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

Respiratory distress*-syndrome(RDS) is a non-cardiogenic pulmonary edema caused by various damaging factors and leading to acute respiratory failure (ARF) and hypoxia. Morphologically, RDS is characterized by a diffuse alveolar lesion of a non-specific nature, increased permeability of the pulmonary capillaries with the development of pulmonary edema.

Previously, this condition was called non-hemodynamic or non-cardiogenic pulmonary edema , the term is sometimes used today.

Some authors refer to this condition as adult respiratory distress syndrome (ARDS). This is due to the fact that, in addition to ARDS, there is neonatal respiratory distress syndrome (RDSN). ARDS develops almost exclusively in premature babies born before 37 weeks of gestation, often with a hereditary predisposition to the disease, much less often in newborns whose mothers suffered from diabetes mellitus. The disease is based on a deficiency in the newborn pulmonary surfactant. This leads to a decrease in the elasticity of the lung tissue, the collapse of the alveoli and the development of diffuse atelectasis. As a result, the child already in the first hours after birth develops a pronounced respiratory failure. With this disease, a hyaline-like substance is observed on the inner surface of the alveoli, alveolar ducts and respiratory bronchioles, and therefore the disease is also called hyaline membrane disease. Without treatment, severe hypoxia inevitably leads to multiple organ failure and death. However, if it is possible to establish artificial lung ventilation (ALV) in time, ensure the expansion of the lungs and sufficient gas exchange, then after a while the surfactant begins to be produced and RDS is resolved in 4-5 days. However, RDS associated with nonhemodynamic pulmonary edema can also develop in children.

* Distress - English. distress - severe malaise, suffering

In the English-language literature, RDS is often referred to as "acute respiratory distress syndrome" (ARDS).

This term also cannot be considered successful, since there is no chronic RDS. In accordance with recent publications, the condition considered here is more correctly referred to as respiratory distress syndrome (syn. - ARDS, ARDS, non-hemodynamic pulmonary edema). Its difference from RDS is not so much in the age characteristics of the disease, but in the features of the mechanism of development of ARF.

Etiology

Etiological factors are usually divided into 2 groups:

direct damage to the lungs and causing indirect (mediated) damage

denial of the lungs. The first group of factors includes: bacterial and viral-bacterial pneumonia, aspiration of gastric contents, exposure to toxic substances (ammonia, chlorine, formaldehyde, acetic acid, etc.), drowning, lung contusion (blunt chest trauma), oxygen intoxication, pulmonary embolism, altitude sickness, exposure to ionizing radiation, lymphostasis in the lungs (for example, with tumor metastases to regional lymph nodes). Indirect lung damage is observed with sepsis, acute hemorrhagic pancreatitis, peritonitis, severe extrathoracic trauma, especially craniocerebral injury, burn disease, eclampsia, massive blood transfusion, with the use of cardiopulmonary bypass, an overdose of certain drugs, especially narcotic analgesics, with low plasma oncotic pressure blood, in renal failure, in conditions after cardioversion and anesthesia. The most common causes of RDS are pneumonia, sepsis, aspiration of gastric contents, trauma, destructive pancreatitis, drug overdose, and hypertransfusion of blood components.

Pathogenesis

The etiological factor causes in the lung tissue systemic inflammatory response. In the initial stage, the manifestation of this inflammatory reaction is the release of endotoxins, tumor necrosis factor, interleukin-1 and other pro-inflammatory cytokines. Subsequently, cytokine-activated leukocytes and platelets are included in the cascade of inflammatory reactions, which accumulate in capillaries, interstitium, and alveoli and begin to release a number of inflammatory mediators, including free radicals, proteases, kinins, neuropeptides, and complement-activating substances.

Inflammatory mediators cause an increase in lung permeability

pills for protein, which leads to a decrease in the oncotic pressure gradient between plasma and interstitial tissue, and fluid begins to exit the vascular bed. Swelling of the interstitial tissue and alveoli develops.

Thus, in the pathogenesis of pulmonary edema, endotoxins play an important role, which have both a direct damaging effect on the cells of the endothelium of the pulmonary capillaries, and indirectly due to the activation of mediator systems of the body.

In the presence of increased permeability of the pulmonary capillaries, even the slightest increase in hydrostatic pressure in them (for example, due to infusion therapy or dysfunction of the left ventricle of the heart due to intoxication and hypoxia, which are naturally observed in diseases underlying RDS) leads to a sharp increase in alveolar and in-

terstitial pulmonary edema (first morphological phase) . In connection with the

due to the role of hydrostatic pressure in the pulmonary vessels, changes associated with edema are more pronounced in the underlying parts of the lungs.

Gas exchange is disturbed not only due to the accumulation of fluid in the alveoli (“flooding” of the lungs), but also due to their atelectasis due to a decrease in the activity of the surfactant. The development of severe hypoxemia and hypoxia is associated with a sharp decrease in ventilation with relatively preserved perfusion and significant intrapulmonary shunting of blood from right to left (blood shunting). Shun-

blood circulation is explained as follows. Venous blood, passing through areas of the lungs with collapsed (atelectatic) or fluid-filled alveoli, is not enriched with oxygen (not arterialized) and in this form enters the arterial bed, which increases hypoxemia and hypoxia.

Violation of gas exchange is also associated with an increase in dead space due to obstruction and occlusion of the pulmonary capillaries. In addition to this, due to a decrease in the elasticity of the lungs, the respiratory muscles are forced to develop a large effort during inspiration, in connection with which the work of breathing increases sharply and fatigue of the respiratory muscles develops. This is a serious additional factor in the pathogenesis of respiratory failure.

Within 2-3 days, the above-described lung damage passes into the second morphological phase, in which interstitial and bronchoalveolar inflammation develops, proliferation of epithelial and interstitial cells. In the future, if there is no death, the process passes into the third phase, which is characterized by the rapid development of collagen, which leads to severe inflammation within 2-3 weeks. interstitial fibrosis with

formation in the parenchyma of the lungs of small air cysts - honeycomb lung.

Clinic and diagnostics

RDS develops within 24-48 hours after exposure to a damaging factor.

The first clinical manifestation is shortness of breath, usually with shallow breathing. On inspiration, retraction of the intercostal spaces and the suprasternal region is usually observed. During auscultation of the lungs at the beginning of RDS, pathological changes may not be determined (more precisely, only changes characteristic of the underlying disease are determined), or scattered dry rales are heard. As pulmonary edema increases, cyanosis appears, shortness of breath and tachypnea increase, moist rales appear in the lungs, which start from the lower sections, but then are heard throughout the lungs.

On the radiograph at first, a mesh restructuring of the lung pattern appears (due to interstitial edema), and soon extensive bilateral infiltrative changes (due to alveolar edema).

