Retraction bottom wall chest (movement inward of the bone structure of the chest wall while inhaling) is an indicator of severe pneumonia. This symptom is more specific than retraction of the intercostal spaces, which involves retraction of the soft tissues of the intercostal space, but not the bone structure of the chest wall.

· If you did not lift the baby's shirt while counting the baby's breathing rate, ask the mother to do it now.

· Before looking for chest indrawing, observe the baby to determine when he is breathing in and when he is breathing out.

See if there is chest retraction on inhale.

· Look at the lower ribcage (lower ribs). The child has retraction of the chest,if when inhaling, the lower chest sinks.

Chest retraction occurs when the baby makes much more effort to inhale than is necessary with normal breathing. When normal breathing while inhaling, the entire chest (upper and lower parts) and abdomen rise... In the presence of chest retraction, the chest wall sinks,when baby inhales.

Note: In order to infer the presence of chest retraction, it must be clearly visible and present at all times. If chest retraction is only noticeable when the baby is screaming or feeding, then the baby is not having a chest retraction. If only soft tissue intercostal space (retraction of the intercostal spaces or retraction of the intercostal spaces), which means that the child does not have retraction of the chest. For this assessment, chest retraction means retraction of the lower part of the chest wall. Intercostal retraction does not apply here.

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

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

Epidemiology

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

Classification

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

■ RDS due to primary insufficiency of the surfactant system;

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

Etiology

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

Pathogenesis

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

Clinical signs and symptoms

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

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

These common changes are most pronounced in the lower regions and at the apex of the lungs. In addition, a decrease in lung volume, cardiomegaly of varying severity are noticeable. Nodose-reticular changes observed during X-ray examination, according to most authors, are disseminated atelectasis.

For edematous-hemorrhagic syndrome, "blurred" x-ray picture and a decrease in the size of the pulmonary fields, and clinically - the release of frothy fluid mixed with blood from the mouth.

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

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

■ chest x-ray;

■ determination of indicators of CBS and blood gases;

■ general analysis blood with the determination of the number of platelets and the calculation of the leukocyte index of intoxication;

■ determination of hematocrit;

■ biochemical blood test;

■ ultrasound of the brain and internal organs;

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

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

Differential diagnosis

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

Differential diagnosis RDS is performed with respiratory disorders (both pulmonary - congenital pneumonia, pulmonary malformations, and extrapulmonary - congenital heart defects, birth trauma spinal cord, diaphragmatic hernia, tracheoesophageal fistula, polycythemia, transient tachypnea, metabolic disorders).

Optimal patient care is essential in treating RDS. The basic principle of treatment for RDS is the “minimal touch” method. The child should receive only the procedures and manipulations necessary for him; the medical and protective regime should be observed in the ward. It is important to maintain an optimal temperature regime, and when treating children with very low body weight, provide high humidity to reduce fluid loss through the skin.

It is necessary to strive for a newborn in need of mechanical ventilation to be at a neutral temperature (with minimal tissue oxygen consumption).

To reduce heat loss in children with deep prematurity, it is recommended to use an additional plastic covering for the whole body (inner shield), special foil.

Oxygen therapy

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

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

Infusion therapy

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

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

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

Isotonic solution of sodium chloride / calcium chloride / mono-carbonate

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

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

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

■ from the 1st day of life: glucose solution 5% or 10%, providing the minimum energy requirement in the first 2-3 days of life (if the body weight is less than 1000 g, it is advisable to start with a glucose solution of 5%, and with the introduction of a 10% solution, the rate does not must exceed 0.55 g / kg / h);

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

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

Replacement therapy with exogenous surfactants

Exogenous surfactants include:

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

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

■ synthetic.

