RDS diagnosis in infant. Distress syndrome in newborns. The important role of surfactant

21.02.2019

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

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

Some authors call this condition adult respiratory distress syndrome (ARDS). This is due to the fact that, in addition to ARDS, there is respiratory distress syndrome of newborns (RDNS). RDS develops almost exclusively in premature infants born before 37 weeks of pregnancy, who often have a hereditary predisposition to the disease, and much less frequently in newborns whose mothers suffered from diabetes. The disease is based on a deficiency of pulmonary surfactant in the newborn. This leads to decreased elasticity lung tissue, collapse of the alveoli and the development of diffuse atelectasis. As a result, the child develops severe respiratory failure in the first hours after birth. With this disease, on the inner surface of the alveoli, alveolar ducts and respiratory bronchioles Deposition of a hyaline-like substance is observed, 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 pulmonary ventilation (ALV) in time, ensure expansion of the lungs and sufficient gas exchange, then after some time surfactant begins to be produced and ARDS resolves in 4-5 days. However, RDS associated with nonhemodynamic pulmonary edema can also develop in children.

* Distress – English. distress – severe illness, suffering

In the English-language literature, RDS is often called “acute respiratory distress syndrome” (ARDS).

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

Etiology

Etiological factors are usually divided into 2 groups: those that have

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

lung denting. 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 injury), oxygen intoxication, fat embolism of the pulmonary artery, altitude sickness, exposure to ionizing radiation, lymphostasis in the lungs (for example, with metastases of tumors to regional lymph nodes). Indirect lung damage is observed in sepsis, acute hemorrhagic pancreatitis, peritonitis, severe extrathoracic trauma, especially traumatic brain injury, burn disease, eclampsia, massive blood transfusion, during the use of artificial circulation, 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 initial stage This inflammatory response is manifested by the release of endotoxins, tumor necrosis factor, interleukin-1 and other proinflammatory cytokines. Later in the cascade inflammatory reactions Cytokine-activated leukocytes and platelets are activated, which accumulate in the 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 the permeability of the pulmonary

protein pillars, which leads to a decrease in the oncotic pressure gradient between plasma and interstitial tissue, and fluid begins to leave the vascular bed. Edema of interstitial tissue and alveoli develops.

Thus, in the pathogenesis of pulmonary edema, endotoxins play a crucial role, which have both a direct damaging effect on the endothelial cells of the pulmonary capillaries, and indirectly through the activation of the body’s mediator systems.

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 alveolar and in-

terstitial pulmonary edema (first morphological phase) . Due to the significance

Due to the significant 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 disrupted 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 surfactant activity. 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 testing is explained as follows. Venous blood, passing through areas of the lungs with collapsed (atelectasis) or fluid-filled alveoli, is not enriched with oxygen (not arterialized) and in this form enters the arterial bed, which increases hypoxemia and hypoxia.

Impaired 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 great force during inspiration, and therefore the work of breathing sharply increases and fatigue of the respiratory muscles develops. This is serious additional factor pathogenesis of respiratory failure.

Within 2-3 days, the lung damage described above passes into the second morphological phase, in which interstitial and bronchoalveolar inflammation develops, proliferation of epithelial and interstitial cells. In the future, if it does not occur fatal outcome, the process enters the third phase, which is characterized by rapid development of collagen, which within 2-3 weeks leads to severe interstitial fibrosis with for-

formation in the lung parenchyma of small air cysts– cellular lung.

Clinic and diagnostics

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

First clinical manifestation is shortness of breath, usually with frequent shallow breathing. On inhalation, retraction of the intercostal spaces and suprasternal region is usually observed. When auscultating the lungs at the onset of RDS, pathological changes may not be detected (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 intensify, moist wheezing appears in the lungs, which start with lower sections, but then are heard throughout the lungs.

On the radiograph First, a reticular restructuring of the pulmonary pattern appears (due to interstitial edema), and soon extensive bilateral infiltrative changes (due to alveolar edema).

