Retraction of compliant places of the chest. Respiratory distress syndrome of the fetus and newborn: when the first breath is given with difficulty

Very often in children, parainfluenza is complicated by croup (stenosis, narrowing of the larynx due to inflammation), mainly due to swelling of the subligamentous space. Stenosis of the larynx occurs in the first hours of the disease, suddenly, often at night, and lasts for several hours.

Criteria for the severity of stenosis of the larynx

I degree - inspiratory dyspnea(difficulty inhaling) and retraction of the jugular fossa during physical exertion, with the excitement of the child. The frequency of respiratory movements corresponds to the age norm. There is no respiratory failure.

II degree - the child is restless, excited. Noisy breathing heard at a distance is determined. Inspiratory dyspnea is present at rest (even during sleep) and increases with exertion. Characteristic is the retraction of the compliant places of the chest: retraction of the jugular fossa, supraclavicular and subclavian fossae, intercostal spaces, less often the epigastric region. Pallor and even cyanosis of the nasolabial triangle, moisture and slight marbling of the skin are noted. The frequency of respiratory movements is higher than the age norm, tachycardia (increased heart rate). Respiratory failure of the first degree develops.

III degree - shortness of breath becomes mixed(difficulty inhaling and exhaling). There is a maximum retraction of the compliant places of the chest.

Auxiliary muscles are involved in the act of breathing: swelling of the wings of the nose, tension of the muscles of the neck, participation in the act of breathing of the intercostal muscles. The skin becomes marbled. The heart sounds are muffled, there is a loss of a pulse wave on inspiration. Respiratory failure of the second degree develops.

IV degree - asphyxic stage. The expressed anxiety of the patient is replaced by adynamia. The child quickly loses consciousness. Noisy breathing disappears. The skin is pale, with a grayish tinge. Breathing is shallow, frequent, the retraction of compliant places of the chest disappears. Tachycardia is replaced by bradycardia. Heart sounds are muffled, the pulse is weak. Respiratory failure of the third degree develops. Death comes from asphyxia. The appearance of stenosis on the 1st-2nd day of the disease is typical for a purely viral infection, on the 3rd-4th day - for a viral-bacterial infection.

Also, frequent complications of parainfluenza include viral-bacterial pneumonia, which is characterized by a change in the clinical picture of the disease. The inflammatory process acquires an acute feverish character with a significant increase in temperature, chills, severe headache and even signs of meningism, chest pain, increased cough with sputum (even blood), cyanosis of the lips and the detection of light fine bubbling rales and even pleural friction noise during auscultation. Other complications of parainfluenza can be otitis media and lesions of the paranasal sinuses. Severe forms of the disease are rare and are caused by pneumonia. The parainfluenza virus contributes to the exacerbation of chronic diseases.

14149 0

Respiratory distress syndrome (RDS) of newborns (respiratory distress syndrome, hyaline membrane disease) is a disease of newborns, manifested by the development of respiratory failure (RD) immediately after childbirth or within a few hours after childbirth, increasing in severity up to 2-4 day of life, followed by a gradual improvement.

RDS is due to the immaturity of the surfactant system and is predominantly characteristic of premature babies.

Epidemiology

According to the literature, RDS is observed in 1% of all children born alive, and in 14% of children born weighing less than 2500 g.

Classification

RDS in premature babies is characterized by clinical polymorphism and is divided into 2 main variants:

■ RDS due to primary insufficiency of the surfactant system;

■ RDS in premature infants with a mature surfactant system associated with its secondary insufficiency due to intrauterine infection.

Etiology

The main etiological factor in RDS is the primary immaturity of the surfactant system. In addition, secondary disturbance of the surfactant system is of great importance, leading to a decrease in the synthesis or an increase in the breakdown of phosphatidylcholines. Prenatal or postnatal hypoxia, birth asphyxia, hypoventilation, acidosis, infectious diseases lead to a secondary violation. In addition, the presence of diabetes in the mother, childbirth by caesarean section, male sex, birth as the second of twins, incompatibility of the blood of the mother and fetus predispose to the development of RDS.

Pathogenesis

Insufficient synthesis and rapid inactivation of surfactant lead to a decrease in lung compliance, which, in combination with impaired chest compliance in preterm infants, leads to the development of hypoventilation and insufficient oxygenation. Hypercapnia, hypoxia, respiratory acidosis occur. This, in turn, contributes to an increase in resistance in the vessels of the lungs, followed by intrapulmonary and extrapulmonary shunting of blood. Increased surface tension in the alveoli causes their expiratory collapse with the development of atelectasis and hypoventilation zones. There is a further violation of gas exchange in the lungs, and the number of shunts increases. A decrease in pulmonary blood flow leads to ischemia of alveolocytes and vascular endothelium, which causes changes in the alveolar-capillary barrier with the release of plasma proteins into the interstitial space and the lumen of the alveoli.