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

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

Poractant alfa endotracheal 200 mg / kg once,

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

Surfactant BL endotracheal

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

Surfactant BL can be injected through the side opening of a special endotracheal tube adapter without depressurizing the breathing circuit and interrupting ventilation. The total duration of administration should be at least 30 and no more than 90 minutes (in the latter case, the drug is administered using a syringe pump, drip). Another method is to use a nebulizer for inhalation solutions built into the ventilator; the duration of administration should be 1-2 hours. The trachea should not be sanitized within 6 hours after administration. In the future, the drug is administered subject to the continuing need for mechanical ventilation with an oxygen concentration in the air-oxygen mixture of more than 40%; the interval between injections should be at least 6 hours.

Errors and unreasonable assignments

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

Forecast

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

IN AND. Kulakov, V.N. Serov

It occurs in 6.7% of newborn babies.

Respiratory distress is characterized by several main clinical features:

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

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

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

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

CHD occurs in 0.5-0.8% of live births. The incidence is higher in stillborns (3-4%), spontaneous miscarriages (10-25%), and premature infants (about 2%), excluding PDA.

Epidemiology: primary (idiopathic) RDS occurs:

• Approximately 60% of premature babies< 30 недель гестации.
• Approximately 50-80% of premature babies< 28 недель гестации или весом < 1000 г.
• Almost never in prematurity\u003e 35 weeks of gestation.

Causes of Respiratory Distress Syndrome (RDS) in Newborns

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

Pathogenesis: Surfactant deficiency disease of morphologically and functionally immature lungs. Surfactant deficiency leads to the collapse of the alveoli and, thereby, to a decrease in compliance and functional residual lung capacity (FRC).

Risk factors for respiratory distress syndrome (RDS) in newborns

Increased risk in premature birth, in boys, familial predisposition, primary cesarean section, asphyxia, chorioamnionitis, dropsy, diabetes in the mother.

Reduced risk of intrauterine "stress", premature rupture amniotic fluid without chorionamnionitis, maternal hypertension, drug use, low weight for gestational age, use of corticosteroids, tocolysis, taking thyroid medications.

Symptoms and signs of respiratory distress syndrome (RDS) in newborn babies

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

• Respiratory failure with retractions (intercostal space, hypochondrium, jugular zones, xiphoid process).
• Dyspnea, tachypnea\u003e 60 / min, moan on exhalation, retraction of the wings of the nose.
• Hypoxemia. hypercapnia, increased oxygen demand.

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

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

Cyanosis

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

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

With pronounced anatomical changes, cardiopulmonary distress can cause coarctation of the aorta, hypoplasia of the right heart, tetrad of Fallot, and large septal defects. Since cyanosis is one of the leading symptoms of CHD, it is suggested to carry out pulse oximetry screening for all newborns before discharge from the maternity hospital.

Tachypnea

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

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

Retraction of pliable chest sites

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

Noisy exhalation

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

Inflating the wings of the nose

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

Complications of Respiratory Distress Syndrome (RDS) in Newborns

• Patent ductus arteriosus, PFC syndrome \u003d persistent pulmonary hypertension of the newborn.
• Necrotizing enterocolitis.
• Intracranial bleeding, periventricular leukomalacia.
• Without treatment - bradycardia, cardiac arrest and respiratory arrest.

Diagnostics of the respiratory distress syndrome (RDS) in newborns

Survey

At the initial stage, one should assume the most common causes of distress (immaturity of the lungs and congenital infections), after their exclusion, one should think about more rare causes (CHD, surgical diseases, etc.).

Mother's history... The following data will help to diagnose:

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

The course of labor:

• duration;
• anhydrous gap;
• bleeding;
• cesarean section;
• fetal heart rate (HR);
• breech presentation;
• the nature of the amniotic fluid;
• analgesia / anesthesia of labor;
• fever in the mother.

