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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 higher, the lower the gestational age and the more often pathological conditions associated with pathology of the respiratory, circulatory and central nervous systems occur. The disease is polyetiological.

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

Deficiency and immaturity of surfactant 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 RDS. Even after going through the birth process without any deviations, they can develop a 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 factors here are those that disrupt the physiological course of labor. During normal childbirth through the natural birth canal, dosed stimulation of the sympatho-adrenal system occurs. Expansion of 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 surgical delivery, can cause a process of insufficient surfactant synthesis with the subsequent development of RDS.

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

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

One can think of acute respiratory distress syndrome (ARDS) in cases where the child underwent the birth process without abnormalities, and subsequently developed a picture of some disease that contributed to the development of hypoxia of any origin, centralization of blood circulation, and endotoxicosis.

It should also be taken into account that the period acute adaptation in newborns born prematurely or sick increases. It is believed that the period of maximum risk of manifestations of breathing disorders in such children is: for those born from healthy mothers - 24 hours, and for those born 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 trigger point is the deficiency and immaturity of surfactant, in the second - persistent high pulmonary hypertension and the resulting unrealized process of surfactant synthesis. In the third option ("mixed"), these two points are combined. The variant of ARDS formation is due to the development of “shock” lung.

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

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

For more efficient and rational therapy In critical conditions in newborns, it is necessary to distinguish between the options for the formation of RDS.

Currently, the main method of intensive therapy for RDS is respiratory support. Most often, mechanical ventilation for this pathology has to start with “hard” parameters, under which, in addition to the danger of barotrauma, hemodynamics are also significantly inhibited. To avoid “hard” parameters of mechanical ventilation with high average pressure in the respiratory tract, it is recommended 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 premature infants) with surfactant replacement therapy. In these cases, mechanical ventilation will not be so “hard” and long-lasting. A number of children will have the opportunity, after short-term mechanical ventilation, to carry out SDPPDV through binasal cannulas until the pneumocytes are able to “produce” a sufficient amount of mature surfactant.

Preventive initiation of mechanical ventilation with the elimination of hypoxia without the use of “hard” mechanical ventilation will allow for 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

1. Symptoms of respiratory failure, tachypnea, chest swelling, nasal flaring, difficulty breathing and cyanosis.
2. Other symptoms, for example, hypotension, oliguria, muscle hypotonia, temperature instability, intestinal paresis, peripheral edema.
3. Prematurity at gestational age assessment.

During the first hours of life, the child undergoes a clinical assessment 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 assistance.

RDS severity assessment (modified Downes scale)

Points Frequency Cyanosis of breathing per 1 min.	Retraction	Expiratory grunt	Breathing pattern during auscultation
0 < 60 нет при 21%	No	No	puerile
1 60-80 yes, disappears at 40% O2	moderate	listens- stethoscope	changed weakened
2 > 80 disappears or apnea with	significant	audible distance	Badly carried out

A score of 2-3 points corresponds to RDS mild degree

A score of 4-6 points corresponds to moderate RDS

A score of more than 6 points corresponds to severe RDS

B. CHEST X-RAY. Characteristic nodular or round opacities and an air bronchogram indicate diffuse atelectasis.

B. LABORATORY SIGNS.

1. Amniotic fluid Lecithin/Sphyringomyelin ratio less than 2.0 and negative shake test results on amniotic fluid and gastric aspirate. In newborns from mothers with diabetes mellitus, RDS can develop when L/S is more than 2.0.
2. Lack of phosphatildiglycerol in amniotic fluid.

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

III. COURSE OF THE DISEASE.

A. RESPIRATORY FAILURE, increasing over 24-48 hours and then stabilizing.

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

IV. PREVENTION

In case of premature birth at 28-34 weeks, an attempt should be made to slow down labor by using beta-mimetics, antispasmodics or magnesium sulfate, followed by glucocorticoid therapy according to one of the following regimens:

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

In case of 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 a peptic ulcer.

When using glucocorticoids, blood sugar should be monitored.

If delivery by cesarean section is expected, if conditions exist, delivery should begin with an amniotomy performed 5-6 hours before surgery in order to stimulate the fetal sympathetic-adrenal system, which stimulates its surfactant system. In case of critical condition of the mother and fetus, amniotomy is not performed!

Prevention is facilitated by careful extraction of the fetal head during cesarean section, and in very premature infants, extraction of the fetal head in the amniotic sac.

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 renal function may be impaired during this period and perspiration losses increase, it is very important to carefully maintain fluid and electrolyte balance.

A. Maintaining airway patency

1. Lay the newborn down with the head slightly extended. Turn the baby. It improves tracheal drainage bronchial tree.
2. Suction from the trachea is required to sanitize the tracheobronchial tree from thick sputum that appears in exudative phase, which begins at approximately 48 hours of life.

B. Oxygen therapy.

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

B. Vascular access

1. An umbilical venous catheter, the tip of which is located above the diaphragm, can be useful in providing venous access and measuring central venous pressure.