Clinical signs and symptoms

RDS is manifested primarily by symptoms of respiratory failure, which usually develops at birth or 2-8 hours after birth. Increased respiration, swelling of the wings of the nose, retraction of compliant places of the chest, participation in the act of breathing of the auxiliary respiratory muscles, cyanosis are noted. On auscultation in the lungs, weakened breathing and crepitant rales are heard. With the progression of the disease, symptoms of circulatory disorders join the signs of DN (decrease in blood pressure, microcirculation disorder, tachycardia, the liver may increase in size). Hypovolemia often develops due to hypoxic damage to the capillary endothelium, which often leads to the development of peripheral edema and fluid retention.

RDS is characterized by a triad of radiological signs appearing in the first 6 hours after birth: diffuse foci of reduced transparency, air bronchogram, and a decrease in the airiness of the lung fields.

These widespread changes are most clearly seen in the lower sections and at the tops of the lungs. In addition, there is a noticeable decrease in lung volume, cardiomegaly of varying severity. Nodozno-reticular changes observed during x-ray examination, according to most authors, are disseminated atelectasis.

For edematous-hemorrhagic syndrome, a "blurred" x-ray picture and a decrease in the size of the lung fields are typical, and clinically - the release of a foamy liquid mixed with blood from the mouth.

If these signs are not detected by X-ray examination 8 hours after birth, then the diagnosis of RDS is doubtful.

Despite the nonspecificity of radiological signs, the study is necessary to exclude conditions in which surgical intervention is sometimes required. Radiographic signs of RDS disappear after 1-4 weeks, depending on the severity of the disease.

■ chest X-ray;

■ determination of indicators of CBS and blood gases;

■ complete blood count with the determination of the number of platelets and the calculation of the leukocyte index of intoxication;

■ determination of hematocrit;

■ biochemical blood test;

■ Ultrasound of the brain and internal organs;

■ Doppler study of blood flow in the cavities of the heart, vessels of the brain and kidneys (indicated for patients on mechanical ventilation);

■ bacteriological examination (smear from the pharynx, trachea, examination of feces, etc.).

Differential Diagnosis

On the basis of only the clinical picture in the first days of life, it is difficult to distinguish RDS from congenital pneumonia and other diseases of the respiratory system.

Differential diagnosis of RDS is carried out with respiratory disorders (both pulmonary - congenital pneumonia, malformations of the lungs, and extrapulmonary - congenital heart defects, birth injury of the spinal cord, diaphragmatic hernia, tracheoesophageal fistulas, polycythemia, transient tachypnea, metabolic disorders).

In the treatment of RDS, it is extremely important to provide optimal patient care. The main principle of treatment for RDS is the "minimal touch" method. The child should receive only the procedures and manipulations necessary for him, the therapeutic and protective regimen should be observed in the ward. It is important to maintain an optimal temperature regime, and in the treatment of children with very low body weight - to provide high humidity to reduce fluid loss through the skin.

It is necessary to strive for a newborn in need of mechanical ventilation to be in a neutral temperature (at the same time, oxygen consumption by tissues is minimal).

In children with deep prematurity, to reduce heat loss, it is recommended to use an additional plastic cover for the whole body (inner screen), a special foil.

oxygen therapy

Carried out in order to ensure the proper level of tissue oxygenation with a minimal risk of oxygen intoxication. Depending on the clinical picture, it is carried out using an oxygen tent or by spontaneous breathing with the creation of a constant positive airway pressure, traditional mechanical ventilation, high-frequency oscillatory ventilation.

Oxygen therapy should be treated with caution, as too much oxygen can damage the eyes and lungs. Oxygen therapy should be carried out under the control of the gas composition of the blood, avoiding hyperoxia.

Infusion therapy

Correction of hypovolemia is carried out with non-protein and protein colloidal solutions:

Hydroxyethyl starch, 6% solution, i.v. 10-20 ml/kg/day, until clinical effect is obtained or

Isotonic solution of sodium chloride IV 10-20 ml / kg / day, until a clinical effect is obtained or

Isotonic solution of sodium chloride/calcium chloride/monocarbonate

sodium / glucose in / in 10-20 ml / kg / day, until a clinical effect is obtained

Albumin, 5-10% solution, i.v. 10-20 ml/kg/day, until clinical effect or

Fresh frozen blood plasma in / in 10-20 ml / kg / day, until a clinical effect is obtained. For parenteral nutrition use:

■ from the 1st day of life: 5% or 10% glucose solution, which provides the minimum energy requirement in the first 2-3 days of life must exceed 0.55 g/kg/h);

■ from the 2nd day of life: solutions of amino acids (AA) up to 2.5-3 g / kg / day (it is necessary that about 30 kcal per 1 g of AA introduced due to non-protein substances; with this ratio, the plastic function of AA is ensured) . In case of impaired renal function (increased levels of creatinine and urea in the blood, oliguria), it is advisable to limit the dose of AA to 0.5 g/kg/day;

■ from the 3rd day of life: fat emulsions, starting from 0.5 g/kg/day, with a gradual increase in dose up to 2 g/kg/day. In case of impaired liver function and hyperbilirubinemia (more than 100-130 μmol / l), the dose is reduced to 0.5 g / kg / day, and with hyperbilirubinemia more than 170 μmol / l, the introduction of fat emulsions is not indicated.