Newborn:

• assess the degree of prematurity and maturity by gestational age;
• assess the level of spontaneous activity;
• skin color;
• cyanosis (peripheral or central);
• muscle tone, symmetry;
• characteristics of the large fontanelle;
• measure body temperature in the armpit;
• RR (normal values \u200b\u200b- 30-60 per minute), breathing pattern;
• Resting heart rate (normal indicators for full-term babies are 90-160 per minute, for premature babies - 140-170 per minute);
• size and symmetry of chest excursions;
• when sanitizing the trachea, assess the quantity and quality of the secretion;
• insert a tube into the stomach and evaluate its contents;
• auscultation of the lungs: the presence and nature of wheezing, their symmetry. Immediately after birth, wheezing is possible due to incomplete absorption of fetal pulmonary fluid;
• auscultation of the heart: heart murmur;
• white spot symptom:
• blood pressure (BP): If CHD is suspected, BP should be measured in all 4 limbs. Normally, blood pressure in the lower extremities slightly exceeds blood pressure in the upper ones;
• evaluate the pulsation of the peripheral arteries;
• measure pulse pressure;
• palpation and auscultation of the abdomen.

Acid-base state

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

Respiratory distress can be accompanied by respiratory failure (DV), or it can develop without it. DN can be defined as an impairment of the respiratory system's ability to maintain adequate oxygen and carbon dioxide homeostasis.

Chest X-ray

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

Pay attention to:

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

Hyperoxic test

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

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

To distinguish severe PLH from CHD "blue" type, sometimes a test with hyperventilation is performed in order to raise the pH to more than 7.5. Mechanical ventilation begins with a frequency of about 100 breaths per minute for 5-10 minutes. At high pH, \u200b\u200bthe pressure in the pulmonary artery decreases, pulmonary blood flow and oxygenation increase with PLH, and almost does not increase with CHD of the "blue" type. Both tests (hyperoxic and hyperventilating) have rather low sensitivity and specificity.

Clinical blood test

You need to pay attention to the changes:

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

C-reactive protein, procalcitonin

The level of C-reactive protein (CRP) usually rises in the first 4-9 hours after the onset of infection or injury, its concentration can increase in the next 2-3 days and remains elevated as long as the inflammatory response persists. The upper limit of normal values \u200b\u200bin newborns was taken by most researchers as 10 mg / l. The concentration of CRP increases not in all, but only in 50–90% of newborns with early systemic bacterial infections. However, other conditions - asphyxia, RDS, maternal fever, chorioamnionitis, prolonged anhydrous period, intraventricular hemorrhage (IVH), meconium aspiration, NEC, tissue necrosis, vaccination, surgery, intracranial hemorrhage, resuscitation with indirect cardiac massage - can cause ...

The concentration of procalcitonin can rise within hours after the infection becomes systemic, regardless of gestational age. The sensitivity of the method as a marker of early infections is reduced by the dynamics of this indicator in healthy newborns after birth. Their concentration of procalcitonin increases to a maximum by the end of the first - beginning of the second day of life and then decreases to less than 2 ng / ml by the end of the second day of life. A similar pattern was found in premature newborns; the level of procalcitonin decreases to normal values \u200b\u200bonly after 4 days. life.

Culture of blood and cerebrospinal fluid

Blood and cerebrospinal fluid (CSF) cultures should be performed if sepsis or meningitis is suspected, preferably before antibiotics are prescribed.

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

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

Electrocardiography

Echocardiography

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

Treatment of Respiratory Distress Syndrome (RDS) in Newborns

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

• A - to ensure airway patency;
• B - to provide breathing;
• C - to provide circulation.

It is important to quickly recognize the underlying causes of respiratory distress and treat appropriately. Should:

• Conduct continuous monitoring of blood pressure, heart rate, RR, temperature, continuous or periodic monitoring of oxygen and carbon dioxide.
• Determine the level of respiratory support (oxygen therapy, CPAP, mechanical ventilation). Hypoxemia is much more dangerous than hypercapnia and needs immediate correction.
• Depending on the severity of DN, it is recommended:
  • Spontaneous breathing with supplemental oxygen (oxygen tent, cannulas, mask) is usually used for non-severe DN, without apnea, with almost normal pH and PaCO 2, but low oxygenation (SaO 2 with air breathing less than 85-90%). If during oxygen therapy low oxygenation remains, with FiO 2\u003e 0.4-0.5 the patient is transferred to CPAP through nasal catheters (nCPAP).
  • nCPAP - is used for moderate-severe DN, without severe or frequent episodes of apnea, with pH and PaCO 2 below normal, but within reasonable limits. Condition: stable hemodynamics.
  • Surfactant?
• The minimum number of manipulations.
• Insert a naso- or orogastric tube.
• Provide an axillary temperature of 36.5-36.8 ° C. Hypothermia can cause vasoconstriction peripheral vessels and metabolic acidosis.
• Intravenous fluid should be administered if enteral nutrition cannot be absorbed. Maintenance of normoglycemia.
• In the case of low cardiac output, arterial hypotension, increased acidosis, poor peripheral perfusion, low urine output, you should consider intravenous administration NaCl solution for 20-30 minutes. Perhaps the introduction of dopamine, dobutamine, adrenaline, glucocorticosteroids (GCS).
• With congestive heart failure: decreased preload, inotropes, digoxin, diuretics.
• Antibiotics should be given if a bacterial infection is suspected.
• If it is impossible to perform echocardiography and there is a suspicion of ductus-dependent CHD, prostaglandin E 1 should be prescribed with an initial injection rate of 0.025-0.01 μg / kg / min and titrated to the lowest working dose. Prostaglandin E 1 maintains open AP and increases pulmonary or systemic blood flow depending on the pressure difference in the aorta and pulmonary artery. The reasons for the ineffectiveness of prostaglandin E 1 may be an incorrect diagnosis, a large gestational age of the newborn, and the absence of AP. With some heart defects, there may be no effect or even worsening of the condition.
• After initial stabilization, the cause of the respiratory distress should be investigated and treated.

Surfactant therapy

Indications:

• FiO 2\u003e 0.4 and / or
• PIP\u003e 20 cm H20 (in preterm< 1500 г > 15 cm H 2 O) and / or
• PEEP\u003e 4 and / or
• Ti\u003e 0.4 sec.
• Premature babies< 28 недель гестации возможно введение сурфактанта еще в родзале, предусмотреть оптимальное наблюдение при транспортировке!

Practical approach:

• When administering the surfactant, 2 people must always be present.
• Scan the baby well and stabilize it as much as possible (BP). Keep your head straight.
• Install pO 2 / pCO 2 sensors in advance to ensure stable measurement.
• If possible, attach the SpO2 sensor to the right handle (by design).
• Bolus surfactant through a sterile gastric tube shortened to the length of the endotracheal tube or an additional branch of the tube for about 1 minute.
• Dosage: Alveofact 2.4 ml / kg \u003d 100 mg / kg. Curosurf 1.3 ml / kg \u003d 100 mg / kg. Survanta 4 ml / kg \u003d 100 mg / kg.

Effects of using a surfactant:

Increased tidal volume and FRU:

• Fall of paCO 2
• Increase in paO 2.

Actions after injection: increase PIP by 2 cm H 2 O. Now the intense (and dangerous) phase begins. The child should be monitored extremely closely for at least one hour. Fast and continuous optimization of respirator settings.

Priorities:

• Decrease PIP with increasing tidal volume due to improved compliance.
• Reduce FiO 2 if SpO 2 increases.
• Then reduce PEEP.
• Finally, reduce Ti.
• Ventilation often improves dramatically, only to deteriorate again after 1 to 2 hours.
• Sanitation of the endotracheal tube without flushing is permitted! It makes sense to use TrachCare, since PEEP and MAP are retained even during refurbishment.
• Repeated dose: The 2nd dose (calculated as with the first) can be applied after 8-12 hours if the ventilation parameters deteriorate again.

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

Attention: too slow a decrease in PIP and PEEP increases the risk of barotrauma!

