Respiratory distress syndrome in newborns

Syndrome of respiratory distress in newborns (SDR) - respiratory failure of varying severity, mainly in premature infants in the first 2 days of life, due to the immaturity of the lungs and the primary deficit surfactant.

In foreign literature, the terms "respiratory distress syndrome in newborns" (SDR) and "hyaline membrane disease" (BGM) are synonyms. This condition is also called respiratory distress syndrome (RDS).

Epidemiology

This pathology occurs in 1% of all live births and in 14% of newborns with a birth weight less than 2500 g., The syndrome of respiratory distress in newborns and its consequences - the cause of 30-50% of neonatal deaths in the US.

[1], [2], [3],

What causes the syndrome of respiratory distress?

The etiological factors of SDR development are:

• deficiency in the formation and release of surfactant;
• qualitative defect surfactant;
• inhibition and destruction of the surfactant;
• immaturity of the structure of the lung tissue.

These processes are facilitated by:

• prematurity;
• congenital infections;
• chronic intrauterine and acute hypoxia of the fetus and newborn;
• diabetes maternal diabetes;
• acute blood loss in childbirth;
• intra- and periventricular hemorrhages;
• transient hypofunction of the thyroid gland and adrenal glands;
• hypovolemia;
• hyperoxia;
• cooling (general or inhalation of an unheated oxygen-air mixture);
• birth is the second of twins.

Acute perinatal stress, namely, an increase in the duration of labor can reduce the incidence and severity of the respiratory distress syndrome in newborns. Consequently, the planned caesarean section can also be included in the risk factors. Increasing the duration of the anhydrous gap reduces the risk of SDR.

Pathogenesis

In the development of the syndrome of respiratory disorders in neonates, the primary role is played by immature pulmonary tissue and the lack of surfactant. Surfactant is a surface-active substance synthesized by type II pneumocytes, consisting mainly of lipids (90%, 80% of which are phospholipids) and proteins (10%).

The surfactant performs the following functions:

• reduces the surface tension in the alveoli and allows them to straighten;
• prevents the collapse of the alveoli on exhalation;
• Has bactericidal activity against gram-positive bacteria and stimulates a macrophagal reaction in the lungs;
• participates in the regulation of microcirculation in the lungs and permeability of alveolar walls;
• prevents the development of edema of the lungs.

The synthesis of the surfactant in the alveoli begins with the 20th to 24th week of gestation through the reactions of ethanol choline methylation. During this period, the rate of synthesis is low. From the 34th-36th week, the holin route begins to function and the surfactant accumulates in large quantities. Surfactant products are stimulated by glucocorticoids, thyroid hormones, estrogens, epinephrine and norepinephrine.

When the surfactant is deficient after the first inhalation, part of the alveoli recedes, and atelectasis arises. The ventilation capacity of the lungs decreases. Increase in hypoxemia, hypercapnia, respiratory acidosis. On the other hand, the lack of formation of residual air causes an increase in intrapulmonary pressure. High resistance of the pulmonary vessels leads to shunting the blood from right to left along the collaterals, bypassing the pulmonary blood flow. Decrease in intrapulmonary pressure after the first inspiration leads to the fact that the blood already trapped in the capillary channel "fences off" from the active circulation of the small circle by the reflex spasm of the arteries and the tendency to spasmodic venules. In conditions of stasis of blood, there are "coins" (sludge). In response, the coagulation potential of the blood increases, fibrin strands are formed, microthrombi are formed in intact vessels, and around them is the hypocoagulation zone. The DIC-syndrome develops. Microthrombi complicate capillary blood flow, and blood through the intact vascular wall leaves the tissues, leading to hemorrhagic pulmonary edema. Exudate and transudate accumulate in the alveoli (stage of edematous-hemorrhagic syndrome). In the plasma entering the alveoli, hyaline is formed. It lays the surface of the alveoli and disrupts gas exchange, as it is impervious to oxygen and carbon dioxide. These changes are called the disease of hyaline membranes. Light airy, the child breathes intensely, and gas exchange does not occur. Proteolytic enzymes destroy hyaline and fibrin for 5-7 days. In the conditions of severe hypoxia and the increase in acidosis, the synthesis of the surfactant practically ceases.