D. Correction of hypovolemia and anemia

1. Monitor central hematocrit and blood pressure starting after birth.
2. 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

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

E. Feeding

1. If the newborn's hemodynamics are stable and you manage to relieve respiratory failure, then feeding should begin at 48-72 hours of life.
2. Avoid pacifier feeding if shortness of breath exceeds 70 breaths per minute because... high risk of aspiration.
3. If enteral feeding is not possible, consider parenteral nutrition.
4. Vitamin A parenterally, 2000 units every other day, until enteral feeding is started, reduces the incidence of chronic lung diseases.

G. Chest X-ray

1. To make a diagnosis and assess the course of the disease.
2. To confirm the placement of the endotracheal tube, chest tube and umbilical catheter.
3. For the diagnosis of complications such as pneumothorax, pneumopericardium and necrotizing enterocolitis.

H. Excitement

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

I. Infection

1. In most newborns with respiratory failure, sepsis and pneumonia should be excluded, so it is advisable to prescribe empirical antibiotic therapy with broad-spectrum bactericidal antibiotics until culture results are confirmed.
2. Group B hemolytic streptococcus infection may clinically and radiologically resemble RDS.

K. Therapy of acute respiratory failure

1. The decision to use respiratory support techniques should be based on the medical history.
2. In newborns weighing less than 1500 g, the use of CPAP techniques may lead to unnecessary energy expenditure.
3. You should initially try to adjust the ventilation parameters to reduce FiO2 to 0.6-0.8. Typically, this requires maintaining an average pressure within 12-14 cmH2O.

• A. When PaO2 exceeds 100 mmHg, or there are no signs 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 using blood gas analysis or a pulse oximeter.
• V. At low oxygen concentrations (less than 40%), a reduction in FiO2 of 2%-3% is sufficient.

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

• A. Maintain pCO2 less than 60 mmHg by varying ventilation rates or peak pressures.
• b. If your attempts to stop hypercapnia lead to impaired oxygenation, consult with more experienced colleagues.

L. Reasons for the deterioration of the patient’s condition

1. Rupture of the alveoli and the development of interstitial pulmonary emphysema, pneumothorax or pneumopericardium.
2. Violation of the tightness of the breathing circuit.

• A. Check the connections 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 endotracheal tube obstruction or self-extubation is detected, remove the old endotracheal tube and ventilate the child with a bag and mask. Reintubation is best done after the patient's condition has stabilized.

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 pulmonary vessels can sharply decrease, causing shunting through the ductus arteriosus from left to right.

5. Much less often, deterioration of the condition of newborns is caused by intracranial hemorrhage, septic shock, hypoglycemia, kernicterus, transient hyperammonemia, or inborn defects of metabolism.

Scale for selecting some parameters of mechanical ventilation in newborns with RDS

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

Note: This diagram is a guide only. Ventilator parameters can be changed based on the clinical picture of the disease, blood gases and CBS and pulse oximetry data.

Criteria for the use of respiratory therapy measures

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

M. Surfactant therapy

• A. Human, synthetic and animal surfactants are currently being tested. In Russia for clinical application The surfactant "EXOSURF NEONATAL" from Glaxo Wellcome is approved.
• b. It is prescribed prophylactically in the delivery room or later, within a period of 2 to 24 hours. Prophylactic use of surfactant is indicated for: premature newborns with a birth weight of less than 1350 g with a high risk of developing RDS; newborns weighing more than 1350 g with lung immaturity confirmed by objective methods. WITH therapeutic purpose surfactant is used in newborns with a clinically and radiologically confirmed diagnosis of RDS who are on mechanical ventilation through an endotracheal tube.
• V. It is administered into the respiratory tract in the form of a suspension in fiera solution. WITH for preventive purposes"Exosurf" is administered from 1 to 3 times, with therapeutic - 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 time from 5 to 30 minutes, depending on the child’s reaction. It is safer to administer the solution micro-jet at a rate of 15-16 ml/hour. A repeat dose of Exosurf is administered 12 hours after the initial dose.
• d. Reduces the severity of RDS, but the need for mechanical ventilation remains and the frequency chronic diseases lungs does not decrease.

VI. TACTICAL EVENTS

The team of specialists for the treatment of RDS is headed by a neonatologist. trained in resuscitation and intensive care or a qualified resuscitator.

From LU with URNP 1 - 3, it is mandatory to contact the RCCN and face-to-face consultation on the 1st day. Rehospitalization in specialized center for resuscitation and intensive care of newborns after stabilization of the patient’s condition after 24-48 hours by the RCBN.

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

Application schemes:

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

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

3 doses of dexamethasone IM 8 mg every 8 hours.

N. B. The effectiveness of the above drugs is the same, however, it should be taken into account that when dexamethasone is prescribed, there is a higher frequency of hospitalization in the ICU, but more low frequency IVH than with betamethasone (A-1b).

Indications for RDS prevention:

premature rupture of membranes;

clinical signs premature birth(see above) at 24–34 completed (34 weeks 0 days) weeks (any doubt about the true gestational age should be interpreted in the direction of a smaller one and preventive measures should be carried out);

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

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

N. B. The effectiveness of ACT for periods longer than 34 weeks remains a controversial issue. Perhaps the best recommendation today may be the following: prescribing ACT for more than 34 weeks of pregnancy if there are signs of fetal lung immaturity (in particular in pregnant women with type 1 or type 2 diabetes mellitus).