Replacement therapy with exogenous surfactants

Exogenous surfactants include:

■ natural - isolated from human amniotic fluid, as well as from the lungs of piglets or calves;

■ semi-synthetic - obtained by mixing crushed lungs of cattle with surface phospholipids;

■ synthetic.

Most neonatologists prefer to use natural surfactants. Their use provides the effect faster, reduces the incidence of complications and reduces the duration of mechanical ventilation:

Colfosceryl palmitate endotracheally 5 ml/kg every 6-12 hours, but not more than 3 times or

Poractant alfa endotracheally 200 mg/kg once,

then 100 mg/kg once (12-24 hours after the first injection), no more than 3 times, or

Surfactant BL endotracheally

75 mg/kg (dissolve in 2.5 ml isotonic sodium chloride solution) every 6-12 hours, but not more than 3 times.

Surfactant BL can be administered through the side opening of a special endotracheal tube adapter without depressurization of the respiratory circuit and interruption of mechanical ventilation. The total duration of administration should be at least 30 and not more than 90 minutes (in the latter case, the drug is administered using a syringe pump, drip). Another way is to use a nebulizer of inhalation solutions built into the ventilator; while the duration of administration should be 1-2 hours. Within 6 hours after administration, tracheal sanitation should not be carried out. In the future, the drug is administered subject to the continued need for mechanical ventilation with an oxygen concentration in the air-oxygen mixture of more than 40%; the interval between injections should be at least 6 hours.

Mistakes and unreasonable appointments

In case of RDS in newborns weighing less than 1250 g, spontaneous breathing with continuous positive expiratory pressure should not be used during initial therapy.

Forecast

With careful adherence to the protocols for antenatal prevention and treatment of RDS and in the absence of complications in children with a gestational age of more than 32 weeks, the cure can reach 100%. The lower the gestational age, the lower the likelihood of a favorable outcome.

IN AND. Kulakov, V.N. Serov

It occurs in 6.7% of newborns.

Respiratory distress is characterized by several main clinical features:

cyanosis;
tachypnea;
retraction of pliable places of the chest;
noisy exhalation;
swelling of the wings of the nose.

To assess the severity of respiratory distress, the Silverman and Anderson scale is sometimes used, which assesses the synchronism of movements of the chest and abdominal wall, retraction of the intercostal spaces, retraction of the xiphoid process of the sternum, expiratory "grunting", swelling of the wings of the nose.

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

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

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

Epidemiology: Primary (idiopathic) RDS occurs:

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

Causes of respiratory distress syndrome (RDS) in newborns

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

Pathogenesis: surfactant deficiency disease of morphologically and functionally immature lungs. Surfactant deficiency results in alveolar collapse and thus reduced compliance and functional residual lung capacity (FRC).

Risk factors for respiratory distress syndrome (RDS) in newborns

Increased risk in preterm birth, in boys, familial predisposition, primary caesarean section, asphyxia, chorioamnionitis, dropsy, maternal diabetes.

Reduced risk for intrauterine "stress", premature rupture of the membranes without chorionamnionitis, maternal hypertension, drug use, low birth weight, corticosteroid use, tocolysis, thyroid medication.

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

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

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

To determine the cause of respiratory distress in a newborn, you need to look at:

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

Cyanosis

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

Acrocyanosis of a healthy newborn in the first 48 hours of life is not a sign of disease, but shows vasomotor instability, blood sludge (especially with some hypothermia) and does not require examination and treatment of the child. Measurement and monitoring of oxygen saturation in the delivery room is useful for detecting hypoxemia prior to the onset of clinically overt cyanosis.

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

Tachypnea

Tachypnea in newborns is defined as a respiratory rate greater than 60 per minute. Tachypnea can be a symptom of a wide range of diseases, both pulmonary and non-pulmonary etiology. The main causes leading to tachypnea are: hypoxemia, hypercapnia, acidosis, or an attempt to reduce the work of breathing in restrictive lung diseases (in obstructive diseases, the opposite pattern is "beneficial" - rare and deep breathing). With a high respiratory rate, the expiratory time decreases, the residual volume in the lungs increases, and oxygenation increases. MOB also increases, which reduces PaCO 2 and raises pH as a compensatory response to respiratory and/or metabolic acidosis, hypoxemia. The most common respiratory problems leading to tachypnea are RDS and TTN, but in principle this is the case for any lung disease with low compliance; non-pulmonary diseases - PLH, CHD, neonatal infections, metabolic disorders, CNS pathology, etc. Some newborns with tachypnea may be healthy ("happy tachypneic infants"). There may be periods of tachypnea during sleep in healthy children.