If possible, computed tomography should be performed. At the same time, a heterogeneous pattern of infiltration areas, alternating with areas of normal lung tissue, is revealed. The posterior sections of the lungs and areas that are more affected by gravity are more infiltrated. Therefore, a portion of the lung tissue that appears diffusely infiltrated on plain radiography is actually partially preserved and can be restored for gas exchange using positive end-expiratory pressure (PEEP) ventilation.

It must be emphasized that physical and radiological changes in the lungs lag many hours behind functional disorders. Therefore, for the early diagnosis of RDS, it is recommended to carry out urgent arterial blood gas analysis(GAK). At the same time, acute respiratory alkalosis is detected: pronounced hypoxemia (very low PaO2), normal or reduced partial pressure of carbon dioxide (PaCO2) and increased pH. The need for this study is especially justified when severe dyspnea with tachypnea occurs in patients with those diseases that can cause RDS.

Currently, there is a tendency to consider RDS as a pulmonary manifestation of a systemic disease caused by inflammatory mediators, effector cells, and other factors that are involved in the pathogenesis of the disease. Clinically, this is manifested by the development of progressive insufficiency of various organs or the so-called multiple organ failure. The most common failure of the kidneys, liver and cardiovascular system. Multiple organ failure is considered by some authors as a manifestation of a severe course of the disease, while others consider it to be a complication of RDS.

Complications also include the development of pneumonia, and in cases where pneumonia itself is the cause of RDS, its spread to other parts of the lungs due to bacterial superinfection, most often with gram-negative bacteria (Pseudomonas aeruginosa, Klebsiella, Proteus, etc.).

In RDS, it is customary to allocate 4 clinical phases of the disease.

I phase ( acute injury phase), when the impact of the damaging factor occurred, but objective changes indicating RDS have not yet occurred.

Phase II ( latent phase) develops 6-48 hours after exposure to the causative factor. This phase is characterized by tachypnea, hypoxemia, hypocapnia, respiratory alkalosis, an increase in the alveolar-capillary P(A-a)O2 gradient (in this regard, it is possible to achieve an increase in arterial blood oxygenation only with the help of oxygen inhalations, which increase the partial pressure of O2 in the alveolar air ).

III phase (phase of acute pulmonary insufficiency ). The breathlessness gets worse

cyanosis, wet and dry rales in the lungs appear, on the chest x-ray - bilateral diffuse or spotty cloud-like infiltrates. The elasticity of the lung tissue is reduced.

IV phase ( intrapulmonary bypass phase). Hypoxemia develops, which cannot be eliminated by conventional oxygen inhalations, metabolic and respiratory acidosis. Hypoxemic coma may develop.

Summarizing the above, the following the main criteria for the diagnosis of RDS:

1. The presence of diseases or exposures that can serve as a causative factor for the development of this condition.

2. Acute onset with shortness of breath and tachypnea.

3. Bilateral infiltrates on direct chest x-ray.

4. PZLA less than 18 mm Hg.

5. The development of respiratory alkalosis in the first hours of the disease, followed by a transition to metabolic and respiratory acidosis. The most

A clear deviation from external respiration is a pronounced arterial hypoxemia with a decrease in the ratio of PaO2 (partial pressure of oxygen in arterial blood) to FiO2 (fractional oxygen concentration in the inhaled gas mixture). As a rule, this ratio is sharply reduced and cannot be raised significantly even when a gas mixture with a high oxygen concentration is inhaled. The effect is achieved only with mechanical ventilation with PEEP.

Differential Diagnosis

Differential Diagnosis performed primarily with cardiogenic pulmonary edema, massive pneumonia and pulmonary embolism. In favor of cardiogenic pulmonary edema, there is a history of certain diseases of the cardiovascular system (hypertension, coronary artery disease, in particular post-infarction cardiosclerosis, mitral or aortic heart disease, etc.), increased heart size on an x-ray (while changes in the lungs are similar with those in RDS), elevated central venous pressure (CVP), a more pronounced decrease in oxygen tension in the venous blood. In all cases, it is necessary to exclude acute myocardial infarction as the cause of cardiogenic pulmonary edema. In the most difficult cases for differential diagnosis, a Swan-Ganz catheter is inserted into the pulmonary artery to determine pulmonary artery wedge pressure (PWP): low pressure

jamming (less than 18 mm Hg) is typical for RDS, high (more than 18 mm Hg) - for heart failure.

Bilateral extensive pneumonia, mimicking RDS, usually develops against a background of severe immunodeficiency. For differential diagnosis with RDS, it is necessary to take into account the entire clinical picture, the dynamics of the development of the disease, the presence of background diseases; in the most difficult cases, it is recommended to conduct a lung biopsy and study the bronchoalveolar lavage fluid.

Common symptoms of RDS and pulmonary embolism (PE) are pronounced shortness of breath and arterial hypoxemia. Unlike RDS, PE is characterized by the suddenness of the development of the disease, the presence of other clinical

cal signs of pulmonary embolism, signs of overload of the right ventricle on the ECG. In PE, widespread pulmonary edema usually does not develop.

To date, there are no standards for medical treatment

Treatment is primarily should be directed to the underlying disease,

causing RDS. If the cause of RDS was sepsis, severe pneumonia, or another inflammatory-purulent process, then antibiotic therapy is carried out, first empirically, and then, based on the results of sputum culture, aspirates from the trachea, blood and the study of the sensitivity of isolated microorganisms to antibiotics. In the presence of purulent foci, they are drained.

Considering the decisive role in the development of RDS of endotoxicosis, pathogenic

detoxification should be included in the treatment methods with hemosorption,

plasmapheresis, quantum hemotherapy and indirect electrochemical blood oxidation. Ultraviolet irradiation of blood is carried out using the Izolda apparatus, laser extracorporeal blood irradiation - with the ShATL apparatus, indirect electrochemical blood oxidation - with the EDO-4 apparatus. The most effective combination of hemosorption or plasmapheresis with UV or laser irradiation and indirect electrochemical blood oxidation. As a rule, one such session of combination therapy is enough for a turning point in the course of the disease to occur. However, in case of a severe course of the disease, 2-3 more detoxification sessions are required to achieve stabilization and reverse development of the process. At the same time, the use of membrane plasmapheresis with plasma replacement in a volume approaching the volume of circulating plasma is more effective. The detoxification methods used reduce the mortality rate in severe RDS by more than 2 times. The effectiveness of detoxification increases with its early application.