Prolongation of pregnancy. Tocolysis

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

General contraindications to tocolysis:

Obstetric contraindications:

chorioamnionitis;

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

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

Contraindications from the fetus:

developmental defects incompatible with life;

antenatal fetal death.

Choice of tocolytic

β2-agonists

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

Contraindications for the use of β-agonists:

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

hyperthyroidism;

closed-angle form of glaucoma;

insulin-dependent diabetes mellitus;

fetal distress not associated with uterine hypertonicity.

Side effects:

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

from the fetus: tachycardia, hyperbilirubinemia, hypocalcemia.

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

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

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols Ministry of Health of the Republic of Kazakhstan - 2014

Neonatal respiratory distress syndrome (P22.0)

Neonatology, Pediatrics

General information

Brief description

Approved by the Expert Commission

On health development issues

Ministry of Health of the Republic of Kazakhstan

Respiratory distress syndrome (RDS) is a condition of respiratory failure that develops immediately or a short period of time after birth and the severity of its manifestations increases during the first two days of life. The development of RDS is caused by surfactant deficiency and structural immaturity of the lungs, observed mainly, but not exclusively, in premature newborns.

INTRODUCTORY PART

Protocol name: Respiratory distress syndrome in a newborn.

Protocol code

ICD-10 code:

P22.0 Respiratory distress syndrome in a newborn

Abbreviations used in the protocol:

BPD - bronchopulmonary dysplasia

CHD - congenital heart defect

IVH - intraventricular hemorrhage

FiO2 - concentration of supplied oxygen

MV - mechanical ventilation

NIPPV - nasal intermittent positive pressure ventilation

CBC - complete blood count

PDA - patent ductus arteriosus

RDS - Respiratory distress syndrome

ROP - retinopathy of prematurity

See H2O - centimeters of water column

CRP - C-reactive protein

CPAP - continuous positive blood pressure respiratory tract

Air Leak Syndrome

TTN - transient tachypnea of ​​newborns

TBI - severe bacterial infection

RR = respiratory rate

HR - heart rate

EchoCG - echocardiography

Date of development of the protocol: 2013

Protocol users: neonatologists of obstetric organizations.

Classification

Clinical classification: is absent, since with modern tactics of early therapy, clinical symptoms do not reach the classical definition of RDS.

Diagnostics

II. METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

List of basic and additional diagnostic measures

Basic diagnostic measures

A. Risk factors: gestational age less than 34 weeks, maternal or gestational diabetes mellitus, C-section, maternal bleeding during pregnancy, perinatal asphyxia, male gender, second (or each subsequent) in multiple pregnancies.

B. Clinical manifestations:

RDS is clinically manifested by early respiratory disorders in the form of cyanosis, groaning breathing, retraction of the pliable areas of the chest and tachypnea. In the absence of therapy, it may occur death due to progressive hypoxia and respiratory failure. With adequate therapy, regression of symptoms begins within 2-4 days. .

Additional diagnostic measures

X-ray signs:

The classic picture of decreased pneumatization of the lungs in the form of “frosted glass” and the presence of air bronchograms.

Diagnostic criteria

A. Laboratory indicators:

Blood gases: PaO2 level less than 50 mmHg (less than 6.6 kPa).

Blood culture, CRP, CBC to exclude TBI (pneumonia, sepsis).

B. EchoCG: to exclude congenital heart disease, detect PDA, pulmonary hypertension and clarify the direction of blood shunting.

Differential diagnosis

Differential diagnosis: TTN, SUV, pneumonia, sepsis.

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Treatment

Goal of treatment: providing interventions to maximize the number of surviving preterm infants while reducing potential side effects.

Treatment tactics

1. Stabilization of the newborn’s condition after birth

A. Prerequisites to adequately stabilize the newborn:

When a child is born who is at risk for developing RDS, the most trained staff are called in to deliver the baby, having up-to-date knowledge and skills in performing resuscitation in newborns with extremely low and very low birth weight.

To maintain optimal air temperature in the delivery room (25-26ºС), additional heaters, radiant heat sources, and open resuscitation systems can be used. To prevent overheating, it is necessary to carry out servo control within 10 minutes (B).

Warming and humidifying gases used to stabilize the condition may also help maintain normothermia.

To prevent hypothermia, neonates less than 28 weeks' gestational age should be placed in a plastic bag or occlusive film with a parallel heater (A) immediately after birth.

It has been proven that uncontrolled inspiratory volumes, both too high and too low, can be dangerous for the immature lungs of premature babies. Therefore, it is recommended to replace the traditional use of a self-inflating bag with a resuscitation system with a T-piece connector, which provides control of a set continuous positive airway pressure (CPAP) with a measured peak inspiratory pressure (PIP) when the T-piece is closed.

B. Stabilization of the newborn’s condition after birth

Immediately after birth, place a pulse oximeter on the newborn's right wrist to obtain heart rate and saturation targets (B).

Umbilical cord clamp premature newborn If the patient's condition allows, it is recommended to delay for 60 seconds, with the infant positioned below the mother, to facilitate placental-fetal transfusion (A).

CPAP use should be started at birth in all newborns at risk of developing RDS and in all those with gestational ageing.

Up to 30 weeks of age, ensuring airway pressure of at least 6 cm H2O, through a mask or nasal cannula (A). Short binasal cannulas are preferred because they reduce the need for intubation (A).