In children with lesions of the lung parenchyma, tachypnea is usually accompanied by cyanosis when breathing air and violations of the "mechanics" of breathing, in the absence of parenchymal lung disease, newborns often have only tachypnea and cyanosis (for example, with congenital heart disease).

Retraction of pliable places of the chest

Retraction of the pliable places of the chest is a common symptom of lung diseases. The lower the pulmonary compliance, the more pronounced this symptom. A decrease in retractions in dynamics, ceteris paribus, indicates an increase in pulmonary compliance. There are two types of sinkholes. With obstruction of the upper respiratory tract, the retraction of the suprasternal fossa is characteristic, in the supraclavicular regions, in the submandibular region. In diseases with reduced lung compliance, retraction of the intercostal spaces and retraction of the sternum are observed.

Noisy exhalation

The lengthening of the expiration serves to increase the FOB of the lungs, stabilize the alveolar volume and improve oxygenation. A partially closed glottis produces a characteristic sound. Depending on the severity of the condition, noisy expiration may occur intermittently or be constant and loud. Endotracheal intubation without CPAP/PEEP eliminates the effect of a closed glottis and can lead to a fall in FRC and a decrease in PaO 2 . Equivalent to this mechanism, PEEP/CPAP should be maintained at 2-3 cm H2O. Noisy expiration is more common in pulmonary causes of distress and is usually not seen in children with heart disease until the condition worsens.

Nasal flaring

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

Complications of respiratory distress syndrome (RDS) in newborns

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

Diagnosis of respiratory distress syndrome (RDS) in newborns

Survey

At the initial stage, the most common causes of distress (immaturity of the lungs and congenital infections) should be assumed, after their exclusion, more rare causes (CHDs, surgical diseases, etc.) should be considered.

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

gestational age;
age;
chronic diseases;
incompatibility of blood groups;
infectious diseases;
ultrasound data (ultrasound) of the fetus;
fever;
polyhydramnios / oligohydramnios;
preeclampsia/eclampsia;
taking medications/drugs;
diabetes;
multiple pregnancy;
use of antenatal glucocorticoids (AGCs);
how did the previous pregnancy and childbirth end?

The course of childbirth:

duration;
anhydrous gap;
bleeding;
C-section;
heart rate (HR) of the fetus;
breech presentation;
the nature of the amniotic fluid;
analgesia/anesthesia of childbirth;
mother's fever.

Newborn:

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

Acid-base state

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

Respiratory distress may or may not be accompanied by respiratory failure (RD). DN can be defined as the impairment of the respiratory system's ability to maintain adequate oxygen and carbon dioxide homeostasis.

Chest X-ray

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

You should pay attention to:

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

Hyperoxic test

A hyperoxic test may help in differentiating a cardiac cause of cyanosis from a pulmonary one. To conduct it, it is necessary to determine arterial blood gases in the umbilical and right radial arteries or to carry out transcutaneous oxygen monitoring in the region of the right subclavian fossa and on the abdomen or chest. Pulse oximetry is significantly less useful. Arterial oxygen and carbon dioxide are determined while breathing air and after 10-15 minutes of breathing with 100% oxygen to completely replace alveolar air with oxygen. It is believed that with CHD of the “blue” type there will be no significant increase in oxygenation, with PLH without powerful right-hand shunting it will increase, and with pulmonary diseases it will increase significantly.

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

To distinguish between severe PLH and blue CHD, a hyperventilation test is sometimes performed to raise the pH to above 7.5. IVL begins with a frequency of about 100 breaths per minute for 5-10 minutes. At high pH, pressure in the pulmonary artery decreases, pulmonary blood flow and oxygenation increase in PLH, and almost does not increase in CHD of the “blue” type. Both tests (hyperoxic and hyperventilation) have rather low sensitivity and specificity.

Clinical blood test

You need to pay attention to the changes:

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

C-reactive protein, procalcitonin

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

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

Culture of blood and cerebrospinal fluid

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

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

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

Electrocardiography

echocardiography

Echocardiography (EchoCG) is the standard examination for suspected congenital heart disease and pulmonary hypertension. An important condition for obtaining valuable information will be the study by a doctor who has experience in conducting ultrasound of the heart in newborns.

Treatment of respiratory distress syndrome (RDS) in newborns

For a child in extremely serious condition, of course, one should adhere to the basic rules for resuscitation:

A - to ensure the patency of the respiratory tract;
B - provide breathing;
C - circulate.

It is necessary to quickly recognize the causes of respiratory distress and prescribe appropriate treatment. Should:

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

Surfactant Therapy

Indications:

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

Practical Approach:

2 people should always be present when surfactant is administered.
It is good to sanitize the child and stabilize as much as possible (BP). Keep your head straight.
Install pO 2 / pCO 2 sensors preductively to ensure a stable measurement.
If possible, attach the SpO 2 sensor to the right handle (preductally).
Bolus injection of surfactant through a sterile gastric tube shortened to the length of the endotracheal tube or an additional outlet of the tube for about 1 minute.
Dosage: Alveofact 2.4 ml/kg = 100 mg/kg. Curosurf 1.3 ml/kg = 100 mg/kg. Survanta 4 ml/kg = 100 mg/kg.