Thus, all three forms of the syndrome of respiratory distress in newborns (disseminated atelectasis, edema- hemorrhagic syndrome and hyaline membrane disease) are phases of a single pathological process that results in severe hypoxemia and hypoxia, hypercapnia, mixed (respiratory-metabolic) acidosis and other metabolic disorders (hypoglycemia, hypocalcemia, etc.), pulmonary hypertension and systemic hypotension, hypovolemia, microcirculatory disturbances, peripheral edema, muscle hypotension, ra the functional condition of the brain, heart failure (mainly in the right ventricle type with right-hand shunts), temperature instability with a tendency to hypothermia, functional intestinal obstruction.

Symptoms of respiratory distress syndrome in newborns

Symptoms of respiratory distress syndrome in newborn preterm infants are revealed from the first day of life, less often from the second day. The Apgar score at birth can be any. They note intense dyspnoea (up to 80-120 breaths per minute) with the participation of ancillary muscles, sternum suction, abdominal swelling on the inspiration (symptom of a "swing"), and a noisy, groaning, "grunting" exhalation and general cyanosis. For disseminated atelectasis, surface weakened breathing and crepitating rales are characteristic. When the edema-hemorrhagic syndrome marks frothy discharge from the mouth, sometimes pink, over the entire surface of the lungs listen to multiple creping small bubbling rales. In the case of hyaline membranes, breathing in the lungs is hard, wheezing, as a rule, no.

With SDR, a tendency to hypothermia and suppression of central nervous system (CNS) functions due to hypoxia are also observed. The edema of the brain is rapidly progressing, a coma is developing. Often, intraventricular hemorrhage (IVH) is detected, and ultrasound signs of periventricular leukomalacia (PVL) are subsequently revealed. In addition, patients rapidly develop acute cardiac insufficiency in right and left ventricular types with an increase in the liver, edematous syndrome. Preservation of fetal shunts and discharge of blood from right to left through the arterial duct and oval window are due to pulmonary hypertension. With the progression of the syndrome of respiratory disorders in newborns, the severity of the condition is determined by the time of development of shock and DIC syndrome (bleeding from injection sites, pulmonary bleeding, etc.).

To assess the severity of respiratory disorders in newborns use the Silverman scale. Each symptom in the column "Stage I" is rated at 1 point, in the column "Stage II" - in 2 points. With a total score of 10 points, the newborn has an extremely severe SDR, 6-9 points is severe, 5 points is moderate, and below 5, the beginning syndrome of respiratory distress in newborns.

The Silverman Andersen Scale

Step I	Stage II	Stage III
The upper part of the chest (in the position on the back) and the anterior abdominal wall synchronously participate in the act of breathing. Absence of intercostal drag on inspiration. No retraction of the xiphoid process of the sternum on inspiration. Absence of chin movement during breathing. No exhalation noises	Absence of synchronism or minimal descent of the upper part of the thorax when the anterior abdominal wall is raised by inhalation. Easy entrainment of intercostal spaces on inspiration. A slight pull of the xiphoid process of the sternum on inspiration. Lowering of the chin on inhalation, the mouth is closed. Expiratory noise ("expiratory grunting") is audible with auscultation of the thorax	Noticeable westing of the upper part of the thorax during the rise of the anterior abdominal wall on inspiration. Noticeable retraction of intercostal spaces on inspiration. Noticeable zapening of the xiphoid process of the sternum on inspiration. Lowering of the chin on inhalation, the mouth is open. Expiratory noise ("expiratory grunting") is audible when the phonendoscope is brought to the mouth or even without a phonendoscope

With an uncomplicated course of moderate-to-moderate form of SDS, clinical manifestations are most pronounced on the 1-3rd day of life, then the condition gradually improves. In children with birth weight less than 1500 g, the syndrome of respiratory distress in newborns usually occurs with complications, in these cases, the ventilator lasts several weeks.

Typical complications of the respiratory distress syndrome in newborns are air leakage syndromes, bronchopulmonary dysplasia, pneumonia, pulmonary hemorrhages, pulmonary edema, retinopathy of prematurity, renal insufficiency, DIC syndrome, nephrosis of the arterial duct and oval window, IVH.