Oxygen must be supplied only through an oxygen-air mixer. To begin stabilization, an oxygen concentration of 21-30% is advisable, and an increase or decrease in its concentration is made based on the pulse oximeter readings about heart rate and saturation (B).

Normal saturation immediately after birth for a premature baby is 40-60%, rises to 80% by the 5th minute and should reach 85% or more by the 10th minute after birth. Hyperoxia should be avoided during stabilization (B).

Intubation should be considered for neonates who have not responded to noninvasive ventilation (CPAP) (A). Surfactant replacement therapy is indicated for all intubated newborns (A).

After the administration of surfactant, a decision should be made on immediate (or early) extubation (INSURE technique: IN-intubation-SUR-surfactant-E-extubation) with a transition to non-invasive ventilation (CPAP or nasal intermittent positive pressure ventilation ─ NIPPV), but subject to stability in relation to other systems of the newborn (B). Nasal intermittent positive pressure ventilation (NIPPV) can be considered as a means to reduce the risk of extubation failure in infants who do not respond to CPAP, but this approach does not provide significant long-term benefit (A).

B. Surfactant therapy

Natural surfactant preparations are recommended for all newborns with RDS or at high risk of developing it (A).

Early administration of surfactant for life-saving therapeutic purposes should be standard and recommended for all neonates with RDS at early stage diseases.

Surfactant should be administered directly in the delivery room in cases where the mother has not received antenatal steroids or when intubation is necessary to stabilize the newborn (A), and in preterm neonates less than 26 weeks gestational age when FiO2 is > 0.30, and for newborns with a gestational age of more than 26 weeks, with FiO2 > 0.40 (B).

For the treatment of RDS, poractant alfa at an initial dose of 200 mg/kg is better than 100 mg/kg of the same drug or beractant (A).

A second and sometimes a third dose of surfactant should be given if signs of RDS persist, such as a persistent need for oxygen and the need for mechanical ventilation (A).

2. Supplemental oxygen therapy after the newborn’s condition has been stabilized

When administering oxygen therapy to preterm neonates, after initial stabilization, oxygen saturation levels should be maintained between 90-95% (B).

After surfactant administration, it is necessary to quickly reduce the concentration of oxygen supplied (FiO2) to prevent a hyperoxic peak (C).

It is extremely important to avoid fluctuations in saturation in the postnatal period (C).

3. Strategy for mechanical ventilation (MV) of the lungs

CF should be used to support neonates with respiratory failure who have failed nasal CPAP (B).

CF can be provided by conventional intermittent positive pressure ventilation (IPPV) or high-frequency oscillatory ventilation (HFOV). HFOV and traditional IPPV have similar efficiencies, so the ventilation method that is most effective in each department should be used.

The goal of CF is to maintain optimal lung volume after expansion by generating adequate positive end-expiratory pressure (PEEP), or continuous expansion pressure (CDP), to the HFOV throughout the respiratory cycle.

To determine the optimal PEEP during conventional ventilation, it is necessary to change the PEEP step by step, assessing FiO2, CO2 levels and observing respiratory mechanics.

Target tidal volume ventilation should be used as this shortens the duration of ventilation and reduces BPD (A).

Hypocapnia should be avoided as it is associated with an increased risk of bronchopulmonary dysplasia and periventricular leukomalacia.

MV settings should be adjusted more frequently to ensure optimal lung capacity.

Termination of CF with extubation and transfer to CPAP should be carried out as early as possible, if it is clinically safe and blood gas concentrations are acceptable (B)

Extubation can be successful with an average air pressure of 6-7 cmH2O in traditional modes and with 8-9 cmH2O in HFCS, even in the most immature children.

4. Elimination or reduction of the duration of mechanical ventilation.

CPAP or NIPPV should be preferred to avoid or reduce the duration of invasive mechanical ventilation (B).

When weaning from CF, it is allowed moderate degree hypercapnia, provided that the pH remains above 7.22 (B).

To reduce the duration of CF, it is necessary to use traditional ventilation modes with a synchronized and set breathing volume using aggressive weaning from the device (B).

Caffeine should be included in the regimen apnea treatment in neonates and to facilitate extubation (A), and caffeine may be used in infants weighing less than 1250 g at birth who are on CPAP or NIPPV and are likely to require invasive ventilation (B). Caffeine citrate is administered at a saturation dose of 20 mg/kg, followed by 5-10 mg/kg/day as a maintenance dose.

5. Prevention of infections

All newborns with RDS should begin treatment with antibiotics until the possibility of a severe bacterial infection (sepsis, pneumonia) is completely excluded. The usual regimen includes a combination of penicillin/ampicillin with an aminoglycoside. Each neonatal unit should develop its own protocols for the use of antibiotics, based on an analysis of the spectrum of pathogens that cause early sepsis (D).

Antibiotic treatment should be stopped as soon as possible once TBI has been ruled out (C).

In departments with a high incidence of invasive fungal infections, it is recommended to preventive treatment fluconazole in children with birth weight less than 1000 g or with a gestational age ≤ 27 weeks, starting on the 1st day of life at a dose of 3 mg/kg twice a week for 6 weeks (A).

