Respiratory distress syndrome of newborns. Respiratory distress syndrome in children

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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 age.

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.

L. 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 RCHN.

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

Application schemes:

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

4 doses of dexamethasone IM 6 mg every 12 hours;

3 doses of dexamethasone IM 8 mg every 8 hours.

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

Indications for the prevention of RDS:

premature rupture of membranes;

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

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

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

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

Prolongation of pregnancy. Tocolysis

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

General contraindications for tocolysis:

Obstetric contraindications:

chorioamnionitis;

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

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

Fetal contraindications:

malformations incompatible with life;

antenatal fetal death.

Choice of tocolytic

β2-agonists

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

Contraindications for the use of β-agonists:

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

hyperthyroidism;

angle-closure glaucoma;

insulin-dependent diabetes mellitus;

fetal distress not associated with uterine hypertonicity.

Side effects:

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

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

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

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

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 a ductus-dependent CHD is suspected, prostaglandin E 1 should be administered 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 carefully 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 the duration of ventilation (on an endotracheal tube, CPAP) and reducing mortality.

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

Indications for the prevention of RDS:

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

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

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

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

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

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

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

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

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

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

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

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

Synonyms

Hyaline membrane disease.

DEFINITION

RDS is a severe respiratory disorder in preterm infants caused by lung immaturity and primary surfactant deficiency.

EPIDEMIOLOGY

RDS is the most common cause of respiratory failure in the early neonatal period. Its occurrence is the higher, the lower the gestational age and body weight of the child at birth. Conducting prenatal prophylaxis with the threat of preterm birth also affects the incidence of RDS.

In children born earlier than 30 weeks of gestation and who did not receive prenatal prophylaxis with betamethasone or dexamethasone, its frequency is about 65%, during prophylaxis - 35%; in children born at a gestational age of 30-34 weeks: without prophylaxis - 25%, with prophylaxis - 10%.

In children born with a gestation of more than 34 weeks, the incidence of RDS does not depend on prenatal prophylaxis and is less than 5%.

ETIOLOGY

The reasons for the development of RDS include a violation of the synthesis and excretion of surfactant. associated with lung immaturity. The most significant factors influencing the incidence of RDS. are presented in table. 23-5.

Table 23-5. Factors affecting the development of RDS

DEVELOPMENT MECHANISM

A key link in the pathogenesis of RDS is a surfactant deficiency resulting from the structural and functional immaturity of the lungs.

Surfactant is a group of surfactants of a lipoprotein nature that reduce surface tension forces in the alveoli and maintain their stability. In addition, the surfactant improves mucociliary transport, has bactericidal activity, and stimulates the macrophage reaction in the lungs. It consists of phospholipids (phosphatidylcholine, phosphatidylglycerol), neutral lipids and proteins (proteins A, B, C, D).

Type II alveolocytes begin to produce surfactant in the fetus from the 20-24th week of intrauterine development. A particularly intense release of surfactant to the surface of the alveoli occurs at the time of childbirth, which contributes to the primary expansion of the lungs.

There are two ways to synthesize the main phospholipid component of the surfactant - phosphatidylcholine (lecithin).

The first (with the participation of methyltransferase) actively proceeds from the 20-24th week to the 33-35th week of intrauterine development. It is easily depleted under the influence of hypoxemia, acidosis, hypothermia. Surfactant reserves up to the 35th week of gestation ensure the onset of breathing and the formation of functional residual lung capacity.

The second pathway (with the participation of phosphocholine transferase) begins to act only from the 35-36th week of intrauterine development, it is more resistant to hypoxemia and acidosis.

With a deficiency (or reduced activity) of the surfactant, the permeability of the alveolar and capillary membranes increases, stagnation of blood in the capillaries develops, diffuse interstitial edema and hyperdistension of the lymphatic vessels; collapse of the alveoli and atelectasis. As a result, the functional residual capacity, tidal volume and vital capacity of the lungs decrease. As a result, the work of breathing increases, intrapulmonary shunting of blood occurs, and hypoventilation of the lungs increases. This process leads to the development of hypoxemia, hypercapnia and acidosis.

Against the background of progressive respiratory failure, dysfunctions of the cardiovascular system occur: secondary pulmonary hypertension with a right-handed blood shunt through functioning fetal communications; transient myocardial dysfunction of the right and / or left ventricles, systemic hypotension.

On pathoanatomical examination, the lungs are airless, sinking in water. Microscopy reveals diffuse atelectasis and necrosis of alveolar epithelial cells. Many of the dilated terminal bronchioles and alveolar ducts contain fibrinous-based eosinophilic membranes. It should be noted that hyaline membranes are rarely found in newborns who died from RDS in the first hours of life.