Failure to respond to surfactant therapy may indicate:

• ARDS (inhibition of surfactant proteins by plasma proteins).
• Severe infections (eg, caused by group B streptococci).
• Meconium aspiration or lung hypoplasia.
• Hypoxia, ischemia, or acidosis.
• Hypothermia, peripheral hypotension. D Caution: Side Effects ".
• Falling blood pressure.
• Increased risk of IVH and PVL.
• Increased risk of pulmonary bleeding.
• Debated: the increased incidence of PDA.

Prevention of Respiratory Distress Syndrome (RDS) in Newborns

Prophylactic intratracheal surfactant therapy for newborns.

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

Prevention of neonatal peripartum infection antibacterial prophylaxis pregnant women with suspected chorionamnionitis.

Optimal correction of diabetes mellitus in a pregnant woman.

Very gentle delivery management.

Gentle but persistent resuscitation of a premature and full-term baby.

Respiratory Distress Syndrome (RDS) Prognosis in Newborns

Very variable, depending on the baseline.

Danger, for example, pneumothorax, BPD, retinopathy, secondary infection during mechanical ventilation.

Long-term research results:

• Lack of effect of surfactant application; on the frequency of retinopathy of prematurity, NEC, BPD or PDA.
• Favorable effect of surfactan-1 administration on the development of pneumothorax, interstitial emphysema and mortality.
• Shortening the duration of ventilation (endotracheal tube, CPAP) and reducing mortality.

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

Criteria for the severity of laryngeal stenosis

I degree - inspiratory dyspnea (difficulty breathing) and retraction of the jugular fossa during physical activity, with anxiety of the child. The respiratory rate corresponds to the age norm. There is no respiratory failure.

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

III degree - shortness of breath becomes mixed (both inhalation and exhalation are difficult). The maximum retraction of the compliant places of the chest is noted.

The auxiliary muscles are involved in the act of breathing: inflation of the wings of the nose, tension of the neck muscles, participation in the act of breathing of the intercostal muscles. The skin becomes marbled. Muffled heart sounds, prolapse noted pulse wave while inhaling. Respiratory failure of the second degree develops.

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

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

Structural Approach to the Management of Critical Conditions in Children

The purpose of training

In this section, you will learn:

1. on how to recognize serious condition child;
2. about a structural approach to assessing the condition of a child with a serious illness;
3. about a structural approach to resuscitation and intensive care in a child with a serious illness.

Introduction

The prognosis for life in children after cardiac arrest is generally poor. Early and treatment of respiratory, circulatory and cerebral insufficiency helps reduce mortality and improve disease outcome. This section presents the symptoms that are used to quickly assess the condition of a seriously ill child.

Initial assessment of the airway and respiration

Respiratory failure diagnosis

Respiratory efforts

The severity of respiratory pathology can be judged by the severity of respiratory efforts. The following indicators should be evaluated.

Breathing rate

The normal respiratory rate in children is shown in Table 7.1. In newborns, the highest respiratory rate is observed, and with age, it gradually decreases. Single measurements of the respiratory rate must be treated with caution: a newborn can breathe 30 to 90 times a minute, and this depends on his activity.

Table 7.1. Respiratory rate in children of different ages

According to the WHO recommendation, the respiratory rate in infants and young children above 60 per minute, along with other symptoms, is regarded as a sign of pneumonia. In order to assess the dynamics of respiratory failure, it is more important to analyze the trends in the respiratory rate.

Thus, tachypnea is a reflection of the increased need of the body for hyperventilation due to pathology of the lungs and respiratory tract or due to metabolic acidosis. Bradypnea occurs with fatigue of the respiratory muscles, depression of the central nervous system, as well as in the preagonal stage of the dying process.

Retraction of the compliant areas of the chest

The retraction of the intercostal spaces, the lower aperture of the chest and the retraction of the sternum indicate an increased work of breathing. These symptoms are more noticeable in newborns and infants because their ribcage is more malleable. The presence of retractions in older children (after 6-7 years) is possible only in the presence of severe respiratory pathology. As fatigue develops, the degree of retraction decreases.