6. Supportive care

In newborns with RDS, the best outcome is ensured by optimal maintenance normal temperature body at 36.5-37.5ºС, treatment of patent ductus arteriosus (PDA), support of adequate blood pressure and tissue perfusion.

A. Infusion therapy and nutrition

Most premature newborns should be started

Intravenous administration liquids at 70-80 ml/kg per day, maintaining high humidity in the incubator (D).

In preterm infants, infusion and electrolyte volumes should be individualized, allowing for 2.4–4% weight loss per day (15% overall) in the first 5 days (D).

Sodium intake should be limited in the first few days of postnatal life and initiated after the onset of diuresis, with close monitoring of fluid balance and electrolyte levels (B).

Parenteral nutrition should be started on day 1 to avoid growth retardation and include early protein starting at 3.5 g/kg/day and lipids at 3.0 g/kg/day to maintain adequate caloric intake. This approach improves survival of preterm infants with RDS (A)

Minimal enteral nutrition should also be started on the first day (B).

B. Maintain tissue perfusion

Hemoglobin concentrations should be maintained within the normal range. Alleged threshold value hemoglobin concentration in newborns undergoing assisted ventilation is 120 g/l in the 1st week, 110 g/l in the 2nd week and 90 g/l after the 2nd week of postnatal life.

If restoration of bcc fails to satisfactorily increase blood pressure, dopamine (2-20 mcg/kg/min) must be administered (B).

If low systemic blood flow, or there is a need to treat myocardial dysfunction, it is necessary to use dobutamine (5-20 mcg/kg/min) as a first-line drug and epinephrine (adrenaline) as a second-line drug (0.01-1.0 mg/kg/min) .

In cases of refractory hypotension, when traditional therapy is ineffective, hydrocortisone (1 mg/kg every 8 hours) should be used.

Echocardiographic testing can help guide decisions regarding the timing of treatment for hypotension and the choice of treatment (B).

B. Treatment of patent ductus arteriosus

If a decision is made to treat PDA medically, indomethacin and ibuprofen have similar effects (B), but ibuprofen is associated with a lower incidence of renal side effects.

MINISTRY OF HEALTH OF THE REPUBLIC OF UZBEKISTAN

TASHKENT PEDIATRIC MEDICAL INSTITUTE

RESPIRATORY DISTRESS SYNDROME IN NEWBORNS

Tashkent - 2010

Compiled by:

Gulyamova M.A., Rudnitskaya S.V., Ismailova M.A.,

Khodzhimetova Sh.H., Amizyan N.M., Rakhmankulova Z.Zh.

Reviewers:

1. Mukhamedova Kh. T.d. M.Sc., professor, head. Department of Neonatology TashIUV

2. Dzhubatova R.S. Doctor of Medical Sciences, Director of the Russian Scientific and Practical Medical Center of Pediatrics

3. Shomansurova E.A. Associate Professor, Head Department of Outpatient Medicine TashPMI

"Respiratory distress syndrome in newborns"

1. At the Problem Commission of the Pediatric Council of TashPMI, protocol No.

2. At the Academic Council of TashPMI, protocol No.

Secretary of the Academic Council Shomansurova E.A.

List of abbreviations

CPAP- continuous positive airway pressure

FiO 2- oxygen content in the inhaled mixture

PaCO2- partial pressure of carbon dioxide in arterial blood

PaO2- partial pressure of oxygen in arterial blood

PCO 2- partial pressure of carbon dioxide in mixed (capillary) blood

PIP- (PVP) peak (upper limit) pressure during inspiration

PO 2- partial pressure of oxygen in mixed (capillary) blood

SaO2- an indicator of hemoglobin oxygen saturation measured in arterial blood

SpO2- indicator of hemoglobin oxygen saturation measured by a transcutaneous sensor

HELL- blood pressure

BGM- hyaline membrane disease

BPD- bronchopulmonary dysplasia

VFO IVL - high frequency oscillatory artificial ventilation lungs

ICE- disseminated intravascular coagulation

DN- respiratory failure

TO- tidal volume

Gastrointestinal tract- gastrointestinal tract

mechanical ventilation- artificial ventilation

IEL- interstitial pulmonary emphysema

CBS- acid-base state

L/S - lecithin/sphingomyelin

IDA- average pressure in the respiratory tract, see water. Art.

MOS- cytochrome P-450 system

FLOOR- lipid peroxidation

RASPM- Russian Association of Perinatal Medicine Specialists

RDS- respiratory distress syndrome

MYSELF- meconium aspiration syndrome

SDR- respiratory distress syndrome

CCH- cardiovascular failure

SUV- air leak syndrome

LDP- tracheobronchial tree

FOE- functional residual capacity of the lungs

CNS - central nervous system

NPV- respiratory rate

ECG- electrocardiogram

YANEC- ulcerative-necrotizing enterocolitis

Definition

RESPIRATORY DISTRESS SYNDROME (English: distress, severe malaise, suffering; Latin: respiratio breathing; syndrome - a set of typical symptoms) - non-infectious pathological processes(primary atelectasis, hyaline membrane disease, edematous-hemorrhagic syndrome), which develop in the prenatal and early neonatal periods of a child’s development and manifest as respiratory failure. A symptom complex of severe respiratory failure that occurs in the first hours of a child’s life due to the development of primary pulmonary atelectasis, hyaline membrane disease, and edematous hemorrhagic syndrome. It is more common in premature and immature newborns.