CLINICAL CHARACTERISTICS

Early signs of RDS include:

Shortness of breath (more than 60/min), occurring in the first minutes or hours of life;

Expiratory noises (“grunting exhalation”) as a result of the development of a compensatory spasm of the glottis on exhalation, which prevents the alveoli from collapsing;

Retraction of the chest on inspiration (retraction of the xiphoid process of the sternum, epigastric region, intercostal spaces, supraclavicular fossae) with simultaneous inflation of the wings of the nose and cheeks (breathing "trumpeter").

Respiratory failure in most cases progresses during the first 24-48 hours of life. On the 3-4th day, as a rule, stabilization of the condition is noted. In most cases, RDS resolves by day 5-7 of life. It is possible to organize prenatal diagnosis (risk prediction) of RDS, based on the study of the lipid spectrum of amniotic fluid, but it is appropriate only in large specialized hospitals and regional perinatal centers.

The following methods are the most informative.

Ratio of lecithin to sphingomyelin (normal >2). If the coefficient is less than 1, then the probability of developing RDS is about 75%. In newborns from mothers with diabetes mellitus, RDS can develop when the ratio of lecithin to sphingomyelin is more than 2.0.

Saturated phosphatidylcholine (normal >5 µmol/L) or phosphatidylglycerol (normal >3 µmol/L). The absence or sharp decrease in the concentration of saturated phosphatidylcholine and phosphatyldiglycerol in the amniotic fluid indicates a high likelihood of developing RDS.

DIFFERENTIAL DIAGNOSTIC MEASURES

Diagnosis of the disease is based mainly on the history (risk factors), the clinical picture, and the results of x-ray examination.

Differential diagnosis is carried out with sepsis, pneumonia, transient tachypnea of newborns, CAM.

Physical examination

Instrumental and laboratory methods are used for differential diagnosis, exclusion of concomitant pathology and evaluation of the effectiveness of the therapy.

Laboratory research

According to the KOS, there is hypoxemia and mixed acidosis.

Instrumental Research

The X-ray picture depends on the severity of the disease - from a slight decrease in pneumatization to "white lungs". Characteristic signs: a diffuse decrease in the transparency of the lung fields, a reticulogranular pattern and stripes of enlightenment in the region of the lung root (air bronchogram).

At the birth of a child from a high-risk group for the development of RDS, the most trained employees who know all the necessary manipulations are called to the delivery room. Particular attention should be paid to the readiness of the equipment to maintain optimal temperature conditions. For this purpose, radiant heat sources or open resuscitation systems can be used in the delivery room. In the case of the birth of a child whose gestational age is less than 28 weeks, it is advisable to additionally use a sterile plastic bag with a slot for the head, which will prevent excessive heat loss during resuscitation in the delivery room.

For the prevention and treatment of RDS in all children with gestational age
The goal of therapy in the intensive care unit is to maintain pulmonary gas exchange, restore alveolar volume and create conditions for extrauterine maturation of the child.

Respiratory Therapy

Tasks of respiratory therapy in newborns with RDS: maintenance of arterial pa02 at the level of 50-70 mm Hg. (s 02 - 88-95%), paCO2 - 45-60 mm Hg, pH - 7.25-7.4.

Indications in neonates with RDS to support spontaneous breathing with CPAP.

At the first symptoms of respiratory failure in preterm infants with gestational age
When f i02>0.5 in children older than 32 weeks. Contraindications include:

Respiratory acidosis (paCO2 >60 mmHg and pH
severe cardiovascular insufficiency (shock);

Pneumothorax;

Frequent sleep apnea accompanied by bradycardia.

The use of CPAP in premature infants through an endotracheal tube or nasopharyngeal catheter is not recommended due to a significant increase in aerodynamic resistance and work of breathing. The use of binasal cannulas and variable flow devices is preferred.

Algorithm for the use of CPAP in preterm infants weighing more than 1000 g:

Starting pressure - 4 cm water column, f i02 - 0.21-0.25: | SpO2,
administration of a surfactant followed by rapid extubation and continued CPAP; ^increase in respiratory failure;

Tracheal intubation, start of mechanical ventilation.

The CPAP is terminated in stages: first, fi02 is reduced to 0.21, then the pressure is reduced by 1 cm of water. every 2-4 hours. CPAP is canceled if, at a pressure of 2 cm of water. and f.02 0.21 for 2 hours, a satisfactory blood gas composition is maintained.

The CPAP algorithm in preterm infants weighing less than 1000 g is presented in the section “Peculiarities of nursing children with extremely low body weight”. Indications for transfer from CPAP to conventional mechanical ventilation:

Respiratory acidosis: pH 60 mmHg;

Pa02
frequent (more than 4 per hour) or deep (need for mask ventilation) 2 or more times per hour apnea attacks;

F02 -0.4 in a child on CPAP after the introduction of a surfactant. Starting parameters:

Fi02 - 0.3-0.4 (usually 10% more than with CPAP);

Tin - 0.3-0.35 s;

PEEP - + 4-5 cm water column;

NPV - 60 per minute;

PIP - minimum, providing VT=4-6 ml/kg (usually 16-30 cm water column); flow - 6-8 l/min (2-3 l/min per kg).