Diagnosis of the syndrome of respiratory distress in newborns

The diagnosis of SDR is confirmed by the combination of the three main groups of criteria.

1. Clinical features of the syndrome of respiratory distress in newborns.
2. X-ray changes. Children with disseminated atelectasis identify small areas of darkness in the basal zones. Puffy-hemorrhagic syndrome is characterized by a decrease in the size of pulmonary fields, a fuzzy, "blurred" pulmonary pattern up to the "white" lung. With BGM observed "air bronchogram", reticular-nadoznuyu grid.
3. Tests that detect the immaturity of the lung tissue.
4. Absence of surfactant in biological fluids obtained from the lungs: amniotic fluid, aspirate of the contents of the stomach at birth, nasopharyngeal and tracheal fluids. "Foam test" ("shaking test") is also used to assess the maturity of the lungs. When alcohol (ethanol) is added to the liquid to be analyzed and then shaken, bubbles or foam form on its surface in the presence of the surfactant.
5. Indicators of the maturity of the surfactant.
6. The ratio of lecithin / sphingomyelin is the most informative indicator of the maturity of the surfactant. SDR develops in 50% of cases with a value of this ratio less than 2, if less than 1 - in 75%.
7. The level of phosphatidylglycerol.

With SDR for the detection of apnea and bradycardia in newborns, it is imperative to continuously monitor the heart rate and respiration. It is necessary to determine the gas composition of blood from peripheral arteries. The partial pressure of oxygen in arterial blood is recommended to be maintained within 50-80 mm Hg, carbon dioxide - 45-55 mm Hg, saturation of arterial blood with oxygen - 88-95%, pH should be not less than 7.25 . The use of transcutaneous monitors for the determination of p02 and pCO2 and pulse oximeters allows continuous monitoring of oxygenation and ventilation parameters.

At the height of the severity of the respiratory distress syndrome in newborns, a clinical blood test (hemoglobin, hematocrit) is prescribed in dynamics, blood and tracheal contents are sown, a coagulogram (according to indications), and an ECG. Determine the levels of urea, potassium, sodium, calcium, magnesium, total protein, albumin in the blood serum.

[4], [5], [6], [7], [8], [9], [10], [11]

Differential diagnostics

For agenesis, the khohan is characterized by abundant mucous discharge from the nose, while not being able to hold a catheter or probe into the nasopharynx.

Tracheophistinal fistula is clinically manifested by popping, cyanosis, coughing, wheezing in the lungs during feeding. The diagnosis is confirmed by a contrast study of the esophagus and bronchoscopy.

For diaphragmatic hernia at birth, a small scaphoid abdomen, a retracted anterior abdominal wall, is characteristic. The asynchronous movements of the right and left halves of the chest and the displacement of the apical heart beat (more often to the right, the left-sided diaphragmatic hernia occurs 5-10 times more frequently than the right-sided hernia), the shortening of the percussion sound and the absence of respiratory noises in the lower part of the lung. At a roentgenography in a thorax find out an intestine, a liver, etc.

In children with a birth trauma of the brain and spinal cord, along with respiratory disorders, signs of CNS damage are also noted. Neurosonography, lumbar puncture, etc. Help in diagnosis.

With congenital heart defects of the blue type, the skin of the newborns retains a cyanotic color even when inhaled with 100% oxygen. To clarify the diagnosis use the data of clinical examination, auscultation, chest X-ray, ECG, echocardiography.

Massive aspiration is characteristic of born and full-term children. The newborn is born with a low Apgar score. Often SDR is detected from birth. With intubation of the trachea, amniotic fluid (OPV) can be obtained. When radiographing the chest, the flattening of the diaphragm, the displacement of the mediastinal organs in the affected side, rough, with uneven contours of blackout or polysegmentary atelectasis are revealed.

For pneumonia caused by group B Streptococcus and other anaerobes, symptoms of infectious toxicosis are characteristic. Differentiate diseases help clinical blood test, chest X-ray, results of bacteriological studies.