The incidence of respiratory distress depends on the degree of prematurity, and averages 60% in children born at a gestational age of less than 28 weeks, 15-20% - at a period of 32-36 weeks. and 5% - for a period of 37 weeks. and more. With rational care of such children, the mortality rate approaches 10%.

Epidemiology.

RDS is the most common cause of respiratory failure in the early neonatal period. Its occurrence is higher, the lower the gestational age and body weight of the child at birth. However, the incidence of RDS is strongly influenced by methods of prenatal prevention when there is a threat of preterm birth.

In children born before 30 weeks of gestation and who did not receive prenatal prophylaxis with steroid hormones, its frequency is about 65%, in the presence of prenatal prophylaxis - 35%; in children born at a gestational age of 30-34 weeks without prophylaxis - 25%, with prophylaxis - 10%.

In premature babies born at more than 34 weeks of gestation, its frequency does not depend on prenatal prevention and is less than 5%. (Volodin N.N. et al. 2007)

Etiology.

· deficiency of surfactant formation and release;

· quality defect of surfactant;

· inhibition and destruction of surfactant;

· immaturity of the lung tissue structure.

Risk factors.

Risk factors for RDS are all conditions leading to surfactant deficiency and lung immaturity, namely: asphyxia of the fetus and newborn, morpho-functional immaturity, impaired pulmonary-cardiac adaptation, pulmonary hypertension, metabolic disorders (acidosis, hypoproteinemia, hypofermentosis, changes electrolyte metabolism), untreated diabetes mellitus in pregnancy, bleeding in pregnancy, cesarean section, male sex of the newborn, and being born second of twins.

Intrauterine development of the lungs.

The tracheobronchial tree system begins as a lung bud, which subsequently continuously divides and develops, penetrating the mesenchyme, and expanding to the periphery. This process goes through 5 development phases (Fig. 1):

1. Embryonic phase (< 5 недели)

2. Pseudograndular phase (5-16 weeks)

3. Canalicular phase (17-24 weeks)

4. Developmental phase of the terminal sac (24-37 weeks)

5. Alveolar phase (from the end of 37 weeks to 3 years).

The rudiment of the respiratory tract appears in a 24-day embryo; in the next 3 days, two primary bronchi are formed. The first cartilaginous elements in the bronchi appear at the 10th week, and at the 16th week the intrauterine formation of all generations of the bronchial tree practically ends, although cartilage continues to appear until the 24th week of the gestational period.

Figure 1. Five phases of tracheobronchial airway development. ( adapted from Weibel ER: Morphomeiry of the Human Lung. Berlin, Springer-Verlag, 1963.)

Asymmetry of the main bronchi has been observed since the first days of their development; the rudiments of the lobar bronchi are visible in the embryo at 32 days, and the segmental bronchi at 36 days. By the 12th week, the pulmonary lobes are already distinguishable.

Differentiation of lung tissue begins from the 18th-20th week, when alveoli with capillaries appear in the walls. At the age of 20 weeks, the bronchial drainage usually accumulates, the lumen of which is lined with cuboidal epithelium.

Alveoli appear as outgrowths on the bronchioles, and from the 28th week they increase in number. Since new alveoli can form throughout the prenatal period, terminal air spaces lined by cuboidal epithelium can be found in the lungs of newborns.

The lung bud is initially supplied with blood through paired segmental arteries arising from the dorsal part of the aorta. The vascular elements of the lung begin to form from the mesenchyme from 20 weeks of age as branches of these arteries. Gradually, the pulmonary capillaries lose connection with the segmental arteries, and their blood supply is provided by the branches of the pulmonary artery, which generally follow the branching of the respiratory tube. Anastomoses between the pulmonary and bronchial artery systems persist until birth and can function in premature infants in the first weeks of life.

Already in the 28-30 day embryo, blood from the lungs flows into the left atrium, where the venous sinus is formed.

At 26-28 weeks of the intrauterine period capillary network the lung closely meets the alveolar surface; At this point, the lung acquires the ability to exchange gases.

The development of the pulmonary arteries is accompanied by a progressive increase in their lumen, which initially does not exceed several micrometers. The lumen of the lobar arteries increases only at the 10th week of the intrauterine period, and the lumen of the terminal and respiratory arterioles - only at the 36-38th week. A relative increase in the lumen of the arteries is observed during the first year of life.

Lymphatic vessels surrounding the bronchi, arteries and veins reach the alveoli by the time of birth; this system is formed in the 60-day-old vibrio.

Mucous glands in the trachea are formed by secondary invagination of the epithelium at 7-8 weeks, goblet cells - at 13-14 weeks. At the 26th week of intrauterine life, the mucous glands begin to secrete mucus containing acidic glycosaminoglycans (mucopolysaccharides).

Epithelial cilia in the trachea and main bronchi appear around the 10th week, and in the peripheral bronchi - from the 13th week. In the bronchioles along with the cells ciliated epithelium there are cylindrical cells containing secretory granules in the apical part.