If possible, a CT scan should be performed. In this case, a heterogeneous pattern of areas of infiltration is revealed, alternating with areas of normal lung tissue. The posterior parts of the lungs and areas that are more affected by gravity are subject to greater infiltration. Therefore, part of the lung tissue, which appears diffusely infiltrated on a conventional radiograph, is in fact partially preserved and can be restored for gas exchange when using mechanical ventilation with positive pressure at the end of expiration (PEEP).

It must be emphasized that physical and radiographic changes in the lungs lags many hours behind functional disorders. Therefore, for early diagnosis of RDS, it is recommended to carry out urgent gas analysis arterial blood (GAK). In this case, 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 shortness of breath with tachypnea occurs in patients with diseases that may cause RDS.

There is now a tendency to consider RDS as a pulmonary manifestation 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 failure of various organs or the so-called multiple organ failure. The most common failures of the kidneys, liver and cardiovascular system develop. Some authors consider multiple organ failure as a manifestation of a severe course of the disease, while others attribute it to complications 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 case of RDS, it is customary to distinguish 4 clinical phases of the disease.

Phase I ( acute injury phase), when exposure to a damaging factor has 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 gradient P(A-a)O2 (in this regard, an increase in arterial blood oxygenation can only be achieved with the help of oxygen inhalations, which increase the partial pressure of O2 in the alveolar air ).

Phase III (phase of acute pulmonary failure ). Shortness of breath gets worse

cyanosis, moist and dry rales appear in the lungs, and bilateral diffuse or spotty cloud-like infiltrates appear on a chest x-ray. 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, we can name the following main criteria for diagnosing RDS:

1. The presence of diseases or influences that may 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. PAWP less than 18 mmHg.

5. Development of respiratory alkalosis in the first hours of the disease with subsequent transition to metabolic and respiratory acidosis. The most consistent

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

Differential diagnosis

Differential diagnosis It is carried out primarily with cardiogenic pulmonary edema, massive pneumonia and pulmonary embolism. Cardiogenic pulmonary edema is supported by a history of certain diseases of cardio-vascular system (hypertonic disease, coronary artery disease, in particular post-infarction cardiosclerosis, mitral or aortic heart defects, etc.), increased heart size on an x-ray (while changes in the lungs are similar to those with RDS), increased central venous pressure (CVP), a more pronounced decrease in oxygen tension in 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 (PAWP): low pressure

The jamming level (less than 18 mm Hg) is characteristic of RDS, high (more than 18 mm Hg) – for heart failure.

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

Common symptoms of RDS and pulmonary embolism (PE) are severe 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

ical signs of pulmonary embolism, signs of right ventricular overload on the ECG. With PE, widespread pulmonary edema usually does not develop.

There are still no standards for drug treatment

Treatment, first of all, should be aimed at the underlying disease,

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

Considering the decisive role of endotoxemia in the development of RDS, pathogenetic

Chinese methods of treatment include detoxification using hemosorption,

plasmapheresis, quantum hemotherapy and indirect electrochemical oxidation of blood. UV blood carried out using the Izolda apparatus, laser extracorporeal irradiation of blood - with the SHUTL apparatus, indirect electrochemical oxidation of blood - with the EDO-4 apparatus. The most effective combination is hemosorption or plasmapheresis with ultraviolet irradiation or laser irradiation and indirect electrochemical oxidation of blood. As a rule, one such session of combination therapy is enough to cause a turning point in the course of the disease. However, in severe cases of the disease, another 2-3 detoxification sessions are required to achieve stabilization and reverse development of the process. In this case, 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 use.