An obligatory component of the medical complex is oxygen therapy.

fia. In the presence of appropriate equipment and in the absence of threatening signs of respiratory failure (RD) in patients with mild and moderate RDS, oxygen therapy begins with non-invasive (without intubation)

ventilation of the lungs (NVL) using a mask, under which a constantly elevated pressure is maintained, which ensures sufficient PEEP. In the absence of conditions for NVL, respiratory assistance begins immediately with intubation and mechanical ventilation. Indications for invasive mechanical ventilation (through an endotracheal tube) also occur at a respiratory rate above 30 per minute, with impaired consciousness, fatigue of the respiratory muscles, and in cases where to maintain PaO2 within 60-70 mm Hg. Art. using a face mask requires a partial oxygen content in the inhaled mixture of more than 60% for several hours. The fact is that high concentrations of oxygen (more than 50-60%) in the inhaled mixture have a toxic effect on the lungs. The use of mechanical ventilation with PEEP improves blood oxygenation without increasing this concentration, by increasing the average pressure in the respiratory tract, straightening the collapsed alveoli and preventing them from collapsing at the end of exhalation. Invasive mechanical ventilation is also carried out in all severe cases of the disease, when intrapulmonary shunting of blood from right to left takes part in the development of hypoxemia. At the same time, PaO2 ceases to respond to oxygen inhalation through the mask. In these cases, IVL with PEEP (in volume switching mode) is effective, which contributes not only to the opening of collapsed alveoli, but also to an increase in lung volume and a decrease in blood shunt from right to left.

Not only high concentrations of oxygen in the inhaled mixture have an adverse effect on the body, but also a large tidal volume and high pressure in the airways, in particular at the end of expiration, which can lead to barotrauma: overinflation and rupture of the alveoli, the development of pneumothorax, pneumomediastinum, subcutaneous emphysema . In this regard, the strategy of mechanical ventilation is to achieve sufficient oxygenation at relatively low concentrations of oxygen in the inhaled mixture and PEEP. Mechanical ventilation usually begins with a tidal volume of 10-15 ml/kg at PEEP of 5 cm of water. Art. and the content (fractional concentration) of oxygen in the inhaled mixture of 60%. Then the ventilation parameters are adjusted according to the state of health of the patient and the HAC, trying to achieve a PaO2 of 60-70 mm Hg. Art. This partial pressure of oxygen

V arterial blood guarantees sufficient saturation of hemoglobin with oxygen (at the level of 90% and above) and tissue oxygenation. If this goal is not achieved, then first of allgradually increase PEEP each time by 3-5 cm of water. Art. up to the maximum allowable - 15 cm of water. Art. With a sharp deterioration in the patient's condition and an increase in DN, it is sometimes necessary to increase FiO2, but when the condition improves, the FiO2 indicator is again reduced. The optimal situation is when the patient's PaO2 can be maintained at a level of 60-70 mm Hg. Art. with FiO2 less than 50% and PEEP 5-10 cm of water. Art. In most cases this is possible. However, with massive pulmonary edema, DN may increase, despite all the measures taken.

If the maximum PEEP (15 cm of water column) in combination with FiO2 equal to 100% does not provide sufficient oxygenation, then in some cases it is possible to improve it, turning the patient on his stomach. Most patients in this position experience significant improvements in ventilation-perfusion ratio (due to uniform gravitational distribution of pleural pressure) and oxygenation, although this has not been shown to improve survival. The optimal duration of stay in this position remains unspecified. Certain inconveniences are associated with the danger of falling out and squeezing the catheter.

When performing mechanical ventilation, it is necessary to provide a minute volume of breathing (MOD) sufficient to maintain blood pH at least at the level of 7.25-7.3. Because only a small proportion of the lungs are ventilated in RDS, a high ventilation rate is usually required to provide adequate MOD.

When carrying out mechanical ventilation, it is necessary to monitor not only the HAC, but also the saturation

tissue oxygenation. An indicator of the correspondence between the delivery of oxygen to tissues and their need for it is the partial pressure of oxygen.

V mixed venous blood (PvO 2). PvO2 values ​​below 20 mm Hg. Art. reliably indicate tissue hypoxia, regardless of PaO2 and cardiac output.

Indications for transfer for spontaneous breathing are the improvement of the general condition, the disappearance of tachypnea and a sharp decrease in shortness of breath, normal

lization of the x-ray picture in the lungs, a steady improvement in lung function, as evidenced by a significant improvement (close to normalization) of the HAC.

On the technique of transferring to spontaneous breathing and on the difficulties that the resuscitator encounters in this case, we have no opportunity to stop here.

With an extremely severe degree of RDS, when methodically correctly carried out mechanical ventilation is ineffective, it is recommended extracorporeal membrane oxygenation (ECMO), which is carried out using oxygenators "North" or "MOST" with veno-venous perfusion at a rate of 1.0-1.5 l / min. For a stable improvement in gas exchange, such a procedure is usually required for from several days to 2 weeks. However, with parallel execution against the background of ECMO hemosorption (every 6-10 hours), the efficiency of membrane oxygenation increases and the effect is achieved after 20-44 hours. The use of ECMO significantly improves the results of RDS treatment

Impact on the underlying disease, detoxification and oxygen therapy are

are the main methods of treatment for RDS.

Hypovolemia often develops in RDS. This is due to the septic or infectious-inflammatory etiology of the syndrome, preceded by diuretic therapy and a decrease in venous return of blood to the heart during ventilation with increased pressure. Hypovolemia is manifested by persistent severe hypoxemia, impaired consciousness, deterioration of skin circulation and decreased urination (less than 0.5 ml/kg/h). A decrease in blood pressure in response to a slight increase in PEEP also indicates hypovolemia. Despite alveolar edema, hypovolemia dictates the need for intravenous administration plasma-substituting solutions(saline and colloidal) in order to restore perfusion of vital organs, maintain blood pressure and normal diuresis. However, hyperhydration (hypervolemia) may develop.

Both hypovolemia and hyperhydration are equally dangerous for the patient. With hypovolemia, venous return of blood to the heart decreases and cardiac output decreases, which worsens the perfusion of vital organs and contributes to the development of multiple organ failure. In severe hypovolemia to infusion therapy adding inotropic agents, for example, dopamine or dobutamine, starting with a dose of 5 mcg / kg / min, but only simultaneously with the correction of hypovolemia with plasma-substituting solutions.

In turn, hyperhydration increases pulmonary edema and also sharply worsens the prognosis of the disease. In connection with the above, infusion therapy

pyu must be carried out under the obligatory control of the volume of circulating blood (CBV), for example, by CVP . In recent years, it has been proven that the more informative indicator is PAWP. Therefore, where possible, infusion therapy should be carried out under the constant supervision of the DZLA. In this case, the optimal value of the PWLA is 10-12 (up to 14) mm Hg. Art. A low PAWP indicates hypovolemia, while a high one indicates hypervolemia and overhydration. A decrease in PAWP with reduced cardiac output indicates the need for fluid infusion. PZLA more than 18 mm Hg. Art. with low cardiac output, it indicates heart failure and is an indication for the introduction of inotropic agents.