Effects of using a surfactant:

Increase in tidal volume and FRC:

PaCO 2 drop
The increase in paO 2 .

Post-Injection Action: Increase PIP by 2 cm H 2 O. The tense (and dangerous) phase now begins. The child should be observed very closely for at least one hour. Fast and continuous optimization of respirator settings.

Priorities:

Decrease PIP as tidal volume increases due to improved compliance.
Decrease FiO 2 if SpO 2 increases.
Then reduce PEEP.
Finally, reduce Ti.
Often ventilation improves dramatically only to deteriorate again 1-2 hours later.
Sanitation of the endotracheal tube without flushing is permitted! It makes sense to use TrachCare, as PEEP and MAP are preserved during the sanitation.
Repeated dose: The 2nd dose (calculated as the first) may be given 8-12 hours later if ventilation parameters deteriorate again.

Attention: 3rd or even 4th dose in most cases does not bring further success, possibly even worsening ventilation due to airway obstruction by large amounts of surfactant (usually more harm than good).

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

Failure to respond to surfactant therapy may indicate:

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

Prevention of respiratory distress syndrome (RDS) in newborns

Prophylactic intratracheal surfactant therapy used in neonates.

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

Prevention of neonatal infection by peripartum antibiotic prophylaxis in pregnant women with suspected chorionamnionitis.

Optimal correction of diabetes mellitus in a pregnant woman.

Very gentle birth control.

Careful, but persistent resuscitation of premature and full-term babies.

Prognosis of respiratory distress syndrome (RDS) in newborns

Very variable, depending on initial conditions.

Risk of e.g. pneumothorax, BPD, retinopathy, secondary infection during mechanical ventilation.

Results of long-term studies:

No effect of surfactant application; on the frequency of retinopathy of prematurity, NEC, BPD or PDA.
Favorable effect of surfactan-1 administration on the development of pneumothorax, interstitial emphysema and mortality.
Shortening of the duration of ventilation (on an endotracheal tube, CPAP) and a decrease in mortality.

The time required for the full development of all organs of the child in the prenatal period is 40 weeks. If the baby is born before this time, his lungs will not be formed enough for full breathing. This will cause a violation of all body functions.

With insufficient development of the lungs, respiratory distress syndrome of the newborn occurs. It usually develops in premature babies. Such babies cannot fully breathe, and their organs lack oxygen.

This disease is also called hyaline membrane disease.

Why does pathology occur?

The causes of the disease are a lack or change in the properties of the surfactant. It is a surfactant that provides elasticity and firmness to the lungs. It lines the surface of the alveoli from the inside - respiratory "sacs", through the walls of which the exchange of oxygen and carbon dioxide takes place. With a lack of surfactant, the alveoli collapse and the respiratory surface of the lungs decreases.

Fetal distress syndrome can also be caused by genetic diseases and congenital malformations of the lungs. These are very rare conditions.

The lungs begin to fully develop after the 28th week of pregnancy. The sooner they happen, the higher the risk of pathology. Boys are particularly affected. If a baby is born before 28 weeks, the disease is almost inevitable.

Other risk factors for pathology:

the appearance of a distress syndrome during a previous pregnancy;
(twins, triplets);
due to Rhesus conflict;
diabetes mellitus (or type 1) in the mother;
asphyxia (suffocation) of the newborn.

Mechanism of development (pathogenesis)

The disease is the most common pathology in newborns. It is associated with a lack of surfactant, which leads to the subsidence of lung areas. Breathing becomes inefficient. A decrease in the concentration of oxygen in the blood leads to an increase in pressure in the pulmonary vessels, and pulmonary hypertension increases the violation of the formation of surfactant. There is a "vicious circle" of pathogenesis.

Surfactant pathology is present in all fetuses up to 35 weeks of intrauterine development. If there is chronic hypoxia, this process is more pronounced, and even after birth, lung cells cannot produce enough of this substance. In such babies, as well as with deep prematurity, type 1 neonatal distress syndrome develops.

A more common variant is the inability of the lungs to produce enough surfactant immediately after birth. The reason for this is the pathology of childbirth and caesarean section. In this case, the expansion of the lungs during the first breath is disturbed, which interferes with the launch of the normal mechanism for the formation of surfactant. Type 2 RDS occurs with asphyxia during childbirth, birth trauma, and operative delivery.

In premature babies, both of the above types are often combined.

Violation of the lungs and increased pressure in their vessels cause an intense load on the heart of the newborn. Therefore, there may be manifestations of acute heart failure with the formation of cardiorespiratory distress syndrome.

Sometimes children of the first hours of life develop or manifest other diseases. Even if the lungs functioned normally after birth, comorbidity leads to a lack of oxygen. This starts the process of increasing pressure in the pulmonary vessels and circulatory disorders. This phenomenon is called acute respiratory distress syndrome.