An obligatory component of the treatment complex is oxygen therapy.

piya. In the presence of appropriate equipment and in the absence of threatening signs of respiratory failure (RF) in patients with lung and moderate course RDS - oxygen therapy begins non-invasively (without intubation)

pulmonary ventilation (NVL) using a mask under which a constantly elevated pressure is maintained, which ensures sufficient PEEP. In the absence of conditions for non-invasive ventilation, respiratory support begins immediately with intubation and mechanical ventilation. Indications for invasive mechanical ventilation (via an endotracheal tube) also arise when the respiratory rate is 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, a partial oxygen content in the inhaled mixture of more than 60% is required for several hours. The fact is that high concentrations oxygen (more than 50-60%) in the inhaled mixture has a toxic effect on the lungs. The use of mechanical ventilation with PEEP makes it possible to improve blood oxygenation without increasing this concentration, by increasing the average pressure in the respiratory tract, straightening collapsed alveoli and preventing their collapse at the end of expiration. Invasive mechanical ventilation is also carried out in all severe cases of the disease, when intrapulmonary shunting of blood from right to left is involved in the development of hypoxemia. In this case, PaO2 stops responding to oxygen inhalation through a mask. In these cases, mechanical ventilation with PEEP (in volume switching mode) turns out to be effective, which promotes not only the opening of collapsed alveoli, but also an increase in lung volume and a decrease in blood discharge from right to left.

An unfavorable effect on the body is caused not only by high concentrations of oxygen in the inhaled mixture, but also by a large tidal volume and high pressure in the respiratory tract, 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 ventilation strategy is to achieve sufficient oxygenation at relatively low oxygen concentrations in the inhaled mixture and PEEP. Mechanical ventilation is usually started with a tidal volume of 10-15 ml/kg at a PEEP of 5 cmH2O. Art. and the content (fractional concentration) of oxygen in the inhaled mixture is 60%. Then the ventilation parameters are adjusted according to the patient’s well-being and the GAK, trying to achieve a PaO2 of 60-70 mm Hg. Art. This partial pressure of oxygen

V arterial blood guarantees sufficient oxygen saturation of hemoglobin (at a level of 90% and above) and tissue oxygenation. If this goal is not achieved, then first of allincrease PEEP stepwise each time by 3-5 cm of water. Art. up to the maximum permissible - 15 cm of water. Art. When the patient’s condition sharply deteriorates and DN increases, sometimes it is necessary to increase FiO2, but when the condition improves, the FiO2 indicator is reduced again. 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 water. Art. In most cases this is possible. However, with massive pulmonary edema, DN may increase despite all measures taken.

If the maximum PEEP (15 cm H2O) 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. For most patients, ventilation-perfusion ratio (due to uniform gravitational distribution of pleural pressure) and oxygenation are significantly improved in this position, although this has not been proven to improve survival rates. The optimal duration of stay in this position remains unclear. Certain inconveniences are associated with the danger of the catheter falling out and being compressed.

When performing mechanical ventilation, it is necessary to ensure a minute volume of respiration (MVR) sufficient to maintain blood pH at least at the level of 7.25-7.3. Since only a small portion of the lungs is ventilated in RDS, high insufflation rates are typically required to provide sufficient MOV.

When performing mechanical ventilation, it is necessary to monitor not only the BAC, but also the saturation

supplying tissue with oxygen. 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 an improvement in the general condition, the disappearance of tachypnea and a sharp decrease in shortness of breath, normal

lysis of the X-ray picture in the lungs, a sustained improvement in pulmonary function, as evidenced by a significant improvement (close to normalization) in the blood flow rate.

We do not have the opportunity to dwell here on the technique of transferring to independent breathing and the difficulties encountered by the resuscitator.

In case of extremely severe RDS, when methodically correctly performed mechanical ventilation turns out to be ineffective, it is recommended extracorporeal membrane oxygenation (ECMO) which is carried out using Sever or MOST oxygenators with venovenous perfusion at a rate of 1.0-1.5 l/min. For a stable improvement in gas exchange, this procedure usually requires a period of several days to 2 weeks. However, when hemosorption is performed in parallel against the background of ECMO (every 6-10 hours), the effectiveness of membrane oxygenation increases and the effect is achieved within 20-44 hours. The use of ECMO significantly improves the results of treatment of RDS

Impact on the underlying disease, detoxification and oxygen therapy are

are the main methods of treating RDS.

