in girls the large labia do not cover small, wide sutures and the volume of the “cells, a large amount of cheese-like lubricant, etc.

Respiratory distress syndrome in children, or "shock" lung, is a symptom complex that develops after stress, shock.

What causes respiratory distress syndrome in children?

The triggers of RDS are gross violations of microcirculation, hypoxia and tissue necrosis, and activation of inflammatory mediators. Respiratory distress syndrome in children can develop with multiple trauma, severe blood loss, sepsis, hypovolemia (accompanied by shock phenomena), infectious diseases, poisoning, etc. In addition, the cause of respiratory distress syndrome in children may be massive blood transfusion syndrome, unqualified conducting IVL. It develops after clinical death and resuscitation as an integral part of post-resuscitation disease in combination with damage to other organs and systems (OSS).

It is believed that blood cells as a result of hypoplasmia, acidosis and changes in the normal surface charge begin to deform and stick together with each other, forming aggregates - a sludge phenomenon (English sludge - mud, sediment), which causes embolism of small pulmonary vessels. The adhesion of blood cells to each other and to the vascular endothelium triggers the process of blood DIC. At the same time, a pronounced reaction of the body to hypoxic and necrotic changes in tissues, to the penetration of bacteria and endotoxins (lipopolysaccharides) into the blood begins, which has recently been interpreted as a syndrome of generalized inflammatory response (Systemic inflammatory response syndrome - SIRS).

Respiratory distress syndrome in children, as a rule, begins to develop at the end of the 1st-beginning of the 2nd day after the patient is removed from the state of shock. There is an increase in blood filling in the lungs, there is hypertension in the pulmonary vascular system. Increased hydrostatic pressure against the background of increased vascular permeability contributes to the sweating of the liquid part of the blood into the interstitial, interstitial tissue, and then into the alveoli. As a result, lung compliance decreases, surfactant production decreases, the rheological properties of bronchial secretions and the metabolic properties of the lungs as a whole are disturbed. Shunting of blood increases, ventilation-perfusion relations are disturbed, microatelectasis of the lung tissue progresses. In advanced stages of the “shock” lung, hyaline penetrates into the alveoli and hyaline membranes are formed, which sharply disrupt the diffusion of gases through the alveolocapillary membrane.

Symptoms of respiratory distress syndrome in children

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

There are 4 stages of respiratory distress syndrome in children.

In stage I (1-2 days) there is euphoria or anxiety. Growing tachypnea, tachycardia. Harsh breathing is heard in the lungs. Hypoxemia, controlled by oxygen therapy, develops. On the radiograph of the lungs, an increase in the lung pattern, cellularity, small focal shadows are determined.
In stage II (2-3 days), patients are excited, shortness of breath and tachycardia increase. Shortness of breath has an inspiratory character, the breath becomes noisy, "with anguish", auxiliary muscles are involved in the act of breathing. In the lungs, zones of weakened breathing appear, symmetrical scattered dry rales. Hypoxemia becomes resistant to oxygenation. On the roentgenogram of the lungs, a picture of "air bronchography" and confluent shadows are revealed. Lethality reaches 50%.
Stage III (4-5 days) is manifested by diffuse cyanosis of the skin, oligopnea. In the posterior lower parts of the lungs, moist rales of various sizes are heard. There is marked hypoxemia, torpid to oxygen therapy, combined with a tendency to hypercapnia. On the roentgenogram of lungs the symptom of "blizzard" in the form of multiple merging shadows comes to light; possible pleural effusion. Mortality reaches 65-70%.
In stage IV (after the 5th day), patients have stupor, pronounced hemodynamic disturbances in the form of cyanosis, cardiac arrhythmia, arterial hypotension, gasping breathing. Hypoxemia in combination with hypercapnia becomes resistant to mechanical ventilation with a high oxygen content in the supplied gas mixture. Clinically and radiologically, a detailed picture of alveolar pulmonary edema is determined. Lethality reaches 90-100%.

