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

In newborns it develops due to a lack of surfactant in the immature lungs. Prevention of RDS is carried out by prescribing pregnancy therapy, under the influence of which more rapid maturation of the lungs occurs and surfactant synthesis is accelerated.

Indications for RDS prevention:

— Threatened premature birth with the risk of labor development (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 labor was stopped;
— Placenta previa or low attachment with the risk of recurrent bleeding (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).

During active labor, prevention of RDS is carried out through a set of measures for intrapartum fetal protection.

The acceleration of maturation of fetal lung tissue is facilitated by the administration 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. Prescribing dexamethasone to accelerate the maturation of the fetal lungs is advisable in cases where conservation therapy does not have sufficient effect and there is a high risk of premature birth. Due to the fact that it is not always possible to predict the success of conservation therapy when there is a threat of preterm labor, corticosteroids should be prescribed to all pregnant women undergoing tocolysis. In addition to dexamethasone, the following can be used to prevent 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.

In addition to corticosteroids, other drugs can be used to stimulate surfactant maturation. If a pregnant woman has hypertensive syndrome, a 2.4% solution of aminophylline is prescribed for this purpose in 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 premature birth, this drug is almost the only one.

Acceleration of fetal lung maturation occurs under the influence of the administration of small doses (2.5-5 thousand OD) of folliculin daily for 5-7 days, methionine (1 tablet 3 times a day), essentiale (2 capsules 3 times a day) administration of an ethanol solution , partyist. Lazolvan (ambraxol) is not inferior in effectiveness to cortecosteroids on the fetal lungs and has almost no contraindications. It is administered intravenously at 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 100 units 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 possible premature birth. There are no known contraindications for this method of preventing fetal SDD. It is possible to combine nicotinic acid with corticosteroids, which promotes mutual potentiation of the effects of the drugs.

Prevention of fetal RDS makes sense at a gestational age of 28-34 weeks. Treatment is repeated after 7 days 2-3 times. In cases where prolongation of pregnancy is possible, alveofact is used as replacement therapy after the birth of a child. Alveofact is a purified natural surfactant from the lungs of livestock. The drug improves gas exchange and motor activity of the lungs, shortens the duration of intensive therapy with mechanical ventilation, and reduces the incidence of bronchopulmonary dysplasia. Alveofact treatment is carried out immediately after birth by intratracheal incision. 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 administered drug should not exceed 4 doses for 5 days. There are no contraindications for using Alfeofakt.

For water up to 35 weeks, conservative expectant management is permissible only in the absence of infection, late toxicosis, polyhydramnios, fetal hypoxia, suspicion of fetal malformations, or severe somatic diseases of the mother. In this case, antibiotics are used, means to prevent SDR and fetal hypoxia and reduce the contractile activity of the uterus. Diapers for women must be sterile. Every day it is necessary to conduct a blood test and a woman’s vaginal discharge to timely detect possible infection of the amniotic fluid, as well as 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 helped reduce infectious complications in the early neonatal period. If there is a history of chronic diseases of the genitals, increased leukocytosis in the blood or in the vaginal smear, deterioration of the condition of the fetus or mother, they switch to active tactics (induction of labor).

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

Mandatory in the first stage of premature birth is the prevention or treatment of fetal hypoxia: glucose solution 40% 20 ml with 5 ml of 5% ascorbic acid solution, cigetin solution 1% - 2-4 ml every 4-5 hours, administration of chimes 10-20 mg in 200 ml of 10% glucose solution or 200 ml of rheopolyglucin.

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

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

What Causes Respiratory Distress Syndrome in Children?

The triggering mechanisms of RDS are gross disturbances 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), infectious diseases, poisoning, etc. In addition, the cause of respiratory distress syndrome in children can be the syndrome of massive blood transfusions, unskilled carrying out mechanical ventilation. It develops after clinical death and resuscitation measures as a component of post-resuscitation illness in combination with damage to other organs and systems (MODS).

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

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

Symptoms of respiratory distress syndrome in children

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

There are 4 stages of respiratory distress syndrome in children.

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

Diagnosis and treatment of respiratory distress syndrome in children

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

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

Neonatal respiratory distress syndrome 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, accessory muscle breathing, and nasal flaring that occur soon after birth. Diagnosis is made based on clinical data; Prenatal risk can be assessed using 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 reduces the surface tension of the film of water that covers the inside of the alveoli, thus reducing the tendency of the alveoli to collapse and the work required to fill them.

With insufficient surfactant, 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-to-left intrapulmonary shunt), the child develops hypoxemia. The elasticity of the lungs decreases, so the work expended on breathing increases. In severe cases, weakness of the diaphragm and intercostal muscles, CO2 accumulation 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 by fetal malnutrition, preeclampsia or eclampsia, maternal hypertension, late rupture of membranes, and maternal use of glucocorticoids. Rare causes include congenital surfactant defects caused by mutations in the surfactant protein (SBP and BSS) and ATP-binding cassette transporter A3 genes. Boys and whites are at greater risk.