Hypovolemia often develops in RDS. This is explained by the septic or infectious-inflammatory etiology of the syndrome, previous diuretic therapy and a decrease in venous return of blood to the heart during high-pressure ventilation. 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 replacement solutions(saline and colloid) in order to restore the perfusion of vital organs, maintain blood pressure and normal diuresis. However, overhydration (hypervolemia) may develop.

Both hypovolemia and overhydration are equally dangerous for the patient. With hypovolemia, venous return of blood to the heart decreases and cardiac output decreases, which impairs the perfusion of vital organs and contributes to the development of multiple organ failure. For severe hypovolemia, infusion therapy add inotropes, for example, dopamine or dobutamine, starting with a dose of 5 mcg/kg/min, but only simultaneously with the correction of hypovolemia with plasma replacement solutions.

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

PPI must be carried out under mandatory monitoring of circulating blood volume (CBV), for example, by CVP . IN last years it has been proven that the DPA is a more informative indicator. Therefore, where possible, infusion therapy should be carried out under continuous control of DZLA. Wherein optimal value DZLA is 10-12 (up to 14) mm Hg. Art. A low PAWP indicates hypovolemia, a high PAWP indicates hypervolemia and overhydration. A decrease in PAWP with decreased cardiac output indicates the need for fluid infusion. PAWP more than 18 mm Hg. Art. with low cardiac output, it indicates heart failure and is an indication for the administration of inotropes.

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

Zix intravenously), hemofiltration is more effective.

It is advisable to regularly remove mucus from the respiratory tract, often

ness with the help injection of mucolytics into the bronchi.

Question about the advisability of using glucocorticosteroids (GCS) for RDS remains open. Some researchers consider it advisable to begin a trial of corticosteroid therapy if improvement is not achieved with conventional therapy. Other authors consider it advisable to prescribe GCS for RDS against the background of Pneumocystis pneumonia and meningococcal sepsis in children. A number of studies indicate the advisability of prescribing corticosteroids after the 7th day of unresolved RDS, when collagen deposits appear in the lungs and the

proliferation does not form. In these cases, GCS, prescribed in medium doses for 20-25 days, restrains (slows down) the development of pulmonary fibrosis.

Drugs being studied for RDS include al-

mitrine bismesylate, produced under trade name armanor. He belongs to

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 ganglion. Armanor imitates the effects of hypoxemia in the cells of the carotid bodies, as a result of which neurotransmitters, in particular dopamine, are released 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 shunting of blood 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 for RDS only against the background of optimal respiratory support. In our opinion, it is recommended to include armanor in medical complex if, with methodically correctly performed invasive ventilation, it is not possible to achieve sufficient blood oxygenation due to pronounced shunt blood flow and a critical situation is created for the patient. In these cases, armanor is prescribed in maximum doses - 1 tablet. (50 mg) every 6-8 hours. Treatment at this dose is carried out for 1-2 days.

Considering the serious condition of the patients, special meaning in the treatment of RDS in

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

especially in the first 3 days of the disease.

Without treatment, almost all patients with RDS die. When conducting proper treatment the mortality rate is about 50%. In recent years, individual studies have reported reductions in average mortality to 36% and even 31%. In all these cases, mechanical ventilation was performed 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 correctable 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 due directly to the underlying disease or injury that led to RDS. Late death is most often 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

our treatment.