[12], [13], [14], [15], [16], [17], [18], [19]

Treatment of respiratory distress syndrome in newborns

Treatment of the syndrome of respiratory distress in newborns is aimed primarily at eliminating hypoxia and metabolic disorders, as well as normalizing cardiac activity and hemodynamic parameters. Measures should be carried out under the control of the frequency of breathing and its conductance in the lower parts of the lungs, as well as the frequency of cardiac contractions, blood pressure, gas composition of blood, hematocrit.

Temperature conditions

It should be remembered that cooling the child leads to a significant reduction in the synthesis of surfactant, the development of hemorrhagic syndrome and pulmonary hemorrhage. That's why the child is placed in a tuba with a temperature of 34-35 ° C to maintain skin temperature at 36.5 ° C. It is important to ensure maximum peace, since any contact with a child in a serious condition can trigger apnea, a drop in PaO2 or blood pressure. It is necessary to monitor the patency of the respiratory tract, so periodically perform a sanation of the tracheobronchial tree.

Respiratory Therapy

Respiratory therapy begins with the inhalation of heated moisturized 40% oxygen through an oxygen tent, mask, nasal catheters. If, after this, there is no normalization of PaO2 (<50 mmHg when evaluating a Silverman scale of 5 or more), spontaneous breathing under elevated positive pressure (CPAP) is performed using a nasal cannula or an intubation tube. The manipulation begins with a pressure of 4-6 cm of water. At an O2 concentration of 50-60%. Improvement of oxygenation can be achieved, on the one hand, by increasing the pressure to 8-10 cm of water, on the other - by increasing the concentration of O2 inhaled to 70-80%. For premature infants with a body weight of less than 1500 g, the initial positive airway pressure is 2-3 cm of water. The pressure increase is very cautious, as this increases the resistance in the airways, which can lead to a decrease in the elimination of CO2 and the growth of hypercarbia.

With a favorable effect, the SDPD primarily seek to reduce the concentration of O2 to non-toxic numbers (40%). Then, too slowly (1-2 cm of water) under the control of the gas composition of the blood, the pressure in the respiratory tract is reduced to 2-3 cm of water. With the subsequent transfer to oxygenation through the nasal catheter or oxygen tent.

Artificial ventilation of the lungs (IVL) is indicated if, against the background of the SDPA, for an hour:

• a rise in cyanosis;
• shortness of breath to 80 per minute;
• bradypnoe less than 30 per minute;
• the Silverman scale score is more than 5 points;
• More than 60 mm Hg;
• PaO2 less than 50 mmHg;
• pH less than 7.2.

When transferring to artificial ventilation, the following initial parameters are recommended:

• the maximum pressure at the end of the inspiration is 20-25 cm of water;
• the ratio of inspiration to expiration is 1: 1;
• respiratory rate 30-50 per minute;
• oxygen concentration 50-60%;
• end-expiratory pressure 4 cm of water;
• gas flow 2 l / (minxkg).

After 20-30 minutes after the transfer to the ventilator, the state of the child and the gas composition of the blood are evaluated. If the PaO2 remains low (less than 60 mmHg), the ventilation parameters must be changed:

• the ratio of inspiration to expiration is 1.5: 1 or 2: 1;
• the end-expiratory pressure is increased by 1-2 cm of water;
• increase oxygen concentration by 10%;
• the flow of gas in the breathing circuit should be increased by 2 l / min.

After normalization of the state and indicators of the gas composition of the blood, the child is prepared for extubation and transferred to SDPP. Thus hourly aspirate sputum from the mouth and nasal passages, turn the child over, using the drainage position, vibrating and percussion chest massage.

Infusion therapy and nutrition

In newborns with SDR in the acute period of the disease, enteral feeding is impossible, therefore partial or complete parenteral nutrition is necessary, especially with extremely low body weight. Already 40-60 minutes after birth, infusion therapy is started with a 10% glucose solution at a rate of 60 ml / kg, followed by an increase in volume to 150 ml / kg by the end of the first week. The introduction of fluid should be limited in oliguria, as increased water stress makes it difficult to infect the arterial duct. The balance of sodium and chlorine [2-3 mmol / kgsut]], as well as potassium and calcium [2 mmol / kghsut]] is usually achieved by their intravenous administration with 10% glucose solution from the second day of life.