To reduce hyperhydration (hypervolemia), diuretics are prescribed (la-

zix intravenously), more efficient hemofiltration.

It is advisable to regularly remove sputum from the respiratory tract, in part

with the help of introduction of mucolytics into the bronchi.

The question of the advisability of using glucocorticosteroids (GCS) in RDS remains open. Some researchers consider it appropriate to start trial therapy with corticosteroids if improvement cannot be achieved with conventional therapy. Other authors consider it appropriate to prescribe corticosteroids for RDS against the background of pneumocystis pneumonia and meningococcal sepsis in children. A number of works indicate the expediency of prescribing GCS after the 7th day of unresolved RDS, when collagen deposits appear in the lungs and begin

proliferation is not formed. In these cases, corticosteroids, administered in medium doses for 20-25 days, inhibit (slow down) the development of pneumofibrosis.

Among the drugs, the action of which is being studied in RDS, is al-

mitrin bismesilate, marketed under the trade name armanor. He belongs

belongs to the class of specific agonists of peripheral chemoreceptors, the action of which is realized mainly at the level of chemoreceptors of the carotid node. Armanor mimics the effects of hypoxemia in the cells of the carotid bodies, resulting in the release of neurotransmitters, in particular dopamine, from them. This leads to improved alveolar ventilation and gas exchange.

For the treatment of RDS, another mechanism of action of the drug is of much greater interest - increased hypoxic vasoconstriction in poorly ventilated areas of the lungs, which improves the ventilation-perfusion ratio, reduces intrapulmonary shunt from right to left (shunt blood flow) and improves blood oxygenation. However, narrowing of the pulmonary vessels can have a negative effect on hemodynamics in the pulmonary circulation. Therefore, armanor is used in RDS only against the background of optimal respiratory support. In our opinion, armanor is recommended to be included in the medical complex if, with methodically correctly carried out invasive ventilation, it is not possible to achieve sufficient blood oxygenation due to a pronounced shunt blood flow and a critical situation is created for the patient. In these cases, armanor is prescribed in maximum doses - 1 tab. (50 mg) every 6-8 hours. Treatment at this dose is carried out for 1-2 days.

Given the serious condition of patients, of particular importance in the treatment of RDS is

given to the organization the right enteral and parenteral nutrition, especially

especially in the first 3 days of illness.

Without treatment, almost all patients with RDS die. With proper treatment, mortality is about 50%. In recent years, individual studies have reported a reduction in mean mortality of up to 36% and even up to 31%. In all these cases, mechanical ventilation was carried out with low respiratory

volumes and pressure in the respiratory tract, detoxification methods were used, and if invasive ventilation was ineffective, ECMO was used. Unfavorable prognostic signs are age over 65 years, severe and poorly corrected gas exchange disorders, sepsis, and multiple organ failure.

Causes of death in RDS are divided into early (within 72 hours) and late (after 72 hours). The vast majority of early deaths are directly attributable to the underlying disease or injury leading to RDS. Late death in most cases is caused by irreversible respiratory failure, sepsis, or heart failure. It is also necessary to keep in mind the possibility of death from secondary bacterial superinfection of the lungs and multiple organ (especially renal) failure.

It should be emphasized that severe complications that significantly worsen the prognosis and often lead to death are also associated with

my treatment.

With catheterization of the central veins and mechanical ventilation with PEEP, a sudden development of a tension (valvular) pneumothorax is possible. The patient's general condition deteriorates sharply, shortness of breath increases, tachycardia, arterial hypotension develops, it becomes necessary to sharply increase the maximum expiratory pressure during mechanical ventilation to ensure gas exchange.

The use of constantly elevated pressure or PEEP during mechanical ventilation leads to a decrease in venous return of blood to the heart, which aggravates the existing hypovolemia, can lead to a sharp drop in cardiac output and serve as an additional factor for the development of multiple organ failure.

The toxic effect of oxygen during prolonged inhalation of a gas mixture with a fractional oxygen concentration of more than 50% and massive infusion therapy, carried out without the control of PA and BCC, can aggravate pulmonary edema and cause death. Large tidal volume and high airway pressure can cause barotrauma and lead to bronchopleural fistula formation. And finally, long-term mechanical ventilation dramatically increases

the risk of nosocomial pneumonia, and RDS and the diseases that caused it contribute to the development of DIC.

The majority of surviving patients with no previous respiratory pathology have a favorable long-term prognosis. However condition improves gradually. In the first days and weeks after "weaning" from mechanical ventilation, the quality of life is significantly reduced, shortness of breath persists, which is usually moderate, but in some patients it significantly limits physical activity. By the end of the 3rd month after extubation, the most significant improvement in the quality of life and respiratory function (EPF) occurs. However, even 6 months after extubation, this function remains reduced in 50%, and after 1 year - in 25% of those examined. The worst PEP indicators were those patients who were treated with high oxygen concentrations (more than 50-60%) in the inhaled gas mixture and a higher level of PEEP.

Only a small number of surviving patients had persistent pulmonary fibrosis and a restrictive type of respiratory failure.

Literature

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2. Respiratory distress syndrome in adults. Medical guide. Diagnosis and therapy / Ch. editor R. Bercow, in 2 volumes. Per. from English. – M.:

World, 1997. - Volume I. - S. 440-441.

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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 activity, 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 volume of “cells, a large amount of cheese-like lubricant, etc.

The lecture discusses the main aspects of the etiology, pathogenesis, clinic, diagnosis, therapy and prevention of respiratory distress syndrome.

Respiratory syndrome distress premature infants: modern tactics therapy and prevention

The lecture considers the main aspects of etiology, pathogenesis, clinical manifestations, diagnosis, therapy and prevention of respiratory distress syndrome.

Respiratory distress syndrome (RDS) of newborns is an independent nosological form (code according to ICD-X - R 22.0), clinically expressed as respiratory failure as a result of the development of primary atelectasis, interstitial pulmonary edema and hyaline membranes, which are based on a deficiency of surfactant, manifested in conditions of imbalance of oxygen and energy homeostasis.

Respiratory distress syndrome (synonyms - hyaline membrane disease, respiratory distress syndrome) 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 at birth. RDS is one of the most frequent and severe diseases of the early neonatal period in premature babies, and it accounts for approximately 25% of all deaths, and in children born at 26-28 weeks of gestation, this figure reaches 80%.

Etiology and pathogenesis. The concept that the basis for the development of RDS in newborns is the structural and functional immaturity of the lungs and the surfactant system currently remains leading, and its position has been strengthened after data on the successful use of exogenous surfactant appeared.