During central venous catheterization and mechanical ventilation with PEEP, sudden development of tension (valvular) pneumothorax is possible. The patient is rapidly deteriorating general state, shortness of breath intensifies, tachycardia and arterial hypotension develop, and there is a need 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 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 control of the pulmonary arterial pulmonary artery and blood volume can aggravate pulmonary edema and cause death. Large tidal volumes and high airway pressures can cause barotrauma and lead to the formation of a bronchopleural fistula. And finally, long-term mechanical ventilation sharply increases

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

The majority of surviving patients who had no previous respiratory pathology have a favorable long-term prognosis. However the condition is improving 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 quality of life and respiratory function (RVP) occurs. However, even 6 months after extubation, this function remains reduced in 50%, and after 1 year - in 25% of those examined. The worst EF indicators were those patients whose treatment used high concentrations of oxygen (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 restrictive type violations of physical function.

Literature

1. Voinov V.A., Orlov S.V., Karchevsky K.S. Respiratory distress syndrome // Respiratory diseases. – 2005. – No. 1. - WITH. 21-24.

2. Adult respiratory distress syndrome. Guide to Medicine. Diagnostics and therapy / Ch. editor R. Berkow, in 2 volumes. Per. from English – M.:

World, 1997. – Volume I. – pp. 440-441.

3. Henich E., Ingram R. Respiratory adult distress syndrome. Internal Medicine by Tinsley R. Harrison / Ed. E. Fauci, J. Braunwald, K. Issembacher and others, in 2 volumes. Per. from English – M.: Praktika, 2002. – Volume II. – S. 17921796.

4. Chuchalin A.G. (ed.). Rational pharmacotherapy of respiratory diseases. - M.: Publishing house "Litterra", 2004. – pp. 136-141.

5. Bartlett R.H., Schreiner R.J., Lewis D.A. et al. Extracorporeal life support (ESLS) for ARDS // Chest. – 1996. – Vol. 110. – No. 4. – R. 598.

6. Bernard J.R., Artigas A., Brigham K.L. et al. The American – European consensus conference on ARDS: definition, mechanisms, relevant outcomes, and clinical trial coordination // Am. J. Respira. Crit. Care Med. – 1994. – Vol. 149. – No. 9. – R. 818824.

7. Eaton S., Marc Moss M.D. Acute respiratory distress syndrome: Secrets of pulmonology / Ed. P.E. Parsons, D.E. Heffner. Per. from English – M.: MED press-inform, 2004. – P. 488-493.

8. Kolla S., Award S.S., Rich P.B. et al. Extracorporeal life support for 100 adult patients with severe respiratory failure // Thorax. – 1997. – Vol. 226. – No. 9. – R. 544556.

Synonyms

Hyaline membrane disease.

DEFINITION

RDS - severe disorder breathing in premature newborns, due to immaturity of the lungs and primary deficiency of surfactant.

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. 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. Most significant factors, influencing the incidence of RDS development. 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 is a group of surface-active substances of lipoprotein nature that reduce surface tension forces in the alveoli and maintain 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 20-24 weeks 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 alveolar and capillary membranes increases, blood stagnation in the capillaries, diffuse interstitial edema and overdistension develops lymphatic vessels; 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 of the cardiovascular system occurs: secondary pulmonary hypertension with a right-to-left shunt of blood 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 inspiration (retractions 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 diagnostics (risk prediction) of RDS based on the study of the lipid spectrum of 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). The absence or sharp decrease in the concentration of saturated phosphatidylcholine and phosphatildiglycerol in the amniotic fluid indicates a high probability of developing 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 for differential diagnosis, exclusion of concomitant pathology and assessment of 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).

When a child is born who is at high risk for developing RDS, the most trained staff who know all the necessary manipulations are called to the delivery room. Particular attention should be paid to the readiness of the equipment to maintain optimal temperature conditions. For this purpose, radiant heat sources or open resuscitation systems can be used in the delivery room. In the case of the birth of a child whose gestational age is less than 28 weeks, it is advisable to additionally use a sterile plastic bag with a 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 apnea attacks 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 of water column. and f.02 0.21, a satisfactory blood gas composition is maintained for 2 hours.