Symptoms of respiratory distress syndrome

Clinical symptoms of respiratory distress syndrome include rapid, wheezing, shortness of breath movements occurring immediately after birth or within a few hours after birth, with chest indrawing and nasal flaring. 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 at birth may have such rigid lungs that they are unable to initiate and/or maintain breathing in the delivery room.

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

Diagnosis of respiratory distress syndrome

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

Differential diagnoses include pneumonia and sepsis caused by group B streptococcus, transient tachypnea of the newborn, persistent pulmonary hypertension, aspiration, pulmonary edema, and congenital pulmonary-cardiac anomalies. Typically, cultures of blood, cerebrospinal fluid, and possibly tracheal aspirate should be obtained from patients. It is extremely difficult to make a clinical diagnosis of streptococcal (group B) pneumonia; therefore, antibiotic therapy is usually started while awaiting culture results.

The possibility of developing respiratory distress syndrome can be assessed prenatally using lung maturity tests, which measure surfactant obtained through 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 before 39 weeks if fetal heart sounds, human 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, the foam stability index is 47, and/or the surfactant/albumin ratio (measured by fluorescence polarization) is greater than 55 mg/g.

Treatment of respiratory distress syndrome

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

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

Surfactant therapy accelerates recovery and reduces the risk of pneumothorax, interstitial emphysema, intraventricular hemorrhage, bronchopulmonary dysplasia, as well as hospital mortality in the neonatal period and at 1 year. However, infants who received surfactant for respiratory distress syndrome are at higher risk of developing apnea of prematurity. Surfactant replacement options include beractant (bovine lung fatty extract supplemented with proteins B and C, colfosceryl palmitate, palmitic acid and tripalmitin) at a dose of 100 mg/kg every 6 hours, up to 4 doses as needed; poractant alpha (modified extract of ground pork lungs containing phospholipids, neutral fats, fatty acids and proteins B and C) 200 mg/kg, then up to 2 doses of 100 mg/kg if necessary after 12 hours; calfactant (calf lung extract containing phospholipids, neutral fats, fatty acids and proteins B and C) 105 mg/kg after 12 hours up to 3 doses as needed. Lung elasticity may improve rapidly after surfactant administration; To reduce the risk of pulmonary air leak syndrome, it may be necessary to rapidly 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 corticosteroid drugs. Antenatal corticosteroid therapy (ACT) has been used to promote fetal lung maturation since 1972. ACT is highly effective in reducing the risk of RDS, IVH, and neonatal death in preterm infants between 24 and 34 completed weeks of gestation (34 weeks 0 days) (A-1a). The course dose of ACT is 24 mg.

Application schemes:

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

4 doses of dexamethasone IM, 6 mg each, 12 hours apart;

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 borne in mind that when prescribing dexamethasone, there is a higher incidence of hospitalization in the ICU, but a lower incidence of IVH than when using betamethasone (A-1b).

Indications for RDS prevention:

premature rupture of membranes;

clinical signs of premature birth (see above) at 24–34 completed (34 weeks 0 days) weeks (any doubt about 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 EHZ (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. The effectiveness of ACT for periods longer than 34 weeks remains a controversial issue. Perhaps the best recommendation today may be the following: prescribing ACT for more than 34 weeks of pregnancy if there are signs of fetal lung immaturity (in particular in pregnant women with type 1 or type 2 diabetes mellitus).

Prolongation of pregnancy. Tocolysis

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

General contraindications to tocolysis:

Obstetric contraindications:

chorioamnionitis;

abruption of a normal or low-lying placenta (danger of developing Cuveler's uterus);

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

Contraindications from the fetus:

developmental defects incompatible with life;

antenatal fetal death.

Choice of tocolytic

β2-agonists

Today, the most common and best studied in terms of maternal and perinatal effects are selective β2-adrenergic agonists, representatives of which in our country are hexoprenaline sulfate and fenoterol.

Contraindications for the use of β-agonists:

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

hyperthyroidism;

closed-angle form of glaucoma;

insulin-dependent diabetes mellitus;

fetal distress not associated with uterine hypertonicity.

Side effects:

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

from the fetus: tachycardia, hyperbilirubinemia, hypocalcemia.

N.B. The frequency of side effects depends on the dose of β-adrenergic agonists. If tachycardia or hypotension occurs, the rate of drug administration should be reduced; if chest pain occurs, drug administration should be stopped.