Diagnosis and treatment of respiratory distress syndrome in children

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

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

Respiratory distress syndrome of the newborn is caused by a deficiency of surfactant in the lungs of infants born at less than 37 weeks' gestation. The risk increases with the degree of prematurity. Symptoms of respiratory distress syndrome include shortness of breath, the involvement of additional muscles in the act of breathing, and flaring of the wings of the nose, which occur shortly after birth. Diagnosis is based on clinical findings; prenatally risk can be assessed with lung maturity tests. Treatment includes surfactant therapy and supportive care.

What causes neonatal respiratory distress syndrome?

Surfactant is a mixture of phospholipids and lipoproteins that are secreted by type II pneumocytes; it lowers the surface tension of the water film that lines the inside of the alveoli, thus reducing the tendency of the alveoli to collapse and the work required to fill them.

With surfactant deficiency, diffuse atelectasis develops in the lungs, which provokes the development of inflammation and pulmonary edema. Since the blood passing through the areas of the lung with atelectasis is not oxygenated (forming a right-left intrapulmonary shunt), the child develops hypoxemia. The elasticity of the lungs decreases, therefore, the work expended on breathing increases. In severe cases, weakness of the diaphragm and intercostal muscles, accumulation of CO2, and respiratory acidosis develop.

Surfactant is not produced in sufficient quantities until relatively late in pregnancy; therefore, the risk of respiratory distress syndrome (RDS) increases with the degree of prematurity. Other risk factors include multiple pregnancies and maternal diabetes. The risk is reduced with fetal malnutrition, preeclampsia or eclampsia, maternal hypertension, late rupture of membranes, and maternal glucocorticoid use. Rare causes include birth defects of surfactant caused by mutations in the surfactant protein genes (SFP and SVR) and the ATP-binding cassette transporter A3. Boys and whites are at greater risk.

Symptoms of Respiratory Distress Syndrome

Clinical symptoms of respiratory distress syndrome include rapid, shortness of breath and wheezing respiratory movements that occur immediately after birth or within a few hours after birth, with retraction of compliant places of the chest and swelling of the wings of the nose. With the progression of atelectasis and respiratory failure, the manifestations become more severe, cyanosis, lethargy, irregular breathing and apnea appear.

Babies weighing less than 1000 g may have lungs so rigid that they are unable to start and/or maintain breathing in the delivery room.

Complications of respiratory distress syndrome are intraventricular hemorrhage, periventricular white matter injury, tension pneumothorax, bronchopulmonary dysplasia, sepsis, and neonatal death. Intracranial complications are associated with hypoxemia, hypercapnia, hypotension, BP fluctuations, and low cerebral perfusion.

Diagnosis of respiratory distress syndrome

Diagnosis is based on clinical manifestations, including identification of risk factors; arterial blood gases showing hypoxemia and hypercapnia; and chest radiography. Chest x-ray shows diffuse atelectasis, classically described as a ground-glass appearance with prominent air bronchograms; X-ray picture is closely related to the severity of the course.

The differential diagnosis is with group B streptococcal pneumonia and sepsis, transient neonatal tachypnea, persistent pulmonary hypertension, aspiration, pulmonary edema, and congenital pulmonary heart disease. As a rule, blood cultures, cerebrospinal fluid, and possibly tracheal aspirate should be taken from patients. It is extremely difficult to make a clinical diagnosis of streptococcal (group B) pneumonia; therefore, antibiotic therapy is usually initiated while waiting for culture results.

The possibility of developing respiratory distress syndrome can be assessed prenatally using lung maturity tests that measure surfactant obtained from amniocentesis or taken from the vagina (if the membranes have already ruptured). These tests help determine the optimal time to give birth. They are indicated for selected deliveries up to 39 weeks if fetal heart sounds, chorionic gonadotropin levels, and ultrasound cannot confirm gestational age, and for all deliveries between 34 and 36 weeks. The risk of developing respiratory distress syndrome is lower if the lecithin/sphingomyelin ratio is greater than 2, phosphatidyl inositol is present, foam stability index = 47, and/or surfactant/albumin ratio (measured by fluorescence polarization method) is greater than 55 mg/g.