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 mmHg;

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 and sedatives are prescribed (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 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. The 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 parameters. 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
in case of hypercapnia (paCO2 > 60 mmHg), 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 preventive use of surfactant is described in the section “Features of nursing children with ELBW.”

The use of surfactant with therapeutic purpose 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.

Prescription of surfactant for therapeutic treatment contraindicated in 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 the clinical picture within 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.

Curosurf 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 standards of 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 of the 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 depends 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. At the 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 a trial administration of water through a tube, you need to gradually add breast milk or formula to the EN, 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, stimulates the “maturation” of the lungs more quickly. 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 preterm labor occurs at 24-34 weeks of gestation, an attempt should be made to slow it down. labor activity 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 use corticosteroids.

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

Respiratory distress syndrome(RDS)- one of the serious problems that doctors caring 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 gradually gets worse. Usually, by 2-4 days of life, its outcome is determined: gradual recovery or the death of the baby.

Why do the child’s lungs 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 consist of a huge number of small sacs - 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. A special “lubricant” prevents the alveoli from collapsing - surfactant. Name unique substance comes from 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 epithelial cells 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 the removal of foreign particles from the surface of the alveoli, protecting the alveolar wall from oxidants and peroxides, and to some extent, 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 “survive” to this date and various reasons appear on White light earlier than expected 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 when exhaling, the lungs seem to slam shut (collapse) and the child has to re-inflate them with each breath. This requires a lot of energy; as a result, the newborn’s strength is depleted and severe respiratory failure develops. In 1959, American scientists M.E. Avery and J. Mead discovered pulmonary surfactant deficiency in premature newborns suffering from respiratory distress syndrome, thus identifying the main cause of RDS. The frequency of development of RDS is higher, the shorter the period at which the child was born. Thus, it affects 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, first of all, by symptoms of respiratory failure, developing, as a rule, at birth, or 2-8 hours after birth - increased breathing, flaring of the wings of the nose, retraction of the intercostal spaces, participation of auxiliary respiratory muscles in the act of breathing, development of cyanosis (cyanosis). Due to insufficient ventilation of the lungs, a secondary infection often occurs, and pneumonia in such infants is by no means uncommon. Natural process recovery begins after 48-72 hours of life, but not all children have this process quickly enough - due to the development of the infectious complications already mentioned.

With rational care and careful adherence to treatment protocols for children with RDS, up to 90 percent of small patients survive. The respiratory distress syndrome suffered in the future has virtually no impact on the health of children.

Risk factors

It is difficult to predict whether a given person will develop specific child RDS or not, scientists were able to identify a certain risk group. Predisposes to the development of the syndrome are diabetes mellitus, infections and maternal smoking during pregnancy, birth by cesarean section, birth of the second of twins, asphyxia during childbirth. In addition, it has been found that boys suffer from RDS more often than girls. Prevention of the development of RDS comes down to the prevention of premature birth.

Treatment

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

The basis of treatment for children with RDS is the “minimal touch” technique; the child should receive only absolutely necessary procedures and manipulations. One of the methods of treating the syndrome is intensive respiratory therapy, different kinds 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 restrictions and difficulties that the active use of artificial surfactant preparations began only in the late 80s - early 90s of the last century. Surfactant therapy allows you to improve the child’s condition 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 modern equipment and qualified medical personnel, since there is a high risk of developing severe complications.