Surfactant is a monomolecular layer at the interface between the alveoli and air, the main function of which is to reduce the surface tension of the alveoli. Surfactant is synthesized by type II alveolocytes. Human surfactant is approximately 90% lipid and 5-10% protein. The main function - reducing surface tension and preventing the collapse of the alveoli on exhalation - is performed by surface-active phospholipids. In addition, the surfactant protects the alveolar epithelium from damage and promotes mucociliary clearance, has bactericidal activity against gram-positive microorganisms and stimulates the macrophage reaction in the lungs, participates in the regulation of microcirculation in the lungs and the permeability of the walls of the alveoli, and prevents the development of pulmonary edema.

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. The surfactant system matures by the 35-36th week of intrauterine development.

The primary deficiency of surfactant may be due to low activity of synthesis enzymes, energy deficiency, or increased degradation of surfactant. The maturation of type II alveolocytes is delayed in the presence of hyperinsulinemia in the fetus and accelerated under the influence of chronic intrauterine hypoxia due to factors such as hypertension in pregnant women, intrauterine growth retardation. Surfactant synthesis is stimulated by glucocorticoids, thyroid hormones, estrogens, adrenaline and norepinephrine.

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 of the lungs, 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 of the cardiovascular system occurs: secondary pulmonary hypertension with a right-to-left 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. In newborns who die from RDS in the first hours of life, hyaline membranes are rarely found.

Clinical signs and symptoms. Most often, RDS develops in preterm infants with a gestational age of less than 34 weeks. Risk factors for the development of RDS among newborns born at a later date and full-term are diabetes mellitus in the mother, multiple pregnancy, isoserological incompatibility of the blood of the mother and fetus, intrauterine infections, bleeding due to abruption or placenta previa, caesarean section before the onset of labor , asphyxia of the fetus and newborn.

The classical picture of RDS is characterized by a staging of clinical and radiological symptoms that appear 2-8 hours after birth: a gradual increase in breathing, swelling of the wings of the nose, "trumpeter's breathing", the appearance of a sonorous groaning exhalation, retraction of the sternum, cyanosis, CNS depression. The child groans to lengthen the exhalation, which results in a real improvement in alveolar ventilation. With inadequate treatment, there is a decrease in blood pressure, body temperature, muscle hypotension, cyanosis and pallor of the skin intensify, chest rigidity develops. With the development of irreversible changes in the lungs, general edema and oliguria may appear and increase. On auscultation, weakened breathing and crepitant rales are heard in the lungs. As a rule, signs of cardiovascular insufficiency are observed.

Depending on the morphological and functional maturity of the child and the severity of respiratory disorders, clinical signs of respiratory disorders can occur in various combinations and have different degrees of severity. Clinical manifestations of RDS in preterm infants weighing less than 1500 g and gestational age less than 32 weeks have their own characteristics: there is a more prolonged development of symptoms of respiratory failure, a peculiar sequence of symptoms. The earliest signs are diffuse cyanosis against a purple background, then swelling of the chest in the anterior upper sections, later - retraction of the lower intercostal spaces and retraction of the sternum. Violation of the rhythm of breathing is most often manifested in the form of apnea attacks, convulsive and paradoxical breathing is often observed. For children with extremely low body weight, signs such as flaring of the wings of the nose, sonorous exhalation, "trumpeter's breath", severe shortness of breath are uncharacteristic.

Clinical assessment of the severity of respiratory disorders is carried out on the scales Silverman (Silverman) and Downes (Downes). In accordance with the assessment, RDS is subdivided into a mild form of the disease (2-3 points), moderate (4-6 points) and severe (more than 6 points).

An x-ray examination of the chest organs shows a characteristic triad of signs: a diffuse decrease in the transparency of the lung fields, the borders of the heart are not differentiated, an "air" bronchogram.

As complications of RDS, the development of air leakage syndromes from the lungs, such as pneumothorax, pneumomediastinum, pneumopericardium and interstitial pulmonary emphysema, is possible. Chronic diseases, late complications of hyaline membrane disease include bronchopulmonary dysplasia and tracheal stenosis.

Principles of therapy for RDS. An obligatory condition for the treatment of premature infants with RDS is the creation and maintenance of a protective regimen: reduction of light, sound and tactile effects on the child, local and general anesthesia before performing painful manipulations. Of great importance is the creation of an optimal temperature regime, starting with the provision of primary and resuscitation care in the delivery room. When conducting resuscitation care for premature babies with a gestational age of less than 28 weeks, it is advisable to additionally use a sterile plastic bag with a slot for the head or a disposable polyethylene-based diaper, which can prevent excessive heat loss. At the end of the complex of primary and resuscitation measures, the child from the delivery room is transferred to the intensive care post, where it is placed in an incubator or under a source of radiant heat.

Antibacterial therapy is prescribed for all children with RDS. Infusion therapy is carried out under the control of diuresis. Children usually have fluid retention in the first 24-48 hours of life, which requires limiting the volume of infusion therapy. Prevention of hypoglycemia is of great importance.

In severe RDS and high oxygen dependence, parenteral nutrition is indicated. As the condition stabilizes on the 2-3rd day after the trial introduction of water through the probe, it is necessary to gradually connect enteral nutrition with breast milk or mixtures for preterm infants, which reduces the risk of necrotizing enterocolitis.

Respiratory therapy for RDS. Oxygen therapy used in mild forms of RDS with a mask, oxygen tent, nasal catheters.

CPAP- continuous positive airway pressure - constant (i.e. continuously maintained) positive pressure in the airways prevents the alveoli from collapsing and the development of atelectasis. Continuous positive pressure increases functional residual capacity (FRC), reduces airway resistance, improves lung tissue extensibility, promotes stabilization and synthesis of endogenous surfactant. The use of binasal cannulas and variable flow devices (NCPAPs) is preferred.

Prophylactic or early (within the first 30 minutes of life) administration of CPAP is given to all neonates 27–32 weeks gestational age who are spontaneously breathing. In the absence of spontaneous breathing in preterm infants, mask ventilation is recommended; after spontaneous breathing is restored, CPAP is started.

The use of CPAP in the delivery room is contraindicated, despite the presence of spontaneous breathing in children: with choanal atresia or other malformations of the maxillofacial region, diagnosed with pneumothorax, with congenital diaphragmatic hernia, with congenital malformations incompatible with life, with bleeding (pulmonary, gastric, bleeding skin), with signs of shock.

Therapeutic use of CPAP. It is indicated in all cases when the child develops the first signs of respiratory disorders and the dependence on oxygen increases. In addition, CPAP is used as a method of respiratory support after extubation of newborns of any gestational age.

mechanical ventilation is the main treatment for severe respiratory failure in newborns with RDS. It should be remembered that mechanical ventilation, even with the most advanced devices, inevitably leads to lung damage. Therefore, the main efforts should be aimed at preventing the development of severe respiratory failure. The introduction of surfactant replacement therapy and the early use of CPAP contribute to a decrease in the proportion of mechanical ventilation in the intensive care of newborns with RDS.