Treatment of respiratory distress syndrome

Respiratory distress syndrome with treatment has a favorable prognosis; lethality less than 10%. With adequate respiratory support, surfactant production eventually begins, with respiratory distress resolved within 4–5 days, but severe hypoxemia can lead to multiple organ failure and death.

Specific treatment consists of intratracheal administration of a surfactant; this requires tracheal intubation, which may also be necessary to achieve adequate ventilation and oxygenation. Less preterm infants (over 1 kg), as well as children with a lower need for oxygen supplementation (fraction O [H ] in the inhaled mixture less than 40-50%), support alone may be sufficient 02

Surfactant therapy accelerates recovery and reduces the risk of developing pneumothorax, interstitial emphysema, intraventricular hemorrhage, bronchopulmonary dysplasia, and hospital mortality in the neonatal period and at 1 year. At the same time, infants who received surfactant for respiratory distress syndrome are at a higher risk of developing apnea of prematurity. Surfactant replacement options include beractant (bovine lung fat extract supplemented with proteins B and C, colfoceryl palmitate, palmitic acid, and tripalmitin) at 100 mg/kg every 6 hours for up to 4 doses as needed; poractant alfa (modified minced porcine lung extract containing phospholipids, neutral fats, fatty acids, and proteins B and C) 200 mg/kg, then up to 2 doses of 100 mg/kg if needed after 12 hours; calfactant (calf lung extract containing phospholipids, neutral fats, fatty acids and proteins B and C) 105 mg/kg 12 hours later up to 3 doses as needed. Lung compliance may improve rapidly after surfactant administration; to reduce the risk of air leak syndrome, it may be necessary to quickly reduce peak inspiratory pressure. Other ventilation parameters (FiO2 frequency) may also need to be reduced.

Efforts to improve fetal viability in preterm labor include antenatal prophylaxis of RDS with corticosteroids. Antenatal corticosteroid therapy (ACT) has been used since 1972 to accelerate fetal lung maturation. ACT is highly effective in reducing the risk of RDS, IVH, and neonatal death in preterm infants 24 to 34 completed weeks (34 weeks 0 days) of gestation (A-1a). The course dose of ACT is 24 mg.

Application schemes:

2 doses of betamethasone 12 mg IM 24 hours apart (the most commonly used regimen in the RCTs included in the systematic review);

4 doses of dexamethasone IM 6 mg every 12 hours;

3 doses of dexamethasone IM 8 mg every 8 hours.

N. B. The effectiveness of the above drugs is the same, however, it should be noted that when prescribing dexamethasone, there is a higher rate of hospitalization in the ICU, but a lower rate of IVH than with betamethasone (A-1b) .

Indications for the prevention of RDS:

premature rupture of membranes;

clinical signs of preterm labor (see above) at 24-34 full (34 weeks 0 days) weeks (any doubt in the true gestational age should be interpreted in the direction of a smaller one and preventive measures should be taken);

pregnant women who need early delivery due to complications of pregnancy or decompensation of EGD (hypertensive conditions, FGR, placenta previa, diabetes mellitus, glomerulonephritis, etc.).

N. B. Repeated courses of glucocorticoids compared with a single course do not reduce neonatal morbidity and are not recommended (A-1a).

N. B. A controversial issue remains the effectiveness of ACT at terms of more than 34 weeks. Perhaps the best recommendation today would be to prescribe ACT at more than 34 weeks' gestation if there are signs of fetal lung immaturity (particularly in pregnant women with type 1 or type 2 diabetes).

Prolongation of pregnancy. Tocolysis

Tocolysis allows you to gain time for the prevention of RDS in the fetus and the transfer of the pregnant woman to the perinatal center, thus indirectly contributing to the preparation of the premature fetus for birth.

General contraindications for tocolysis:

Obstetric contraindications:

chorioamnionitis;

detachment of a normally or low-lying placenta (danger of developing the uterus of Kuveler);

conditions when prolongation of pregnancy is impractical (eclampsia, preeclampsia, severe extragenital pathology of the mother).