Table of contents of the topic "Treatment of threatened and beginning preterm labor. Management of preterm labor.":
1. Treatment of threatened and beginning premature labor. Drugs that reduce uterine activity. Tocolytics. Indications and contraindications for the use of tocolytics.
2. Side effects of tocolytics. Complications from tocolytics. Evaluation of tocolysis results. Ethanol as a tocolytic.
3. Atosiban, NSAIDs (non-steroidal anti-inflammatory drugs), nifedipine, nitroglycerin for premature birth.
4. Treatment of bacterial vaginosis during pregnancy and premature birth. Electrorelaxation of the uterus.
5. Acupuncture for premature birth. Transcutaneous electrical stimulation in case of threat of premature birth.
6. Prevention of respiratory distress syndrome (RDS) during premature birth. Corticosteroid (glucocorticoid) therapy for threatened preterm birth. Contraindications to hormonal therapy.
7. Management of premature birth. Risk factors for preterm birth. Correction of labor activity in case of its anomalies.
8. Management of rapid or rapid preterm labor. Prevention of birth trauma to the fetus.
9. Surgical interventions for premature birth. Resuscitation measures for premature birth. Intracranial hemorrhages in premature infants.
10. Management of premature birth with premature rupture of membranes. Diagnosis of uterine infection. Prevention of respiratory distress syndrome (RDS) during premature birth. Corticosteroid (glucocorticoid) therapy for threatened preterm birth. Contraindications to hormonal therapy.

If there is a threat of premature birth, an integral part of therapy must be prevention of respiratory distress syndrome in newborns by prescribing glucocorticoid drugs that promote the synthesis of surfactant and more rapid maturation of the fetal lungs.

Surfactant(a mixture of lipids and proteins) is synthesized in large alveoli and covers them; it promotes the opening of the alveoli and prevents their collapse during inhalation. At a gestational age of 22-24 weeks, surfactant is produced with the participation of methyl transferase, from the 35th week intrauterine life it is carried out with the participation of phosphocholyltransferase. The latter system is more resistant to acidosis and hypoxia,

Pregnant women are prescribed 8-12 mg of dexamethasone during the course of treatment.(4 mg 2 times a day intramuscularly for 2-3 days or in tablets 2 mg 4 times a day on the 1st day, 2 mg 3 times on the 2nd day, 2 mg 2 times on the 3rd day ).

Use of dexamethasone in order to accelerate the maturation of the fetal lungs, it makes sense to continue therapy for 2-3 days. Since it is not always possible to prevent the development of preterm labor, corticosteroids should be prescribed to all pregnant women receiving tocolytics. In addition to dexamethasone, you can use prednisolone at a dose of 60 mg per day for 2 days,

According to the US National Institutes of Health (Hayward P.E., Diaz-Rosselln J.L., 1995; Grimes D.A., 1995; Crowley P.A., 1995), a consensus has been reached on the use of corticosteroids to prevent RDS when there is a threat of preterm birth.

For a gestational age of 24-34 weeks, it is recommended that 5 mg of dexamethasone be administered intramuscularly every 12 hours 4 times. If, despite therapy, the threat of premature birth remains, then it is advisable to repeat glucocorticoid therapy after 7 days. Based on the studies, respiratory distress syndrome and neonatal mortality decreased by 50%, and the number of intraventricular hemorrhages decreased. There was no effect on premature rupture of membranes if less than 24 hours passed after the administration of glucocorticoids or in the case when delivery was carried out 7 days after the administration of glucocorticoids, as well as when the gestational age was more than 34 weeks.

After betamethasone administration(12 mg every 24 hours) a decrease in fetal heart rate was detected, motor activity fetal and respiratory movements. These changes return to baseline data on day 2 and indicate the physiological response of the fetus to steroid therapy (Mulder E.P. et al., 1997; Magel LA. el al., 1997).

According to S. Chapman ct al. (1996), corticosteroid therapy is ineffective for premature rupture of the membranes and fetal weight less than 1000 g. When observing children under 12 years of age, whose mothers for preventive purposes received corticosteroids, their negative effect on the child’s intellectual development, behavior, motor and sensory functions was not revealed.

Contraindications to glucocorticoid therapy are peptic ulcer stomach and duodenum, circulatory failure stage III, endocarditis, nephritis, active phase tuberculosis, severe forms of diabetes, osteoporosis, severe form of gestosis, cervical dilation more than 5 cm, signs of infection. If there are contraindications to the use of glucocorticoids, aminophylline can be used at a dose of 10 ml of a 2.4% solution in 10 ml of a 20% glucose solution for 3 days.