In case of disadaptation to the respirator, painkillers and sedatives are prescribed (promedol - saturation dose of 0.5 mg / kg, maintenance - 20-80 mcg / kg per hour; midazolam - saturation dose of 150 mcg / kg, maintenance - 50-200 mcg / kg per hour; hour; diazepam - saturation dose of 0.5 mg / kg).

Subsequent correction of parameters (see section IVL) in accordance with the indicators of monitoring, CBS and blood gases.

The beginning and methods of weaning from mechanical ventilation depend on many factors: the severity of RDS, the gestational age and body weight of the child, the effectiveness of surfactant therapy, the developed complications, etc. A typical algorithm for respiratory therapy in newborns with severe RDS: controlled mechanical ventilation - assisted ventilation - CPAP - spontaneous breathing. Disconnection from the device usually occurs after PIP drops to 16-18 cm of water column, f to 1015 per minute, f02 to 0.3.

There are a number of reasons that make it difficult to wean from mechanical ventilation:

Pulmonary edema;

Interstitial emphysema, prevothorax;

Intraventricular hemorrhages;

PDA; BPD.

For successful extubation in small patients, the use of methylxanthines is recommended to stimulate regular breathing and prevent apnea. The greatest effect from the appointment of methylxanthines is observed in children.
Caffeine-sodium benzoate at the rate of 20 mg/kg is a loading dose and 5 mg/kg is a maintenance dose.

Eufillin 6-8 mg / kg - loading dose and 1.5-3 mg / kg - maintenance, after 8-12 hours.

The indication for high-frequency oscillatory ventilation is the inefficiency of traditional mechanical ventilation. To maintain an acceptable blood gas composition, it is necessary:

Mean airway pressure (MAP) >13 cm w.g. in children weighing >2500 g;

MAP >10 cm w.c. in children weighing 1000-2500 g;

MAP >8 cm w.c. in children with body weight
The clinic uses the following starting parameters of high-frequency oscillatory ventilation in RDS.

MAP - by 2-4 cm w.g. differs from traditional IVL.

Delta P - the amplitude of oscillatory oscillations, usually it is selected in such a way that the patient's chest vibration is visible to the eye.

FhF - frequency of oscillatory oscillations (Hz). Set 15 Hz for children weighing less than 750 g and 10 Hz for children weighing more than 750 g.

Tin% (inspiratory time percentage). On devices where this parameter can be adjusted, they always set 33% and do not change throughout the respiratory support. An increase in this parameter leads to the appearance of gas traps.

Set f i02 the same as with traditional IVL.

Flow (constant flow). On devices with adjustable flow, set within 15 l / min ± 10% and do not change further.

Adjustment of parameters is carried out to optimize lung volume and normalize blood gas parameters. With normally expanded lungs, the dome of the diaphragm should be located at the level of 8-9 ribs. Signs of hyperinflation (overinflation of the lungs):

Increased transparency of the lung fields;

Flattening of the diaphragm (pulmonary fields extend below the level of the 9th rib).

Signs of hypoinflation (underinflation of the lungs):

Disseminated atelectasis;

The diaphragm is above the level of the 8th rib.

Correction of the parameters of high-frequency oscillatory ventilation, based on the indicators of blood gases:

With hypoxemia (pa02
with hyperoxemia (pa02 > 90 mm Hg) reduce f.02 to 0.3;

With.hypocapnia (paCO2
in case of hypercapnia (paCO2 > 60 mm Hg), increase the DR by 10-20% and reduce the oscillation frequency (by 1-2 Hz).

Termination of high-frequency oscillatory ventilation is carried out with the improvement of the patient's condition, gradually (with a step of 0.05-0.1) reduce f i02, bringing it to 0.3. Also stepwise (in increments of 1-2 cm of water column) reduce MAP to a level of 9-7 cm of water column. After that, the child is transferred either to one of the auxiliary modes of conventional ventilation, or to nasal CPAP.

Surfactant Therapy

The prophylactic use of surfactant is described in the section "Peculiarities of nursing children with ELBW".

The use of a surfactant for therapeutic purposes is indicated for premature infants with RDS if, despite CPAP or mechanical ventilation, it is impossible to maintain parameters:

F i02 >0.35 in the first 24 hours of life;

F i02 0.4-0.6 at 24-48 hours of life.

The appointment of a surfactant for therapeutic treatment is contraindicated in pulmonary hemorrhage, pulmonary edema, hypothermia, decompensated acidosis, arterial hypotension and shock. The patient must be stabilized before administering the surfactant.