Fetal contraindications:

malformations incompatible with life;

antenatal fetal death.

Choice of tocolytic

β2-agonists

To date, the most common and most studied in terms of maternal and perinatal effects are selective β2-agonists, whose representatives in our country are hexoprenaline sulfate and fenoterol.

Contraindications for the use of β-agonists:

cardiovascular diseases of the mother (aortic stenosis, myocarditis, tachyarrhythmias, congenital and acquired heart defects, cardiac arrhythmias);

hyperthyroidism;

angle-closure glaucoma;

insulin-dependent diabetes mellitus;

fetal distress not associated with uterine hypertonicity.

Side effects:

co mother's side: nausea, vomiting, headaches, hypokalemia, increased blood glucose levels, nervousness / anxiety, tremor, tachycardia, shortness of breath, chest pain, pulmonary edema;

from the side of the fetus: tachycardia, hyperbilirubinemia, hypocalcemia.

N.B. The frequency of side effects depends on the dose of β-agonists. With the appearance of tachycardia, hypotension, the rate of administration of the drug should be reduced, with the appearance of retrosternal pain, the administration of the drug should be stopped.

tocolysis should begin with a bolus injection of 10 mcg (1 ampoule of 2 ml) diluted in 10 ml of isotonic saline over 5-10 minutes (acute tocolysis) followed by an infusion at a rate of 0.3 mcg/min (massive tocolysis). Dose calculation:.

Respiratory distress syndrome - a syndrome of suffocation of prematurity. The maturation of the lung tissue ends only after the 35th week of pregnancy; in a premature baby born before the 35th week of pregnancy, surfactant deficiency should be expected. In primary surfactant deficiency, the surface tension rises so much that the alveoli collapse. Secondary surfactant deficiency is also possible among term infants due to vascular shock, acidosis, sepsis, hypoxia, and meconium aspiration.

Complications:

pneumothorax;
bronchopulmonary dysplasia;
atelectasis;
pneumonia;
persistent fetal circulation;
open aortic duct;
intracranial hemorrhage.

Causes of respiratory distress syndrome (RDS) in newborns

Hypercapnia. hypoxemia and acidosis increase PVR, right-to-left shunting through the foramen ovale and AP often occur, and pulmonary hypertension is a characteristic complication of severe RDS. Pulmonary blood flow decreases, ischemia of type II alveolocytes and pulmonary vessels occurs, leading to effusion of serum proteins into the alveolar space. The opposite situation is possible - the development of a left-right shunt through OLI, which, in an extremely severe case, can lead to pulmonary hemorrhage.

Full-term and near-term babies also sometimes get RDS, but much less often than premature babies. Basically, these are newborns after caesarean section or quick delivery, who have suffered asphyxia, and from mothers with diabetes. The relatively stable chest and strong respiratory drive generate very high transpulmonary pressure in term infants, which contributes to the development of pneumothorax.

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

Symptoms of RDS usually appear in the first minutes after birth, but in some, especially large, children, the onset of clinical manifestations is possible even a few hours after birth. If signs of respiratory distress occur 6 hours postpartum, they are usually not caused by a primary surfactant deficiency. Symptoms of RDS usually peak on the 3rd day of life, after which there is a gradual improvement.

Classical clinical picture:

cyanosis when breathing air;
groaning breath;
sinking of the pliable places of the chest;
swelling of the wings of the nose;
tachypnoea/apnea;
decreased conduction of breath sounds, crepitant wheezing.

After the onset of the disease, in the absence of complications, the state of the respiratory system begins to improve in children older than 32 weeks. gestation returns to normal by the end of the first week of life. With a gestational age of less than 2K weeks. the disease proceeds longer and is often complicated by barotrauma, PDA, SFA, nosocomial infections. Recovery often coincides with an increase in spontaneous diuresis. The use of exogenous surfactant changes (softens, erases) the clinical picture of the disease, reduces mortality and the incidence of complications. The course of RDS, in which no effective treatment is carried out, is characterized by a progressive increase in cyanosis, dyspnea, apnea, arterial hypotension. In addition to DN, the cause of death can be SUV, IVH, and pulmonary hemorrhage.