The adaptation period, during which the lungs of a newborn adapt to breathing air and begin to produce surfactant, is prolonged in preterm infants. If the mother of the child is healthy, it is 24 hours. If a woman is ill (for example, diabetes), the adaptation period is 48 hours. During this time, the child may develop respiratory problems.

Manifestations of pathology

The disease manifests itself immediately after the birth of a child or during the first days of his life.

Symptoms of distress syndrome:

cyanosis of the skin;
flaring nostrils when breathing, fluttering of the wings of the nose;
retraction of the pliable sections of the chest (xiphoid process and the area under it, intercostal spaces, zones above the collarbones) on inspiration;
fast shallow breathing;
decrease in the amount of urine excreted;
"groaning" during breathing, resulting from spasm of the vocal cords, or "expiratory grunts".

Additionally, the doctor fixes such signs as low muscle tone, lowering blood pressure, lack of stool, changes in body temperature, swelling of the face and extremities.

Diagnostics

To confirm the diagnosis, the neonatologist prescribes the following studies:

a blood test with the determination of leukocytes and C-reactive protein;
continuous pulse oximetry to determine the oxygen content in the blood;
the content of gases in the blood;
blood culture "for sterility" for differential diagnosis with sepsis;
lung radiography.

X-ray changes are not specific for this disease. They include darkening of the lungs with areas of enlightenment in the root area and a mesh pattern. Such signs occur with early sepsis and pneumonia, but an x-ray is done for all newborns with respiratory disorders.

Fetal distress syndrome in childbirth is differentiated with such diseases:

temporary tachypnea (rapid breathing): usually occurs in full-term babies after caesarean section, quickly disappears, does not require the introduction of a surfactant;
early sepsis or congenital pneumonia: the symptoms are very similar to RDS, but there are signs of inflammation in the blood and focal shadows on the x-ray of the lungs;
meconium aspiration: appears in full-term babies when meconium is inhaled, has specific radiological signs;
pneumothorax: diagnosed radiologically;
pulmonary hypertension: increased pressure in the pulmonary artery, does not have signs characteristic of RDS on x-rays, is diagnosed using an ultrasound of the heart;
aplasia (absence), hypoplasia (underdevelopment) of the lungs: it is diagnosed even before childbirth, in the postpartum period it is easily recognized by radiography;
Diaphragmatic hernia: on x-ray, the displacement of organs from the abdominal cavity to the chest is determined.

Treatment

Emergency care for fetal distress syndrome is to warm the newly born baby and constantly monitor its temperature. If the birth occurred before 28 weeks, the baby is immediately placed in a special plastic bag or wrapped in plastic wrap. It is recommended that the umbilical cord be cut as late as possible so that the baby receives blood from the mother before starting intensive treatment.

Support for the baby's breathing begins immediately: in the absence of breathing or its inferiority, prolonged inflation of the lungs is carried out, and then a constant supply of air is carried out. If necessary, begin artificial ventilation with a mask, and if it is ineffective - a special apparatus.

The management of newborns with respiratory distress syndrome is carried out in the intensive care unit by the joint efforts of a neonatologist and an intensive care specialist.

There are 3 main methods of treatment:

Replacement therapy with surfactant preparations.
Artificial ventilation of the lungs.
Oxygen therapy.

The introduction of a surfactant is carried out from 1 to 3 times, depending on the severity of the infant's condition. It can be administered through an endotracheal tube placed in the trachea. If the child breathes on his own, the medicine is injected into the trachea through a thin catheter.

In Russia, 3 surfactant preparations are registered:

Curosurf;
Surfactant BL;
Alveofakt.

These drugs are obtained from animals (pigs, cows). Curosurf has the best effect.

After the introduction of the surfactant, ventilation of the lungs is started through a mask or nasal cannula. The child is then transferred to CPAP therapy. What it is? This is a method of maintaining a constant pressure in the airways, which prevents the lungs from collapsing. With insufficient efficiency, artificial ventilation of the lungs is carried out.

The goal of treatment is to stabilize breathing, which usually occurs after 2-3 days. After that, breastfeeding is allowed. If shortness of breath persists with a respiratory rate of more than 70 per minute, it is impossible to feed the baby from the nipple. If normal feeding is delayed, the infant is fed with intravenous infusions of special solutions.

All these measures are carried out in accordance with international standards, which clearly define the indications and sequence of procedures. For treatment of neonatal respiratory distress syndrome to be effective, it must be carried out in specially equipped institutions with well-trained personnel (perinatal centers).

Prevention

Women who are at risk of preterm birth should be admitted to the perinatal center on time. If this is not possible, conditions should be created in advance for nursing the newborn in the maternity hospital where the birth will be taken.

Timely delivery is the best prevention of fetal distress syndrome. To reduce the risk of preterm birth, qualified obstetric monitoring of the course of pregnancy is necessary. A woman should not smoke, use alcohol or drugs. Preparing for pregnancy should not be neglected. In particular, it is necessary to correct the course of chronic diseases such as diabetes in a timely manner.