The most peripheral layer of the inner lining of the respiratory tract is represented by alveolocytes of two types, appearing from the 6th month of the intrauterine period. Type I alveolocytes cover up to 95% of the surface of the alveoli; the remainder of the area is occupied by type II alveolocytes, which have a developed lamellar complex (Golgi apparatus), mitochondria and osmiophilic inclusions. The main function of the latter is the production of surfactant, which appears in fruits weighing 500-1200 g; The lower the gestational age of the newborn, the higher the surfactant deficiency. Surfactant is primarily formed in upper lobes, then in the lower ones.

Another function of type II alveolocytes is proliferation and transformation into type I alveolocytes when the latter are damaged.

The surfactant produced by type II alveolocytes, which is based on phospholipids (mainly dipalmitoyl phosphatidylcholine), performs the most important function - it stabilizes the terminal air-containing spaces. Forming a thin continuous lining of the alveoli, the surfactant changes surface tension depending on the radius of the alveoli. As the radius of the alveoli increases during inspiration, surface tension increases to 40-50 dynes/cm, significantly increasing the elastic resistance to breathing. At low volumes alveolar tension drops to 1-5 dynes/cm, which ensures stability of the alveoli during exhalation. Surfactant deficiency in premature infants is one of the leading causes of RDS.

Synonyms

Hyaline membrane disease.

DEFINITION

RDS is a severe respiratory disorder in premature newborns caused by immature lungs and primary surfactant deficiency.

EPIDEMIOLOGY

RDS - the most common reason the occurrence of respiratory failure in the early neonatal period. Its occurrence is higher, the lower the gestational age and body weight of the child at birth. Carrying out prenatal prevention when there is a threat of premature birth also affects the incidence of RDS.

In children born before 3 weeks of gestation and who did not receive prenatal prophylaxis with betamethasone or dexamethasone, its frequency is about 65%, with prophylaxis - 35%; in children born at a gestation period 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 prevention and is less than 5%.

ETIOLOGY

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

Table 23-5. Factors influencing the development of RDS

DEVELOPMENT MECHANISM

The key link in the pathogenesis of RDS is surfactant deficiency, which occurs as a result of structural and functional immaturity of the lungs.

Surfactant - a group of surface-active substances of lipoprotein nature that reduce strength surface tension in the alveoli and maintaining their stability. In addition, 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 onto the surface of the alveoli occurs at the time of birth, which contributes to the primary expansion of the lungs.

There are two routes for the synthesis of the main phospholipid component of surfactant - phosphatidylcholine (lecithin).

The first (with the participation of methyltransferase) actively occurs in the period from the 20-24th week to the 33-35th week of intrauterine development. It is easily depleted under the influence of hypoxemia, acidosis, and 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 surfactant, the permeability of the alveolar and capillary membranes increases, blood stagnation in the capillaries, diffuse interstitial edema and overstretching of the lymphatic vessels develop; alveoli collapse and atelectasis forms. 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, dysfunction occurs cardiovascular system: secondary pulmonary hypertension with right-to-left blood shunt through functioning fetal communications; transient myocardial dysfunction of the right and/or left ventricles, systemic hypotension.

A postmortem examination revealed that the lungs were airless and sank 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 die from RDS in the first hours of life.

CLINICAL CHARACTERISTICS

TO early signs 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 compensatory spasm of the glottis during exhalation, preventing the collapse of the alveoli;

Recession of the chest during inhalation (retraction of the xiphoid process of the sternum, epigastric region, intercostal spaces, supraclavicular fossa) with simultaneous inflation of the wings of the nose and cheeks ("trumpeter" breathing).

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 5-7 days of life. It is possible to organize prenatal diagnosis (risk prediction) of RDS based on research lipid spectrum amniotic fluid, but it is advisable only in large specialized hospitals and regional perinatal centers.

The following methods are the most informative.

Lecithin to sphingomyelin ratio (normally >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.

Level of saturated phosphatidylcholine (normal >5 µmol/L) or phosphatidylglycerol (normal >3 µmol/L). Absence or sharp decline the concentration of saturated phosphatidylcholine and phosphatildiglycerol in the amniotic fluid indicates high probability development of RDS.

DIFFERENTIAL DIAGNOSTIC MEASURES

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

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

Physical examination

Instrumental and laboratory methods are used to differential diagnosis, exceptions concomitant pathology and assessing the effectiveness of therapy.

Laboratory research

According to CBS, hypoxemia and mixed acidosis are noted.

Instrumental studies

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

At the birth of a child from the group high risk for the development of RDS, the most trained employees who know all the necessary manipulations are called to the delivery room. Special attention You should pay attention 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 slit for the head, which will prevent excessive heat loss during resuscitation measures in the delivery room.

For the purpose of prevention and treatment of RDS, all children with a gestational age
Goal of therapy intensive care unit- maintaining pulmonary gas exchange, restoring alveolar volume and creating conditions for extrauterine maturation of the child.

Respiratory therapy

The objectives of respiratory therapy in newborns with RDS: maintaining arterial pa02 at a level of 50-70 mm Hg. (s02 - 88-95%), paS02 - 45-60 mm Hg, pH - 7.25-7.4.

Indications for support of spontaneous breathing with CPAP in newborns with RDS.

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

Respiratory acidosis (paCO2 >60 mm Hg and pH
severe cardiovascular failure (shock);

Pneumothorax;

Frequent attacks of 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 using CPAP in premature infants weighing more than 1000 g:

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

Tracheal intubation, initiation of mechanical ventilation.