Diagnosis of respiratory distress syndrome (RDS) in newborns

Chest x-ray: classification according to degree of ventilation impairment in respiratory distress syndrome I-IV.

Laboratory studies: blood culture, tracheal secretion, complete blood count, CRV level.

Survey

COS: possible hypoxemia, hypercapnia, respiratory, mixed or metabolic acidosis.
Clinical blood test, platelets.
The concentration of glucose, Na, K, Ca, Mg in blood serum.
Echocardiography will help diagnose the PDA, the direction and size of the bypass.
Blood cultures, CSF analysis if bacterial infections are suspected.
Neurosonography will confirm the presence of the most frequent complications - IVH and PVL.

Chest X-ray

Radiographically, the lungs have a characteristic, but not pathognomonic picture: a reticulate-granular pattern of the parenchyma (due to small atelectasis) and an “air bronchogram”.

Radiographic changes are classified according to the severity of the process:

I stage. It is characterized by a clear granularity, with "air bronchograms". The contours of the heart are distinct,
II stage. A more vague reticulogranular pattern is characteristic with an air bronchogram extended to the periphery of the lungs.
III stage. Darkening of the lungs is intense, but not yet final.
IV stage. The lungs are completely darkened (“white out”), the borders of the heart and diaphragm are not visible.

In the first hours of life, the radiograph can sometimes be normal, and a typical picture develops after 6-12 hours. In addition, the quality of the image will be affected by the phase of respiration, the level of PEEP, CPAP and MAP during HF ventilation. Extremely preterm infants with minimal alveoli often have translucent lung fields.

Differential diagnosis should be made with sepsis, congenital pneumonia, CHD, PLH, TTN, pneumothorax, congenital alveolar proteinosis, and with the most likely non-pulmonary causes of respiratory distress anemia, hypothermia, polycythemia, hypoglycemia.

Treatment of respiratory distress syndrome (RDS) in newborns

First aid: avoid hypoxia, acidosis, hypothermia.

Grade I-II: oxygen therapy, nasal continuous positive airway pressure is often sufficient.

Grade III-IV: intubation, mechanical ventilation, replacement of surfactant deficiency.

At high risk of respiratory distress syndrome: it is possible to administer a surfactant already in the delivery room.

Treatment with antibiotics until confirmation of elimination of the infection.

General stabilization of the state

Maintaining body temperature.
Correction of the concentration of glucose and electrolytes in the blood serum.
The minimum number of manipulations. Anesthesia, sedation, if the patient is on a ventilator.
Ensuring the need for fluid (usually starts with 70-80 ml / kg / day). Infusion therapy and parenteral nutrition are carried out taking into account the indicators of blood pressure, the level of Na, K, glucose, diuresis, body weight dynamics. It is tactically preferable to limit the amount of fluid administered. A meta-analysis by Bell and Acarregui showed that fluid restriction (but without exsicosis) reduced the incidence of PDA, NEC, the risk of death, and there was a trend towards a decrease in the incidence of chronic lung disease (CLD).

Meta-analysis by Jardine et al. failed to detect a reduction in morbidity and mortality by correcting low plasma albumin levels with albumin transfusion. Correction of low total plasma protein is currently not supported by any research evidence and may be potentially harmful.

Stabilization of hemodynamics

Low blood pressure in the absence of other hemodynamic symptoms probably does not require treatment. Arterial hypotension in combination with oliguria, high BE, increase in lactate, etc. should be treated with careful administration of crystalloids, inotropes/vasopressors, and corticosteroids. In the absence of obvious signs of hypovolemia, early administration of dopamine is preferable to a bolus of 0.9% NaCl solution.

Nutrition

A balanced and early enteral and / or parenteral nutrition is necessary. We usually prescribe small amounts of enteral nutrition to children with RDS on day 1-2 of life, regardless of the presence of umbilical arterial and venous catheters.