Prevention of fetal respiratory distress syndrome at high risk of preterm birth is the use of corticosteroids. These drugs promote faster lung development and surfactant production. They are administered for a period of 23-34 weeks intramuscularly 2-4 times. If after 2-3 weeks the threat of preterm labor persists, and the gestational age has not yet reached 33 weeks, the administration of corticosteroids is repeated. The drugs are contraindicated in case of peptic ulcer in the mother, as well as any viral or bacterial infection in her.

Before the completion of the course of hormones and for the transportation of the pregnant woman to the perinatal center, the introduction of tocolytics is indicated - drugs that reduce uterine contractility. With premature outflow of water, antibiotics are prescribed. With a short cervix or already undergone preterm birth, progesterone is used to lengthen the pregnancy.

Corticosteroids are also given at 35-36 weeks for planned caesarean section. This reduces the risk of breathing problems in the infant after surgery.

5-6 hours before cesarean, the fetal bladder is opened. This stimulates the fetal nervous system, which triggers the synthesis of surfactant. During the operation, it is important to remove the baby's head as carefully as possible. With deep prematurity, the head is removed directly in the bubble. This protects against injury and subsequent respiratory disorders.

Possible Complications

Respiratory distress syndrome can quickly worsen a newborn's condition during the first days of his life and even cause death. The likely consequences of the pathology are associated with a lack of oxygen or with incorrect treatment tactics, these include:

accumulation of air in the mediastinum;
mental retardation;
blindness;
vascular thrombosis;
bleeding in the brain or lungs;
bronchopulmonary dysplasia (improper development of the lungs);
pneumothorax (air entering the pleural cavity with compression of the lung);
blood poisoning;
kidney failure.

Complications depend on the severity of the disease. They may be pronounced or not appear at all. Each case is individual. It is necessary to obtain detailed information from the attending physician on further tactics of examination and treatment of the baby. The mother of the child will need the support of loved ones. A psychological consultation would also be helpful.

URL

I. FEATURES OF PATHOGENESIS

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

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

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

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

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

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

One can think of acute respiratory distress syndrome (ARDS) in those cases when the child underwent the process of childbirth without deviations, and subsequently he developed a picture of any disease that contributed to the development of hypoxia of any genesis, centralization of blood circulation, endotoxicosis.

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

Thus, in the first variant of the development of RDS, the starting point is the deficiency and immaturity of the surfactant, in the second, the remaining high pulmonary hypertension and the unrealized process of surfactant synthesis caused by it. In the third option ("mixed"), these two points are combined. The variant of ARDS formation is due to the development of a "shock" lung.

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

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

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

Currently, the main method of intensive care for RDSN is respiratory support. Most often, mechanical ventilation in this pathology has to be started with "hard" parameters, under which, in addition to the danger of barotrauma, hemodynamics is also significantly inhibited. To avoid "hard" parameters of mechanical ventilation with a high average airway pressure, it is necessary to start mechanical ventilation preventively, without waiting for the development of interstitial pulmonary edema and severe hypoxia, i.e., those conditions when ARDS develops.

In the case of the expected development of RDS immediately after birth, one should either “simulate” an effective “first breath”, or prolong effective breathing (in preterm infants) with surfactant replacement therapy. In these cases, IVL will not be so "hard" and long. In a number of children, it will be possible, after short-term mechanical ventilation, to carry out SDPPV through binasal cannulas until the pneumocytes can "acquire" a sufficient amount of mature surfactant.

The preventive start of mechanical ventilation with the elimination of hypoxia without the use of "hard" mechanical ventilation will allow more effective use of drugs that reduce pressure in the pulmonary circulation.

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

II. DIAGNOSTICS.

A. Clinical signs

Symptoms of respiratory failure, tachypnea, chest distention, flaring of the alae, difficulty exhaling, and cyanosis.
Other symptoms, eg hypotension, oliguria, muscle hypotension, temperature instability, intestinal paresis, peripheral edema.
Prematurity when assessing gestational age.

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

RDS Severity Assessment (Modified Downes Scale)

Points Frequency Respiratory cyanosis in 1 min.	retraction	expiratory grunt	The nature of breathing on auscultation
0 < 60 нет при 21%	No	No	puerile
1 60-80 present, disappears at 40% O2	moderate	listens- stethoscope	changed weakened
2 > 80 disappears or apnea at	significant	heard distance	Badly held

A score of 2-3 points corresponds to mild RDS

A score of 4-6 points corresponds to moderate RDS

A score of more than 6 points corresponds to severe RDS

B. RADIOGRAPH OF THE CHEST. Characteristic nodular or round opacities and air bronchograms are indicative of diffuse atelectasis.

B. LABORATORY SIGNS.

Lecithin/Sphiringomyelin ratio in amniotic fluid less than 2.0 and negative results of the shake test in the study of amniotic fluid and gastric aspirate. In newborns from mothers with diabetes mellitus, RDS may develop at L/S greater than 2.0.
Absence of phosphatyldiglycerol in amniotic fluid.