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

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

Respiratory acidosis: pH 60 mm Hg;

Ra02
frequent (more than 4 per hour) or deep (need for mask ventilation) 2 or more times per hour attacks of apnea;

F02 -0.4 in a child on CPAP after the administration of 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;

Respiratory rate - 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 are prescribed and sedatives(promedol - saturation dose 0.5 mg/kg, maintenance - 20-80 mcg/kg per hour; midazolam - saturation dose 150 mcg/kg, maintenance - 50-200 mcg/kg per hour; diazepam - saturation dose 0.5 mg/kg).

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

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

Intraventricular hemorrhages;

PDA; BPD.

For successful extubation in low birth weight patients, it is recommended to use methylxanthines to stimulate regular breathing and prevent apnea. Greatest effect from the administration 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 dose, after 8-12 hours.

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

Mean airway pressure (MAP) >13 cmH2O. in children weighing >2500 g;

MAP >10 cm water column in children weighing 1000-2500 g;

MAP >8 cm water column in children with body weight
The clinic uses the following starting parameters for high-frequency oscillatory ventilation for RDS.

MAP - 2-4 cm water column. differs from traditional mechanical ventilation.

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

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

Tin% (percentage of inspiratory time). On devices where this parameter can be adjusted, it is always set to 33% and is not changed throughout the entire duration of respiratory support. Increasing this parameter leads to the appearance of gas traps.

Set f i02 the same as with traditional ventilation.

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

Parameters are adjusted to optimize lung volume and normalize blood gas values. With normally expanded lungs, the dome of the diaphragm should be located at the level of the 8th-9th rib. Signs of hyperinflation (overinflated lungs):

Increased transparency of the lung fields;

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

Signs of hypoinflation (underinflated lungs):

Scattered atelectasis;

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

Correction of high-frequency oscillatory ventilation parameters based on blood gas values:

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

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

Termination of high-frequency oscillatory mechanical ventilation is carried out when the patient’s condition improves, gradually (in steps of 0.05-0.1) reducing f i02, bringing it to 0.3. MAP is also reduced stepwise (in increments of 1-2 cm water column) to a level of 9-7 cm water column. After this, 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 “Features of nursing children with ELBW.”

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

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

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

The use of surfactant for therapeutic treatment is contraindicated in cases of pulmonary hemorrhage, pulmonary edema, hypothermia, decompensated acidosis, arterial hypotension and shock. The patient's condition must be stabilized before administering surfactant.

Before insertion, the correct positioning of the endotracheal tube is checked 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, the drug of choice is Kurosurf. 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 stream at a dose of 2.5 ml/kg (200 mg/kg phospholipids) through an endobronchial catheter with the child in the supine position and in 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 require 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 efficiency and safety.

The clinical effectiveness and safety of Kurosurf has been proven in randomized multicenter international studies performed in more than 3,800 premature newborns.

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

Kurosurf is available in bottles as a ready-made suspension for endotracheal administration; it is simple and easy to use.

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

The use of Kurosurf reduces the length of stay on mechanical ventilation and in the ICU. Kurosurf is included in the delivery standards medical care. IN Russian Federation Kurosurf is presented by the company "Nycomed", Russia-CIS.

Indications for use

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

The initial dose is 200 mg/kg (2.5 ml/kg), if necessary, one or two additional half doses of 100 mg/kg are used 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 the drug 100 mg/kg is administered after 6-12 hours.

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

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

Be sure to immediately establish monitor control of basic functions (blood pressure, 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 to all children with RDS. Blood cultures are performed before antibiotics are prescribed. First-line drugs may include 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 requires mechanical ventilation.

Children with RDS typically experience fluid retention in the first 24-48 hours of life, which requires limiting the volume of fluid therapy, but preventing hypoglycemia is also important. On initial stage a 5-10% glucose solution is prescribed at a rate of 60-80 ml/kg per day. Monitoring diuresis and calculating water balance helps avoid fluid overload.

In case of severe RDS and high oxygen dependence (f.02 >0.4), HS is indicated. As the condition stabilizes (on the 2-3rd day) after the trial administration of water through the probe, you need to gradually connect the ED breast milk or mixtures, which reduces the risk of necrotizing enterocolitis.

To prevent the disease in newborns, all pregnant women with a gestation period of 24-34 weeks with a threat of premature 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 alternatives, 2 schemes for prenatal prevention of RDS can be used:

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

Dexamethasone - 6 mg, intramuscularly, after 12 hours, a total of 4 doses per course.

If there is a threat of premature birth, antenatal administration of betamethasone is preferable. It, as studies have shown, quickly stimulates the “maturation” of the lungs. In addition, antenatal administration of betamethasone helps reduce 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 premature labor occurs at 24-34 weeks of gestation, an attempt should be made to inhibit labor by using β-adrenergic agonists, antispasmodics or magnesium sulfate. In this case, premature rupture of amniotic fluid will not be a contraindication to inhibition of labor and prophylactic administration of corticosteroids.

Children who have suffered severe RDS are at high risk of developing chronic pulmonary pathology. Neurological disorders are detected in 10-70% of cases in premature newborns.