Before insertion, the correct position of the endotracheal tube is clarified, and the tracheobronchial tree is sanitized. After administration, aspiration of bronchial contents is not carried out for 1-2 hours.

Of the surfactants registered in our country, curosurf is the drug of choice. This is a ready-to-use suspension, it must be heated to a temperature of 37 ° C before use. The drug is administered endotracheally in a jet at a dose of 2.5 ml/kg (200 mg/kg of phospholipids) through an endobronchial catheter in the position of the child on the back and the middle position of the head. Repeated doses (1.5 ml/kg) of the drug are administered after 6-12 hours if the child continues to need mechanical ventilation with fp2>0.35.

Curosurf is a natural surfactant of porcine origin for the treatment and prevention of RDS in premature newborns with proven high efficacy and safety.

The clinical efficacy and safety of Curosurf has been proven in randomized, multicenter, international trials performed in more than 3,800 preterm infants.

Curosurf quickly forms a stable layer of surfactant, improves the clinical picture already in the first few minutes after administration.

Curosurf is available in vials as a ready-made suspension for endotracheal administration, it is simple and convenient to use.

Curosurf reduces the severity of RDS, significantly reduces early neonatal mortality and the incidence of complications.

Against the background of the use of curosurf, the duration of stay on mechanical ventilation and stay in the ICU is reduced. Curosurf is included in the standards of medical care. In the Russian Federation, curosurf is represented by Nycomed, Russia-CIS.

Indications for use

Treatment of respiratory distress syndrome in premature newborns. Prevention of RDS in preterm infants with suspected possible development of the syndrome.

The initial dose is 200 mg / kg (2.5 ml / kg), if necessary, one or two additional half doses are used - 100 mg / kg with an interval of 12 hours.

Prevention

The drug in a single dose of 100-200 mg / kg (1.25-2.5 ml / kg) must be administered within the first 15 minutes after the birth of a child with suspected possible development of RDS. The second dose of 100 mg/kg is administered 6-12 hours later.

In the first hours after administration, it is necessary to constantly monitor the gas composition of the blood, ventilation and pulmonary mechanics in order to reduce PIP and f.02 in a timely manner.

When conducting non-respiratory therapy for RDS, the child should be placed in a "nest" and placed in an incubator or an open resuscitation system. The position on the side or stomach is better than on the back.

Be sure to immediately establish monitor control of the main functions (BP, heart rate, respiratory rate, body temperature, sp02).

In the initial period of stabilization, it is better to follow the tactics of "minimal touches". It is important to maintain a neutral temperature regime and reduce fluid loss through the skin.

Antibacterial therapy is prescribed for all children with RDS. Blood cultures are performed before antibiotics are prescribed. First-line drugs may be ampicillin and gentamicin. Further tactics depend on the results obtained. If a negative blood culture is obtained, antibiotics can be discontinued as soon as the child no longer needs mechanical ventilation.

In children with RDS, as a rule, there is fluid retention in the first 24-48 hours of life, which requires limiting the volume of infusion therapy, but prevention of hypoglycemia is also of great importance. At the initial stage, a 5-10% glucose solution is prescribed at the rate of 60-80 ml / kg per day. Monitoring diuresis and calculating water balance helps to avoid fluid overload.

In severe RDS and high dependence on oxygen (f.02 > 0.4), GSh is indicated. As the condition stabilizes (on the 2-3rd day) after a trial introduction of water through a tube, it is necessary to gradually connect EN with breast milk or mixtures, which reduces the risk of necrotizing enterocolitis.

For the prevention of the disease in newborns, all pregnant women with a gestational age of 24-34 weeks with a threat of preterm birth are recommended to prescribe one course of corticosteroids for 7 days. Repeated courses of dexamethasone increase the risk of developing periventricular leukomalacia (PVL) and severe neuropsychiatric disorders.

As an alternative, 2 schemes for prenatal prevention of RDS can be used:

Betamethasone - 12 mg intramuscularly, after 24 hours, only 2 doses per course;

Dexamethasone - 6 mg, intramuscularly, after 12 hours, only 4 doses per course.

With the threat of preterm birth, antenatal administration of betamethasone is preferable. It, as studies have shown, stimulates the “maturation” of the lungs faster. In addition, antenatal administration of betamethasone reduces the incidence of IVH and PVL in premature infants with a gestational age of more than 28 weeks, leading to a significant reduction in perinatal morbidity and mortality.

If preterm labor occurs in the period of 24-34 weeks of gestation, an attempt should be made to inhibit labor activity by using p-agonists, antispasmodics, or magnesium sulfate. In this case, premature rupture of amniotic fluid will not be a contraindication to the inhibition of labor and the prophylactic administration of corticosteroids.

In children who have had severe RDS, there is a high probability of developing chronic pulmonary pathology. Neurological disorders are found in premature newborns in 10-70% of cases.