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

III. COURSE OF DISEASE.

A. RESPIRATORY INSUFFICIENCY, increasing within 24-48 hours, and then stabilizing.

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

IV. PREVENTION

In case of premature birth in the period of 28-34 weeks, an attempt should be made to inhibit labor activity by using beta-mimetics, antispasmodics or magnesium sulfate, after which glucocorticoid therapy should be carried out according to one of the following schemes:

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

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

When using glucocorticoids, blood sugar monitoring should be carried out.

With the intended delivery by cesarean section, if conditions are present, delivery should begin with an amniotomy performed 5-6 hours before the operation in order to stimulate the sympathetic-adrenal system of the fetus, which stimulates its surfactant system. In a critical condition of the mother and fetus, amniotomy is not performed!

Prevention is facilitated by careful removal of the fetal head during caesarean section, and in very premature babies, removal of the fetal head in the fetal bladder.

V. TREATMENT.

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

A. Maintenance of airway patency

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

B. Oxygen therapy.

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

B. Vascular access

1. A venous umbilical catheter with an end above the diaphragm may be useful for providing venous access and measuring central venous pressure.

D. Correction of hypovolemia and anemia

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

D. Acidosis

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

E. Feeding

If the hemodynamics of the newborn is stable and you manage to stop respiratory failure, then feeding should begin at 48-72 hours of life.
Avoid nipple feeding if dyspnoea exceeds 70 breaths per minute as high risk of aspiration.
If it is not possible to start enteral feeding, consider parenteral nutrition.
Vitamin A parenterally at 2000 IU every other day, until enteral feeding is started, reduces the incidence of chronic lung obstruction.

G. Chest x-ray

For diagnosis and assessment of the course of the disease.
To confirm the location of the endotracheal tube, pleural drainage, and umbilical catheter.
To diagnose complications such as pneumothorax, pneumopericardium and necrotizing enterocolitis.

Z. Excitation

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

I. Infection

In most newborns with respiratory failure, sepsis and pneumonia should be ruled out, so empiric antibiotic therapy with broad-spectrum bactericidal antibiotics should be considered until cultures are silent.
Group B hemolytic streptococcus infection may clinically and radiologically resemble RDS.

K. Treatment of acute respiratory failure

The decision to use respiratory support techniques should be justified in the medical history.
In newborns weighing less than 1500 g, the use of CPAP techniques can lead to unnecessary energy expenditure.
It is necessary to initially try to adjust the ventilation parameters in order to reduce FiO2 to 0.6-0.8. Usually this requires maintaining an average pressure in the range of 12-14 cmH2O.

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

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

A. Maintain pCO2 less than 60 mmHg by changing the ventilation rate or peak pressure.
b. If your attempts to stop hypercapnia lead to impaired oxygenation, consult with more experienced colleagues.

K. Causes of deterioration of the patient's condition

Rupture of the alveoli and the development of interstitial emphysema, pneumothorax or pneumopericardium.
Violation of the tightness of the respiratory circuit.

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

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

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

5. Much less often, deterioration in the condition of newborns is due to intracranial hemorrhage, septic shock, hypoglycemia, nuclear jaundice, transient hyperammonemia, or congenital metabolic defects.

Selection scale for some IVL parameters in newborns with RDS

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

Note: This diagram is for guidance only. The parameters of mechanical ventilation can be changed based on the clinic of the disease, blood gases and CBS, and pulse oximetry data.

Criteria for the application of respiratory therapy measures

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

M. Surfactant therapy

A. Human, synthetic and animal surfactants are currently being tested. In Russia, the surfactant EXOSURF NEONATAL, manufactured by Glaxo Wellcome, is approved for clinical use.
b. It is prescribed prophylactically in the delivery room or later, within a period of 2 to 24 hours. Prophylactic use of a surfactant is indicated for: premature newborns with a birth weight of less than 1350 g with a high risk of developing RDS; newborn weighing more than 1350 g with objectively confirmed immaturity of the lungs. For therapeutic purposes, surfactant is used in a newborn with a clinically and radiographically confirmed diagnosis of RDS, who is on a ventilator through an endotracheal tube.
V. Introduced into the respiratory tract in the form of a suspension in saline solution. For prophylactic purposes, "Exosurf" is administered from 1 to 3 times, for therapeutic purposes - 2 times. A single dose of "Exosurf" in all cases is 5 ml / kg. and is administered as a bolus in two half doses over a period of 5 to 30 minutes, depending on the response of the child. It is safer to inject the solution micro-stream at a rate of 15-16 ml/h. A second dose of Exosurf is administered 12 hours after the initial dose.
d. Reduces the severity of RDS, but the need for mechanical ventilation persists and the incidence of chronic lung disease does not decrease.

VI. TACTICAL ACTIVITIES

A neonatologist heads the team of specialists in the treatment of RDS. trained in resuscitation and intensive care or a qualified resuscitator.

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