Lazolvan (ambraxol) is not inferior in effectiveness to a glucocorticoid drug and has virtually no contraindications. Used at a dose of 800-1000 mg per day for 5 days intravenously.

D.B. Knight et al. (1994) with a view to prevention of RDS in the fetus when there is a threat of premature birth administered intravenously 400 mg of thyroid-stimulating releasing hormone alone or in combination with betamethasone and obtained positive results. However, S.A. Crowther et al. (1995) did not find similar results.

For the prevention of RDS use surfactant 100 units intramuscularly 2 times a day for 3 days. If necessary, these doses are repeated after 7 days. Prevention of RDS is effective at 28-33 weeks of pregnancy: more early dates longer use of the drug is required.

In cases where it is not possible prolong pregnancy, surfactate should be used to treat RDS in a newborn.

Concerning prophylactic use of ampicillin and metronidazole for premature birth, then a randomized multicenter study found prolongation of pregnancy, a decrease in the frequency of intensive care for newborns, but maternal and neonatal infectious morbidity did not decrease (SvareJ.ctaL, 1997).

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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, contributes to a decrease in pulmonary compliance, an increase in the work of breathing, and an increase in 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 strengthens 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 clinic for RDS 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 when effective first inhalation helps to reduce pressure in the pulmonary circulation, improve the perfusion of pneumocytes and enhance their synthetic functions. Any deviation from normal course childbirth, even planned surgical delivery, can cause a process of insufficient synthesis of surfactant 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 cesarean 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 of 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 disabilities hemodynamics of the newborn.

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

For more effective and rational treatment of 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

Symptoms of respiratory failure, tachypnea, chest swelling, nasal flaring, difficulty breathing and cyanosis.
Other symptoms, for example, hypotension, oliguria, muscle hypotonia, temperature instability, intestinal paresis, peripheral edema.
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 held

A score of 2-3 points corresponds to mild RDS

A score of 4-6 points corresponds to RDS medium degree

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.

The Lecithin/Sphyringomyelin ratio in amniotic fluid is less than 2.0 and negative results shaking tests for the study of amniotic fluid and gastric aspirate. In newborns from mothers with diabetes mellitus, RDS can develop when L/S is more than 2.0.
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 inhibit labor activity by using beta-mimetics, antispasmodics or magnesium sulfate, and then administer 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

Lay the newborn down with the head slightly extended. Turn the baby. This improves drainage of the tracheobronchial tree.
Tracheal suction is required to sanitation the tracheobronchial tree from thick phlegm, appearing in the exudative phase, which begins at approximately 48 hours of life.

B. Oxygen therapy.

The warmed, moistened and oxygenated mixture is given to the newborn in a tent or through an endotracheal tube.
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

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

D. Acidosis

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

E. Feeding

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

G. Chest X-ray

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

H. Excitement

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

I. Infection

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.
Group B hemolytic streptococcus infection may clinically and radiologically resemble RDS.

K. Therapy of acute respiratory failure

The decision to use respiratory support techniques should be based on the medical history.
In newborns weighing less than 1500 g, the use of CPAP techniques may lead to unnecessary energy expenditure.
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

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

A. Check the connection points of the equipment to the source of oxygen and compressed air.
b. Rule out endotracheal tube obstruction, extubation, or tube advancement into the right main bronchus.
V. If 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, the 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 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. For therapeutic purposes, 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. For preventive purposes, Exosurf is administered 1 to 3 times, for therapeutic purposes - 2 times. A single dose of Exosurf in all cases is 5 ml/kg. and is administered as a bolus in two half doses over a period of 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 incidence of chronic lung diseases 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 to a specialized center for resuscitation and intensive care of newborns after stabilization of the patient’s condition after 24-48 hours by the RCBN.