Anemia correction

Almost half of the blood volume in premature newborns is in the placenta, and a delay in cord clipping for 1) 45 s increases blood volume by 8-24%. A meta-analysis of late cord clipping in preterm infants compared with early cord clipping showed that later (30–120 s, maximum delay 180 s) clipping reduces the number of subsequent transfusions, IVH of any grade, and the risk of developing necrotizing enterocolitis. Milking the umbilical cord is an alternative to delayed clamping if it cannot be done.

Antibiotic therapy

It is generally accepted to prescribe antibiotics until a bacterial infection has been ruled out. As a rule, this is a combination of penicillin or ampicillin with an aminoglycoside. Premature neonates are more likely to be infected with prolonged anhydrous periods, maternal fever, fetal tachycardia, leukocytosis, leukopenia, hypotension, and metabolic acidosis.

Correction of metabolic acidosis

Known negative effects of acidosis on the synthesis of endogenous surfactant, PSS, myocardium. First of all, measures should be taken aimed at general stabilization of the condition, respiratory support, and normalization of hemodynamic parameters. Transfusion of sodium bicarbonate should be carried out only if the measures described above are unsuccessful. At present, there is no convincing evidence that correction of metabolic acidosis by base infusion reduces neonatal mortality and morbidity.

In conclusion, here are some European recommendations of the latest protocol for the treatment of RDS:

A child with RDS should be given a natural surfactant.
The practice of early resuscitation should be the standard, but sometimes it needs to be given in the delivery room to children who need tracheal intubation to stabilize their condition.
A premature baby with RDS should receive resuscitation surfactant at the earliest possible stage of the disease. Protocol suggests administering surfactant to children<26 нед. гестации при FiO 2 >0.30, children >26 weeks. - with FiO 2 >0.40.
Consider the INSURE technique if CPAP fails.
LISA or MIST may be an alternative to INSURE in spontaneously breathing children.
For premature babies requiring oxygen, saturation should be maintained within 90-94%.
Ventilation with a target tidal volume shortens the duration of mechanical ventilation, reduces the frequency of BPD and IVH.
Avoid hypocapnia and severe hypercapnia as they are associated with brain damage. When removed from a ventilator, slight hypercapnia is acceptable as long as the pH is >7.22.
A second, and less commonly, third dose of surfactant should be given if there is an obvious course of RDS with persistent oxygen dependence and mechanical ventilation is required.
In children with a gestational age of less than 30 weeks. at risk of RDS, if they do not require intubation to stabilize, nCPAP should be used immediately after birth.
Use caffeine to take off the ventilator.
Administer parenteral nutrition immediately after birth. Amino acids can be prescribed from the first day. Lipids can also be prescribed from the first day of life.

Respiratory support

In "large" children (body weight 2-2.5 kg) and children with non-severe RDS, oxygen therapy alone may be sufficient.

Surfactant

There are two main methods of prescribing a surfactant for RDS.

Prophylactic. A newborn at high risk of RDS is intubated immediately after birth and given a surfactant. After that, extubation and transfer to nCPAP is carried out as soon as possible.
Resuscitation. Surfactant is administered after the diagnosis of RDS to a patient on mechanical ventilation.

A meta-analysis of studies done before routine use of CPAP, starting from the delivery room, showed a reduction in the risk of VSS and neonatal mortality with prophylactic use. Analysis of new studies (greater use of antenatal steroids, routine stabilization on CPAP from the delivery room, and administration of surfactant only when a patient needs to be moved to a ventilator) showed a slightly lower effectiveness of prophylactic use of surfactant compared to nCPAP, but at the same time, a difference in outcomes such as mortality.

CPAP

In most modern clinics, in spontaneously breathing preterm infants, CPAP breathing begins in the delivery room. The appointment of nSRAP to all children with gestation less than 30 weeks immediately after birth, the acceptability of relatively high PaCO 2, reduces the frequency of transfer to mechanical ventilation of children with RDS and the number of doses of surfactant administered. The recommended initial level of CPAP for RDS is 6-8 cm of water column. with subsequent individualization and dependence on the clinical condition, oxygenation and perfusion.