In modern neonatology, a fairly large number of methods and modes of mechanical ventilation are used. In all cases where a child with RDS is not in critical condition, it is best to start with synchronized assisted (triggered) ventilation modes. This will allow the child to actively participate in maintaining the required volume of minute ventilation of the lungs and will help to reduce the duration and frequency of complications of mechanical ventilation. With the inefficiency of traditional IVL, the method of high-frequency IVL is used. The choice of a specific mode depends on the severity of the patient's respiratory efforts, the experience of the doctor and the capabilities of the ventilator used.

A necessary condition for the effective and safe conduct of mechanical ventilation is monitoring of the vital functions of the child's body, blood gas composition and respiratory parameters.

Surfactant replacement therapy. Surfactant replacement therapy is a pathogenetic treatment for RDS. This therapy is aimed at replenishing the deficiency of surfactant, and its effectiveness has been proven in numerous randomized controlled trials. It makes it possible to avoid high pressures and oxygen concentrations during mechanical ventilation, which contributes to a significant reduction in the risk of barotrauma and toxic effects of oxygen on the lungs, reduces the incidence of bronchopulmonary dysplasia, and increases the survival rate of preterm infants.

Of the surfactants registered in our country, curosurf, a natural surfactant of pig origin, is the drug of choice. Produced as a suspension in vials of 1.5 ml with a concentration of phospholipids 80 mg/ml. The drug is injected in a stream or slowly in a stream into the endotracheal tube (the latter is possible only if special double-lumen endotracheal tubes are used). Curosurf must be warmed to 35-37ºC before use. Jet administration of the drug promotes a homogeneous distribution of surfactant in the lungs and provides an optimal clinical effect. Exogenous surfactants are prescribed for both prevention and treatment of neonatal respiratory distress syndrome.

Preventive the use of a surfactant is considered before the development of clinical symptoms of respiratory distress syndrome in newborns with the highest risk of developing RDS: gestational age less than 27 weeks, no course of antenatal steroid therapy in premature infants born at 27-29 weeks of gestation. The recommended dose of curosurf for prophylactic administration is 100-200 mg/kg.

Early therapeutic use called the use of surfactant in children at risk for RDS due to an increase in respiratory failure.

In preterm infants with regular spontaneous breathing against the background of early CPAP use, it is advisable to administer surfactant only when the clinical signs of RDS increase. For children born at a gestational age of less than 32 weeks and requiring tracheal intubation for mechanical ventilation in the delivery room due to the inefficiency of spontaneous breathing, the introduction of a surfactant is indicated within the next 15-20 minutes after birth. The recommended dose of Curosurf for early therapeutic administration is at least 180 mg/kg (optimally 200 mg/kg).

Delayed therapeutic use of surfactants. If the newborn was not administered surfactant for prophylactic or early therapeutic purposes, then after the transfer to mechanical ventilation of a child with RDS, surfactant replacement therapy should be carried out as soon as possible. The effectiveness of late therapeutic use of surfactant is significantly lower than preventive and early therapeutic use. In the absence or insufficient effect of the introduction of the first dose, the surfactant is re-administered. Usually, the surfactant is re-administered 6-12 hours after the previous dose.

The appointment of a surfactant for therapeutic treatment is contraindicated in pulmonary hemorrhage, pulmonary edema, hypothermia, decompensated acidosis, arterial hypotension and shock. Before administering a surfactant, the patient must be stabilized. In case of complications of RDS with pulmonary bleeding, surfactant can be used no earlier than 6-8 hours after bleeding has stopped.

Prevention of RDS. The use of the following measures can improve survival among newborns at risk of developing RDS:

1. Antenatal ultrasound diagnostics for more accurate determination of gestational age and assessment of the condition of the fetus.

2. Continuous monitoring of the fetus to confirm the satisfactory condition of the fetus during labor or to identify fetal distress, followed by a change in the tactics of labor management.

3. Assessment of the maturity of the lungs of the fetus before delivery - the ratio of lecithin / sphingomyelin, the content of phosphatidylglycerol in the amniotic fluid.

4. Prevention of preterm labor using tocolytics.

5. Antenatal corticosteroid therapy (ACT).

Corticosteroids stimulate the processes of cellular differentiation of numerous cells, including type II alveolocytes, increase the production of surfactant and the elasticity of the lung tissue, and reduce the release of proteins from the pulmonary vessels into the air space. Antenatal administration of corticosteroids to women at risk of preterm birth at 28–34 weeks significantly reduces the incidence of RDS, neonatal death, and intraventricular hemorrhage (IVH).

The appointment of corticosteroid therapy is indicated for the following conditions:

- premature rupture of amniotic fluid;

- clinical signs of the onset of preterm labor (regular labor activity, a sharp shortening / smoothing of the cervix, opening up to 3-4 cm);

- bleeding during pregnancy;

- complications during pregnancy (including preeclampsia, intrauterine growth retardation, placenta previa), in which early termination of pregnancy is performed on a planned or emergency basis.

Maternal diabetes mellitus, preeclampsia, prophylactically treated chorioamnionitis, treated tuberculosis are not contraindications to ACT. In these cases, strict glycemic control and blood pressure monitoring are carried out accordingly. Corticosteroid therapy is prescribed under the guise of antidiabetic drugs, antihypertensive or antibiotic therapy.

Corticosteroid therapy is contraindicated in systemic infectious diseases (tuberculosis). Precautions should be taken if chorioamnionitis is suspected (therapy is carried out under the cover of antibiotics).

The optimal interval between corticosteroid therapy and delivery is 24 hours to 7 days from the start of therapy.

Drugs used to prevent RDS:

Betamethasone- 2 doses of 12 mg intramuscularly after 24 hours.

Dexamethasone- 6 mg intramuscularly every 12 hours for 2 days. Since in our country the drug dexamethasone is distributed in ampoules of 4 mg, it is recommended to administer it intramuscularly at 4 mg 3 times a day for 2 days.

With the threat of preterm birth, antenatal administration of betamethasone is preferable. Studies have shown that it stimulates lung maturation faster, helps to reduce the incidence of IVH and periventricular leukomalacia in premature babies with a gestational age of more than 28 weeks, leading to a significant decrease in perinatal morbidity and mortality.

Doses of corticosteroids in multiple pregnancies do not increase.

A second course of ACT is carried out no earlier than 7 days after the decision of the council.

Respiratory distress syndrome (RDS) continues to be one of the most frequent and severe diseases of the early neonatal period in preterm infants. Antenatal prophylaxis and adequate therapy for RDS can reduce mortality and reduce the incidence of complications in this disease.