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

Respiratory distress syndrome - syndrome of suffocation of prematurity. Maturation of lung tissue ends only after the 35th week of pregnancy; Surfactant deficiency should be expected in a premature baby born before the 35th week of pregnancy. In primary surfactant deficiency, surface tension increases so much that the alveoli collapse. Secondary surfactant deficiency is also possible among full-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 is reduced, and ischemia of type II alveolocytes and pulmonary vessels appears, leading to the effusion of serum proteins into the alveolar space. The opposite situation is possible - the development of a left-to-right shunt through the ALI, which in extremely severe cases can lead to pulmonary hemorrhage.

Full-term and almost full-term babies also sometimes get RDS, but much less often than premature babies. These are mainly newborns after cesarean section or rapid labor, who have suffered asphyxia, and from mothers with diabetes. The relatively stable chest and strong respiratory drive generate very high transpulmonary pressure in full-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 may occur several hours after birth. If signs of respiratory distress are observed 6 hours after delivery, the cause will usually not be primary surfactant deficiency. Symptoms of RDS usually peak on the 3rd day of life, after which gradual improvement occurs.

Classic clinical picture:

cyanosis when breathing air;
groaning breath;
sinking of the pliable parts of the chest;
swelling of the wings of the nose;
tachypnea/apnea;
decreased conductivity of respiratory sounds, crepitating wheezing.

After the onset of the disease, in the absence of complications, the condition of the respiratory system begins to improve in children older than 32 weeks. gestation normalizes by the end of the first week of life. With a gestational age of less than 2K weeks. the disease lasts longer and is often complicated by barotrauma, PDA, gastrointestinal tract, and 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, and arterial hypotension. In addition to DN, the cause of death can be CVD, IVH, and pulmonary hemorrhage.

Diagnosis of respiratory distress syndrome (RDS) in newborns

Chest X-ray: classification according to the degree of deterioration of ventilation in respiratory distress syndrome I-IV.

Laboratory tests: blood culture, tracheal secretion, general blood test, CRP level.

Survey

CBS: possible hypoxemia, hypercapnia, respiratory, mixed or metabolic acidosis.
Clinical blood test, platelets.
Concentration of glucose, Na, K, Ca, Mg in blood serum.
EchoCG will help diagnose PDA, direction and size of shunting.
Blood culture, CSF analysis if bacterial infections are suspected.
Neurosonography will confirm the presence of the most common complications - IVH and PVL.

X-ray of the chest organs

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

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

Stage I. It is characterized by clear granularity, with “air bronchograms”. The contours of the heart are clear,
Stage II. A more diffuse reticulogranular picture with an air bronchogram extended to the periphery of the lungs is characteristic.
Stage III. The darkening of the lungs is intense, but not yet final.
Stage IV. The lungs are completely darkened (“white out”), the boundaries of the heart and diaphragm are not visible.

In the first hours of life, a 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 respiratory phase, the level of PEEP, CPAP and MAP during HF ventilation. In extremely premature infants with a minimal number of alveoli, the lung fields are often transparent.

Differential diagnosis should be carried out with sepsis, congenital pneumonia, congenital heart disease, PPH, 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.

Grades I-II: Oxygen therapy, nasal continuous positive airway pressure is often sufficient.

Stage III-IV: intubation, mechanical ventilation, compensation of surfactant deficiency.

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

Treatment with antibiotics until confirmation of infection elimination.

General stabilization of condition

Maintaining body temperature.
Correction of glucose and electrolyte concentrations in blood serum.
Minimum number of manipulations. Pain relief, sedation if the patient is on mechanical ventilation.
Meeting fluid requirements (usually starts at 70-80 ml/kg/day). Infusion therapy and parenteral nutrition are carried out taking into account blood pressure, Na, K levels, glucose, diuresis, and body weight dynamics. It is tactically preferable to limit the volume of fluid administered. A meta-analysis by Bell and Acarregui showed that fluid restriction (but without fluid restriction) reduces the incidence of PDA, NEC, and the risk of death, and there is a tendency to reduce 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 concentrations with albumin transfusion. Correction of low total plasma protein is not currently supported by any research evidence and may be potentially dangerous.

Hemodynamic stabilization

Low blood pressure in the absence of other hemodynamic symptoms probably does not require treatment. Arterial hypotension in combination with oliguria, large 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

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

Correction of anemia

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

Antibiotic therapy

It is generally accepted to prescribe antibiotics until a bacterial infection has been ruled out. Typically, this is a combination of penicillin or ampicillin with an aminoglycoside. The likelihood of infection in preterm infants increases with prolonged anhydrous periods, maternal fever, fetal tachycardia, leukocytosis, leukopenia, hypotension and metabolic acidosis.