In order to avoid the complications of long-term invasive PIL and to gain benefits from the administration of surfactant (maintaining the alveoli in the open state, increasing the FRC, improving the exchange of gases in the lungs, reducing the work of breathing), methods for administering surfactant without mechanical ventilation were developed. One of them - INSURE (INtubation SI IRfactant Kxtubation) - consists in the fact that a patient on nCPAP is intubated shortly after birth, a surfactant is injected into him endotracheally, then extubation is carried out as soon as possible and transfer to nCPAP. Another technique is called LISA (“less invasive surfactant administration” less invasive surfactant administration), or MIST (“minimal invasive surfactant therapy” - minimally invasive surfactant administration), and it consists in introducing a surfactant into the trachea through a thin catheter into the patient on nCPAP. the timing of his laryngoscopy. An additional advantage of the second method is the absence of complications from intubation. A study conducted in 13 NICUs in Germany showed that non-invasive surfactant administration compared with the standard administration technique reduced the duration of mechanical ventilation, the incidence of pneumothorax and IVH.

An alternative method of respiratory support is non-invasive ventilation (HIMV, HSIMV, SiPAP). There is evidence that non-invasive ventilation in the treatment of RDS may be more effective than nCPAP: it reduces the duration of invasive ventilation, and possibly the frequency of BPD. Like nCPAP, it can be combined with non-invasive surfactant administration.

Artificial lung ventilation

Traditional IVL:

The use of high-frequency ventilation (RR>60 per minute) under positive pressure reduces the incidence of pneumothorax.
PTV accelerates the transition to spontaneous breathing.
Volumetric ventilation reduces the incidence of the combined outcome "death or BPD" and reduces the incidence of pneumothorax.

High-frequency oscillatory ventilation is an effective method for the treatment of DN in children with RDS, but has not shown any advantage over conventional mechanical ventilation.

Experimental or unproven therapy

Nitric oxide is a selective vasodilator that has shown its effectiveness in the treatment of hypoxemia in term infants. Late use for the prevention of BPD may be effective, but further research is needed.

Heliox(oxygen-helium mixture). The use of a mixture of helium with oxygen in premature newborns with RDS on nSRAP 28-32 weeks. gestation showed a significant reduction in the transfer to mechanical ventilation (14.8% vs 45.8%) compared with conventional air-oxygen mixture.

Physiotherapy. Routine chest physiotherapy is currently not recommended as it has not yet shown positive results in the treatment of RDS, and the intervention itself is contrary to the concept of "minimal manipulation" ("minimal handling").

Diuretics. The authors of a meta-analysis of the use of furosemide in children with RDS draw the following conclusions: the drug leads to a transient improvement in lung function, but this does not outweigh the risk of symptomatic PDA and the development of hypovolemia.

Liquid ventilation. Currently, there is a description of individual cases of endotracheal administration of perfluorocarbon in extremely severe cases of DN.

An extended breath is carried out to a premature baby shortly after birth and consists in supplying an artificial breath with a duration of 10-15 s into the airways with a pressure of 20-25 cm of water. in order to increase FRC. Analysis by Schmolzer et al. showed a decrease in the frequency of transfer to mechanical ventilation in the first 72 hours of life and an increase in the frequency of PDA without affecting BPD and mortality in the extended inspiration group.

Care

The minimum amount of manipulation; caring for premature babies on a ventilator.

Regular change of position: position on the back, on the side, on the stomach - improves the perfusion-ventilation ratio, promotes the opening of collapsed areas (atelectasis), prevents the occurrence of new atelectasis.

Prevention of respiratory distress syndrome (RDS) in newborns

Prevention of prematurity.
Prevention of perinatal asphyxia.
AGK. Studies on the use of AI K in newborns 24-34 weeks. gestation showed:

reduction in neonatal mortality;
reduction in the frequency and severity of RDS;
decrease in the frequency of IVH, PDA, NEC, pneumothorax

Prognosis of respiratory distress syndrome (RDS) in newborns

Now, with the widespread use of AHA, surfactant, improvement of methods of respiratory support, mortality from RDS and its complications is less than 10%.