O.A. Stepanova

Kazan State Medical Academy

Stepanova Olga Alexandrovna — Candidate of Medical Sciences, Associate Professor of the Department of Pediatrics and Neonatology

Literature:

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2. Prematurity: Per. from English. / ed. V.Kh.Yu. Victor, E.K. Wood - M.: Medicine, 1995. - 368 p.

3. Neonatology: National Guide / ed. N.N. Volodin. — M.: GEOTAR-Media, 2007. — 848 p.

4. Neonatology: Per. from English. / ed. T.L. Gomella, M.D. Cunnigam. - M., 1995. - 640 p.

5. Perinatal audit in preterm birth / V.I. Kulakov, E.M. Vikhlyaeva, E.N. Baibarina, Z.S. Khodzhaeva and others // Moscow, 2005. - 224 p.

6. Principles of management of newborns with respiratory distress syndrome / Guidelines, ed. N.N. Volodin. - M., 2009. - 32 p.

7. Shabalov N.P. Neonatology. - In 2 volumes - M .: MEDpress-inform, 2006.

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Respiratory Distress Syndrome (RDS)- one of the serious problems that doctors who care for premature babies have to face. RDS is a disease of newborns, manifested by the development of respiratory failure immediately or within a few hours after birth. The disease is gradually getting worse. Usually, by the 2-4th day of life, its outcome is determined: a gradual recovery, or the death of the baby.

Why do the lungs of a child refuse to perform their functions? Let's try to look into the very depths of this vital organ and figure out what's what.

Surfactant

Our lungs are made up of many small sacs called alveoli. Their total surface is comparable to the area of ​​a football field. You can imagine how tightly all this is packed in the chest. But in order for the alveoli to perform their main function - gas exchange - they must be in a straightened state. Prevents the collapse of the alveoli special "lubrication" - surfactant. The name of the unique substance comes from the English words surface- surface and active- active, that is, surface-active. It reduces the surface tension of the inner air-facing surface of the alveoli, preventing them from collapsing during exhalation.

Surfactant is a unique complex consisting of proteins, carbohydrates and phospholipids. The synthesis of this substance is carried out by the cells of the epithelium lining the alveoli - alveolocytes. In addition, this "lubricant" has a number of remarkable properties - it is involved in the exchange of gases and liquids through the pulmonary barrier, in removing foreign particles from the surface of the alveoli, protecting the alveolar wall from oxidants and peroxides, to some extent - and from mechanical damage.

While the fetus is in the uterus, its lungs do not function, but, nevertheless, they are slowly preparing for future independent breathing - at the 23rd week of development, alveolocytes begin to synthesize surfactant. Its optimal amount - about 50 cubic millimeters per square meter of lung surface - accumulates only by the 36th week. However, not all babies "live out" until this period and, for various reasons, are born earlier than the prescribed 38-42 weeks. And this is where the problems begin.

What's happening?

An insufficient amount of surfactant in the lungs of a premature baby leads to the fact that on exhalation the lungs seem to collapse (collapse) and the child has to re-inflate them with each breath. This requires a lot of energy, as a result, the strength of the newborn is depleted and severe respiratory failure develops. In 1959, American scientists M.E. Avery and J. Mead found a lack of pulmonary surfactant in premature infants suffering from respiratory distress syndrome, thus establishing the main cause of RDS. The frequency of development of RDS is higher, the shorter the period at which the child was born. So, they suffer on average 60 percent of children born at a gestational age of less than 28 weeks, 15-20 percent - at a period of 32-36 weeks and only 5 percent - at a period of 37 weeks or more.

The clinical picture of the syndrome is manifested primarily by symptoms of respiratory failure, which usually develop at birth, or 2-8 hours after birth - increased respiration, swelling of the wings of the nose, retraction of the intercostal spaces, participation in the act of breathing of the auxiliary respiratory muscles, development of cyanosis (cyanosis). Due to insufficient ventilation of the lungs, a secondary infection very often joins, and pneumonia in such infants is by no means uncommon. The natural healing process begins after 48-72 hours of life, but not all children have this process fast enough - due to the development of the already mentioned infectious complications.

With rational nursing and careful adherence to treatment protocols for children with RDS, up to 90 percent of young patients survive. The transferred respiratory distress syndrome in the future practically does not affect the health of children.

Risk factors

It is difficult to predict whether a given child will develop RDS or not, but scientists have been able to identify a certain risk group. Predispose to the development of the syndrome diabetes mellitus, infections and smoking of the mother during pregnancy in the mother, childbirth by caesarean section, birth by the second of twins, asphyxia during childbirth. In addition, it was found that boys suffer from RDS more often than girls. Prevention of the development of RDS is reduced to the prevention of preterm birth.

Treatment

Diagnosis of respiratory distress syndrome is carried out in a maternity hospital.

The basis of the treatment of children with RDS is the “minimal touch” technique, the child should receive only absolutely necessary procedures and manipulations. One of the methods for treating the syndrome is intensive respiratory therapy, various types of artificial lung ventilation (ALV).

It would be logical to assume that since RDS is caused by a lack of surfactant, then the syndrome should be treated by introducing this substance from the outside. However, this is associated with so many limitations and difficulties that the active use of artificial surfactant preparations began only in the late 80s and early 90s of the last century. Surfactant therapy allows you to improve the condition of the child much faster. However, these drugs are very expensive, their effectiveness is high only if they are used in the first few hours after birth, and their use requires the availability of modern equipment and qualified medical personnel, since there is a high risk of developing severe complications.

Respiratory distress syndrome of newborns is a pathological condition that occurs in the early neonatal period and is clinically manifested by signs of acute respiratory failure. In the medical literature, to refer to this syndrome, there are also alternative terms "respiratory distress syndrome", "hyaline membrane disease".

The disease is usually detected in preterm infants and is one of the most severe and common pathologies of the neonatal period. Moreover, the lower the gestational age of the fetus and its birth weight, the higher the likelihood of developing respiratory disorders in the child.

Predisposing factors

The basis of the RDS syndrome of newborns is the lack of a substance covering the alveoli from the inside - a surfactant.

The basis for the development of this pathology is the immaturity of the lung tissue and the surfactant system, which explains the occurrence of such disorders mainly in preterm infants. But babies born at term can also develop RDS. The following factors contribute to this:

• intrauterine infections;
• fetal asphyxia;
• general cooling (at temperatures below 35 degrees, the synthesis of surfactant is disrupted);
• multiple pregnancy;
• incompatibility by blood group or Rh factor in mother and child;
• (increases the likelihood of detecting RDS in a newborn by 4-6 times);
• bleeding due to premature detachment of the placenta or its presentation;
• delivery by planned caesarean section (before the onset of labor).