Correction of metabolic acidosis

The negative effects of acidosis on the synthesis of endogenous surfactant, PVR, and myocardium are known. First of all, measures should be taken aimed at general stabilization of the condition, respiratory support, and normalization of hemodynamic parameters. Sodium bicarbonate transfusion should only be performed if the measures described above are unsuccessful. There is currently no convincing evidence that correction of metabolic acidosis with base infusion reduces neonatal mortality and morbidity.

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

A child with RDS should be given a natural surfactant.
Early resuscitation should be the standard practice, but it may sometimes need to be administered in the delivery room for children who require endotracheal intubation to stabilize their condition.
A premature infant with RDS should receive resuscitative surfactant at the earliest possible stage of the disease. The 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 is ineffective.
LISA or MIST may be an alternative to INSURE in spontaneously breathing children.
For premature babies requiring oxygen, saturation should be maintained between 90-94%.
Ventilation with a target tidal volume shortens the duration of mechanical ventilation and reduces the incidence of BPD and IVH.
Avoid hypocapnia and severe hypercapnia as they are associated with brain damage. When removed from mechanical ventilation, a slight hypercapnia is acceptable provided the pH is >7.22.
A second, or less often, a third dose of surfactant should be prescribed if there is an obvious course of RDS with persistent oxygen dependence and mechanical ventilation is necessary.
In children with a gestational age of less than 30 weeks. at risk of RDS, if they do not require intubation for stabilization, nCPAP should be used immediately after birth.
Use caffeine for withdrawal from mechanical ventilation.
Give 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 mild RDS, oxygen therapy alone may be sufficient.

Surfactant

There are two main methods of administering surfactant for RDS.

Prophylactic. A newborn at high risk of RDS is intubated and given surfactant immediately after birth. After this, extubation and transfer to nCPAP are carried out as quickly 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 in the delivery room, showed a reduced risk of SWS and neonatal mortality with prophylactic use. An analysis of new studies (wider use of antenatal steroids, routine stabilization on CPAP starting in the delivery room, and administration of surfactant only when it is necessary to transfer the patient to mechanical ventilation) showed a slightly lower effectiveness of the prophylactic use of surfactant compared with nCPAP, but at the same time there was a difference in such outcomes as mortality.

CPAP

In most modern clinics, spontaneously breathing premature newborns begin breathing using the CPAP system in the delivery room. Prescribing nCPAP to all children with a gestation of less than 30 weeks immediately after birth, with the acceptability of relatively high PaCO 2 indicators, reduces the frequency of transfer to mechanical ventilation of children with RDS and the number of doses of surfactant administered. The recommended starting CPAP level for RDS is 6-8 cm H2O. followed by individualization and dependence on clinical condition, oxygenation and perfusion.

In order to avoid complications of long-term invasive PIL and obtain the benefits of surfactant administration (maintaining the alveoli in an open state, increasing FRC, improving gas exchange in the lungs, reducing the work of breathing), methods for administering surfactant without performing mechanical ventilation have been developed. One of them - INSURE (INtubation SI IRfactant Kxtubation) - is that the patient on nCPAP is intubated soon after birth, surfactant is administered endotracheally, then extubation and transfer to nCPAP are carried out as quickly as possible. Another technique is called LISA (“less invasive surfactant administration”), or MIST (“minimal invasive surfactant therapy”), and it consists of administering surfactant to a patient on nCPAP into the trachea through a thin catheter in the time 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 standard administration techniques 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 mechanical ventilation in the treatment of RDS may be more effective than nCPAP: it reduces the duration of invasive mechanical ventilation and, possibly, the incidence of BPD. Like nCPAP, it can be combined with non-invasive surfactant administration.

Artificial ventilation

Traditional ventilation:

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 composite outcome of death or BPD and reduces the incidence of pneumothorax.

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

Experimental or unproven therapies

Nitric oxide- a selective vasodilator that has shown its effectiveness in the treatment of hypoxemia in full-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 and oxygen in premature newborns with RDS on nCPAP 28-32 weeks. gestation showed a significant reduction in transfer to mechanical ventilation (14.8% vs 45.8%) compared to the usual air-oxygen mixture.

Physiotherapy. Routine physical therapy on the chest is not currently recommended, since it has not yet shown positive results in the treatment of RDS, and the intervention itself contradicts the concept of “minimal handling”.

Diuretics. The authors of a meta-analysis of the administration of furosemide to 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 inhalation is carried out to a premature baby shortly after birth and consists of administering an artificial breath into the airways for 10-15 seconds with a pressure of 20-25 cm of water column. 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 an effect on BPD and mortality in the prolonged inspiration group.

Care

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), and 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;
reducing the frequency and severity of RDS;
reduction in the incidence of IVH, PDA, NEC, pneumothorax

Prognosis of respiratory distress syndrome (RDS) in newborns

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