Feeding with breast milk or an adapted mixture begins with an improvement in the condition and a decrease in dyspnea to 60 per minute, the absence of prolonged apnea, regurgitation, after the control giving inside the distilled water. If by the third day enteral feeding is impossible, the child is transferred to parenteral nutrition with the inclusion of amino acids and fats.

Correction of hypovolemia and hypotension

In the acute phase of the disease, hematocrit should be maintained at a level of 0.4-0.5. For this purpose, 5 and 10% solutions of albumin are used, more rarely - transfusion of fresh frozen plasma and erythrocyte mass. In recent years, widely used infukol - 6% isotonic solution, obtained from potato starch synthetic colloid hydroxyethyl starch. Assign 10-15 ml / kg for the prevention and treatment of hypovolemia, shock, microcirculatory disorders. Hypotension is stopped by the administration of dopamine (vasopressor agent) 5-15 μg / kg hmin), starting with small doses.

[20], [21]

Antibiotic therapy

The question of the appointment of antibiotics for the syndrome of respiratory disorders in newborns is decided individually, taking into account the risk factors for the development of pneumonia. Practically they are not prescribed only with mild forms. As starting circuits are recommended:

• cephalosporins of the second generation:
• cefuroxime 30 mg / kg xut) in 2-3 injections 7-10 days;
• third generation cephalosporins:
• cefotaxime 50 mg / kg xut) up to 7 days of life 2 times a day, from 1 st to 4 th week - 3 times;
• ceftazidime 30 mg // kg xut) in 2 steps;
• ceftriaxone 20-50 mg / kg xut) in 1-2 injections;
• aminoglycosides:
• amikacin 15 mg / kg xut) in 2 administrations;
• netilmicin 5 mg / kg xut) in one administration up to 7 days of life and in 2 injections - from the 1st to the 4th week;
• gentamycin 7 mg / kg xut) single-shot to the newborn until 7 days of life and in 2 doses from 1 st to 4 th week;
• Ampicillin can be prescribed at 100-200 mg / kght).

All of the above atibacterial drugs are administered intramuscularly or intravenously.

[22], [23], [24], [25], [26], [27],

Vitaminotherapy

The expediency of using vitamin E for the prevention of bronchopulmonary dysplasia is not confirmed, but it can be used to prevent retinopathy of prematurity at 10 mg / kg for 7-10 days. Vitamin A, administered parenterally to 2000 units a day, is shown to all children before enteral feeding to reduce the incidence of necrotizing enterocolitis and bronchopulmonary dysplasia.

Diuretics

From the 2nd day of life, furosemide 2-4 mg / kghs is used). Diuremic action due to the improvement of renal blood flow also has dopamine in a dose of 1.5-7 μg / kghmin).

[28], [29], [30], [31], [32], [33], [34]

Glucocorticoid therapy

Currently, glucocorticoid therapy is used in case of development of a child acute adrenal insufficiency, shock.

Substitution therapy with surfactant

Substitute surfactant therapy is used to prevent and treat respiratory distress syndrome in newborns. There are biological and synthetic surfactants. With the preventive purpose the drug is administered in the first 15 minutes after birth, with the therapeutic - at the age of 24-48 hours under the condition of ventilation. The injected dose of 100 mg / kg (about 4 ml / kg) is poured endotracheally through the intubation tube into 4 doses at an interval of about 1 min and with a change in the position of the child when each next dose is given. If necessary, the infusion is repeated after 6-12 hours. In total, no more than 4 infusions are administered in 48 hours.

Dispensary supervision

A child who has suffered a respiratory distress syndrome should, in addition to a district pediatrician, be observed by a neurologist, an oculist once every 3 months.

[35], [36], [37], [38]

Prevention

Syndrome of respiratory disorders in newborns can be prevented if we are fighting against hypoxia and miscarriage. In addition, the above described method of use with the preventive purpose of surfactant. Also, the content of the surfactant in the fetus increases with the introduction of betamethasone (women with a threat of interruption of pregnancy at a period of 28-34 weeks) or dexamethasone (48-72 hours before delivery).