Why develops

The occurrence of RDS in newborns is due to:

• violation of the synthesis of surfactant and its excretion on the surface of the alveoli due to insufficient maturation of lung tissue;
• birth defects of the surfactant system;
• its increased destruction during various pathological processes (for example, severe hypoxia).

Surfactant begins to be produced in the fetus during fetal development at the 20-24th week. However, during this period it does not have all the properties of a mature surfactant, it is less stable (rapidly destroyed under the influence of hypoxemia and acidosis) and has a short half-life. This system fully matures at the 35-36th week of pregnancy. A massive release of surfactant occurs during childbirth, which helps to expand the lungs during the first breath.

Surfactant is synthesized by type II alveolocytes and is a monomolecular layer on the surface of the alveoli, consisting of lipids and proteins. Its role in the body is very large. Its main functions are:

• an obstacle to the collapse of the alveoli on inspiration (due to a decrease in surface tension);
• protection of the epithelium of the alveoli from damage;
• improvement of mucociliary clearance;
• regulation of microcirculation and permeability of the alveolar wall;
• immunomodulatory and bactericidal action.

In a child born prematurely, the reserves of surfactant are only enough to carry out the first breath and ensure the function of breathing in the first hours of life, in the future, its reserves are depleted. Due to the lagging of the processes of surfactant synthesis from the rate of its decay, the subsequent increase in the permeability of the alveolo-capillary membrane and the leakage of fluid into the interalveolar spaces, a significant change occurs in the functioning of the respiratory system:

• in different parts of the lungs are formed;
• stagnation is observed;
• interstitial develops;
• increasing hypoventilation;
• intrapulmonary shunting occurs.

All this leads to insufficient tissue oxygenation, the accumulation of carbon dioxide in them, and a change in the acid-base state towards acidosis. The resulting respiratory failure disrupts the functioning of the cardiovascular system. These children develop:

• increased pressure in the pulmonary artery system;
• systemic;
• transient myocardial dysfunction.

It should be noted that the surfactant synthesis is stimulated by:

• corticosteroids;
• estrogens;
• thyroid hormones;
• epinephrine and norepinephrine.

Its maturation is accelerated under the influence of chronic hypoxia (with intrauterine growth retardation, late preeclampsia).

How it manifests itself and what is dangerous

Depending on the time of appearance of the symptoms of this pathology and the general condition of the child's body at this moment, three main variants of its clinical course can be distinguished.

1. In some premature babies born in a satisfactory condition, the first clinical manifestations are recorded 1-4 hours after birth. This variant of the disease is considered a classic. The so-called "light gap" is associated with the functioning of an immature and rapidly decaying surfactant.
2. The second variant of the syndrome is typical for premature babies who have undergone severe hypoxia during childbirth. Their alveolocytes are not able to quickly accelerate the production of surfactant after the expansion of the lungs. The most common cause of this condition is acute asphyxia. Initially, the severity of the condition of newborns is due to cardio-respiratory depression. However, after stabilization of the condition, they quickly develop RDS.
3. The third variant of the syndrome is observed in very premature babies. They have a combination of immaturity in the mechanisms of surfactant synthesis with a limited ability of alveolocytes to increase the rate of its production after the first breath. Signs of respiratory disorders in such newborns are noticeable from the first minutes of life.

In the classic course of the respiratory syndrome, some time after birth, the child develops the following symptoms:

• gradual increase in respiratory rate (against the background of the skin of normal color, cyanosis appears later);
• swelling of the wings of the nose and cheeks;
• sonorous groaning exhalation;
• retraction of the most pliable places of the chest on inspiration - supraclavicular fossae, intercostal spaces, lower part of the sternum.

As the pathological process progresses, the child's condition worsens:

• the skin becomes cyanotic;
• there is a decrease in blood pressure and body temperature;
• increased muscle hypotension and hyporeflexia;
• chest rigidity develops;
• moist rales are heard above the lungs against the background of weakened breathing.

In very preterm infants, RDS has its own characteristics:

• an early sign of the pathological process is diffuse cyanosis;
• immediately after birth, they experience swelling of the anterior upper chest, which is later replaced by its retraction;
• respiratory failure is manifested by apnea attacks;
• symptoms such as swelling of the wings of the nose may be absent;
• symptoms of respiratory failure persist for a longer period of time.

In severe RDS, due to severe circulatory disorders (both systemic and local), its course is complicated by damage to the nervous system, gastrointestinal tract, and kidneys.

Diagnostic principles

Women who are at risk undergo amniocentesis and examine the lipid content in the resulting sample of amniotic fluid.

Early diagnosis of RDS is extremely important. In women at risk, prenatal diagnosis is recommended. To do this, examine the lipid spectrum of amniotic fluid. According to its composition, the degree of maturity of the lungs of the fetus is judged. Given the results of such a study, it is possible to timely prevent RDS in an unborn child.

In the delivery room, especially in the case of preterm birth, the compliance of the maturity of the main systems of the child's body with his gestational age is assessed, and risk factors are identified. At the same time, the “foam test” is considered quite informative (ethyl alcohol is added to the amniotic fluid or aspirate of gastric contents and the reaction is observed).

In the future, the diagnosis of respiratory distress syndrome is based on an assessment of clinical data and the results of an X-ray examination. The radiological signs of the syndrome include the following:

• reduced pneumatization of the lungs;
• air bronchogram;
• blurred borders of the heart.

For a full assessment of the severity of respiratory disorders in such children, special scales are used (Silverman, Downs).

Medical tactics

Treatment of RDS begins with proper care of the newborn. He should be provided with a protective mode with minimization of light, sound and tactile irritations, optimal ambient temperature. Usually the child is placed under a heat source or in an incubator. His body temperature should not be less than 36 degrees. The first time until the condition stabilizes, the child is provided with parenteral nutrition.

Therapeutic measures for RDS begin immediately, usually they include:

• ensuring normal airway patency (suction of mucus, the appropriate position of the child);
• the introduction of surfactant preparations (carried out as early as possible);
• adequate ventilation of the lungs and normalization of the gas composition of the blood (oxygen therapy, CPAP therapy, mechanical ventilation);
• fight against hypovolemia (infusion therapy);
• correction of the acid-base state.

Considering the severity of RDS in newborns, the high risk of complications and the numerous difficulties of the therapy, special attention should be paid to the prevention of this condition. It is possible to accelerate the maturation of the lungs of the fetus by administering glucocorticoid hormones (dexamethasone, betamethasone) to a pregnant woman. The indications for this are:

• high risk of preterm birth and their initial signs;
• complicated course of pregnancy, in which early delivery is planned;
• outflow of amniotic fluid ahead of time;
• bleeding during pregnancy.

A promising direction in the prevention of RDS is the introduction of thyroid hormones into the amniotic fluid.