Inspiratory and expiratory murmurs

A noisy breath or inspiratory stridor is a sign of obstruction at the level of the larynx or trachea. In severe obstruction, exhalation may be difficult, but the inspiratory component of the stridor is usually more pronounced. Wheezing occurs when the lower airways are obstructed and is better heard on exhalation. A long expiration also indicates a narrowing of the lower airways. The volume of noisy breathing is not a reflection of the severity of the disease.

Granting

Granting (expiratory "grunting" or moaning breathing) occurs when air is exhaled through partially closed vocal cords. This reflects an attempt to create positive end-expiratory pressure to prevent end-expiratory alveoli collapse in a patient with “stiff” lungs. It is a sign of severe respiratory distress and is pathognomonic for pneumonia or pulmonary edema in young children. This symptom can also be observed in patients with intracranial hypertension, abdominal distension, and peritonitis.

Using the accessory musculature

With increased work of breathing, children, like adults, use auxiliary muscles, primarily the sternocleidomastoid muscles. In infants, this may cause nodding movements of the head with each breath, leading to reduced breathing efficiency.

Stretching the wings of the nose

This symptom is especially common in infants with respiratory distress.

Gasping breath

This is a sign of severe hypoxia, appearing in the pre-agonal stage.

Exceptions

Signs of increased work of breathing may be absent or mild in three cases:

1. As fatigue develops in a child with severe respiratory pathology, the severity of symptoms of increased work of breathing decreases. Fatigue is a pre-agonal sign.
2. In case of depression of consciousness in a child with intracranial hypertension, poisoning or encephalopathy, breathing is inadequate and there are no symptoms of increased work of breathing. Inadequate breathing in this case is due to central respiratory depression.
3. In children with neuromuscular diseases (such as spinal amyotrophy or muscular dystrophy), respiratory failure occurs without signs of increased work of breathing.

In children with the pathology described above, respiratory failure is diagnosed based on an assessment of the effectiveness of breathing and other symptoms of inadequate breathing. These symptoms are discussed below.

Breathing efficiency

Evaluation of the chest excursion (or in newborns, the movement of the anterior abdominal wall) allows one to judge the amount of air entering the lungs. The same information can be obtained from auscultation of the lungs. Attention should be paid to the weakening, asymmetry or bronchial nature of breathing. A “silent” chest is an extremely disturbing symptom.

To assess the saturation of arterial blood with oxygen (SaO2), the pulse oximetry method is used, the sensitivity of which, however, decreases when SaO2 is less than 70%, shock and the presence of carboxyhemoglobin in the blood. The SaO2 level when breathing air is a good indicator of breathing efficiency. Oxygen therapy masks this information if the hypoxia is not very severe. Normal level SaO2 in infants and children is 97-100%.

The effect of respiratory failure on other organs

Heart rate

Hypoxia causes tachycardia in infants and children. Along with this, tachycardia can be the result of excitement and an increase in body temperature. Severe and prolonged hypoxia leads to the development of bradycardia, which is a pre-agonal symptom.

Skin color

An early symptom of hypoxia is pallor of the skin, which is caused by vasospasm caused by the release of catecholamines. Cyanosis is a pre-agonal symptom of hypoxia. The progression of central cyanosis in acute respiratory pathology indicates that respiratory arrest may occur in the near future. In a child with anemia, cyanosis does not appear even with deep hypoxia. In some children, cyanosis can be a sign of blue heart disease. The severity of such cyanosis does not change during oxygen therapy.

Consciousness level

With hypoxia and hypercapnia, the child may be agitated or drowsy. Gradually, the depression of consciousness progresses up to its complete loss. This particularly important and beneficial symptom is more difficult to identify in young children. Parents may note that the child is "not himself." On examination, it is necessary to assess the level of consciousness, focusing on such signs as visual concentration, response to voice and, if necessary, response to pain stimulus. With hypoxic depression of the brain, generalized muscle hypotension is also observed.

Re-evaluation

To determine the dynamics of the patient's condition, frequent reassessment of respiration rate, degree of retraction and other symptoms of respiratory failure is necessary.