Respiratory Distress Syndrome

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Respiratory distress syndrome (RDS) is a common breathing problem, especially in premature babies, caused by a lack of surfactant leading to rapid breathing, grunting, nostril flaring, chest retractions, and a bluish skin tone (cyanosis). Treatment involves respiratory support (like oxygen or ventilation) and artificial surfactant administration, while corticosteroids given to mothers before premature birth help mature fetal lungs. Newborn respiratory distress syndrome (RDS) differs greatly from Acute respiratory distress syndrome (ARDS), which affects older children/adults due to severe illness or injury.

Acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS, also adult respiratory distress syndrome) is an acute form of lung disease. ARDS results from an inappropriate inflammatory response in the lung tissue, which can be triggered by infectious or noninfectious agents. During this response, lung alveoli are damaged, fluid accumulates in the lungs, and the diffusion path of oxygen is prolonged. ARDS most commonly occurs as a result of aspiration of gastric contents, severe trauma, lung infection, drowning, and is the clinical manifestation of shock lung .

Pathogenesis of ARDS

During the inflammatory reaction, the alveoli, or rather the first-order pneumocytes, are damaged. The regulatory mechanisms that should remove excess fluid from the alveoli fail. The following signs are characteristic of ARDS itself:

• increased permeability of the pulmonary capillaries,
• accumulation of fluid in the parenchyma and alveoli,
• diffuse damage to the alveolar epithelium – i.e. first-order pneumocytes.

The result of these changes is both extension of the diffusion path for blood gases and the presence of fluid in the lungs. In addition, this fluid also contains proteins. ARDS differs from pulmonary edema itself by the presence of proteins in the filtered fluid. The lungs are heavy and edematous. In addition, hemorrhagic exudate is also present in the lungs.

Clinical picture of ARDS

Acute respiratory distress syndrome is characterized by:

1. dyspnea,
2. tachypnea,
3. hypoxemia.

The most serious symptom is hypoxemia, which does not respond to oxygen therapy and its extent determines the fate of the patient.

Mortality ARDS is 30–60%. The patient most often dies under the picture of sepsis and multiple organ failure (MODS).

Diagnostics of ARDS

The diagnosis is made on the basis of chest X-ray, hypoxemia, decreased lung compliance, and the absence of increased left atrial pressure or normal wedge pressure, which indicates that postcapillary pulmonary pressure is not elevated.

The severity of ARDS can be determined by the oxygenation index PaO₂/FiO₂ (Horowitz index), where PaO₂ is the arterial partial pressure of oxygen, FiO₂ – fraction of oxygen in inspired air:

• above 300 mmHg – ARDS excluded,
• 201–300 mmHg – mild ARDS, mortality 27%;
• 101–200 mmHg – moderate ARDS, mortality 32%;
• ≤100 mmHg – severe ARDS, mortality 45%.

Newborn respiratory distress syndrome

Respiratory distress syndrome of the newborn (RDS – Respiratory Distress Syndrome, hyaline membrane syndrome, idiopathic RDS) is caused by anatomical and functional immaturity of the lungs – a lack of surfactant. It affects almost exclusively immature newborns. It manifests clinically immediately after birth as rapidly progressive respiratory insufficiency. The incidence and severity of RDS is inversely proportional to the gestational age of the newborn. Treatment measures include the use of distension ventilatory support CPAP (Continuous Positive Airway Pressure), early administration of surfactant, gentle ventilation, diagnosis and treatment of open duct of Botall (PDA) and others. Lung maturation can be accelerated by administering corticosteroids to a pregnant woman before delivery. Uncomplicated RDS usually lasts 3–5 days.

Transient tachypnea of ​​the newborn (TTN) or wet lung syndrome is caused by prolonged clearance of the lungs of lung fluid. It occurs in premature babies, but also in some mature newborns after delivery by caesarean section, after asphyxia, and in newborns of diabetic mothers. Symptoms of respiratory distress are evident from birth, sometimes requiring ventilatory support, and usually resolve quickly.

Pathophysiology of RDS

In infants with RDS who are not treated with surfactant, necrosis of the epithelial cells of the alveoli occurs within half an hour after birth. The epithelial cells detach from the basement membrane and form clusters of hyaline membranes. At the same time, diffuse interstitial edema occurs. Lymphatic vessels are dilated due to delayed fluid absorption in the lungs. Within 24 hours, extensive generalized membrane formation occurs, which accumulates mainly in the terminal and respiratory bronchioles, especially at the junction of the airways. The alveoli are collapsed and are not lined with these membranes. Hyaline membranes are composed of debris from dead pneumocytes, coagulated plasma proteins released from damaged capillaries, and exudated fibrin. In unconjugated hyperbilirubinemia they may be yellow in color.

After 24 hours, the first macrophages begin to appear in the lumen of the airways, which devour the membranes over the next 2-3 days. After 48 hours, the epithelium begins to restore and surfactant begins to appear on the surface of the alveoli. In uncomplicated RDS, the hyaline membranes disappear by the 7th day of life. However, in ventilated children, healing occurs more slowly and with the formation of scarring and fibrosis of the alveoli and airways under the picture of bronchopulmonary dysplasia.

File:Stages of lung development.png

Stages of lung development.

Very immature newborn has lungs still in the saccular stage of development with a relatively small internal surface and a large proportion of interstitial tissue. Functional immaturity is manifested by an insufficient ability to maintain functional residual volume (FRC) based on insufficient surfactant production. The result is focal atelectasis surrounded by foci of tissue hyperinflation, which create a typical granular pattern on X-ray.

Surfactant is a surface-active substance found inside the alveoli of the lungs that prevents the collapse of the alveoli at the end of expiration by reducing their surface tension. It begins to be produced in the second half of pregnancy (from the 24th to the 28th week of gestation) in the Golgi apparatus of the endoplasmic reticulum of type II pneumocytes, which secrete it onto the inner alveolar surface and reabsorb it for recycling. Surfactant is approximately 90% phospholipids (mainly lecithin and phosphatidylglycerol) and 10% proteins.

Type II pneumocytes are sensitive to asphyxia. Their maturation is delayed in fetal hyperinsulinemia and accelerated by antenatal administration of corticosteroids and chronic intrauterine stress (gestational hypertension, IUGR, twin pregnancy).

Shortly after birth, right-to-left shunting across the foramen ovale predominates, which can worsen hypoxemia. After 18–24 hours, due to decreasing pulmonary vascular resistance, left-to-right shunting across the PDA begins to dominate, causing pulmonary edema and impairing alveolar gas exchange. Administration of surfactant during this period may worsen the condition.

Risk factors for RDS include: immaturity, male gender, family predisposition, cesarean section before spontaneous onset of labor, perinatal asphyxia, chorioamnionitis, multiple pregnancy, maternal diabetes mellitus.

Clinical picture

Immediately after birth, signs of respiratory distress develop:

• tachypnea = rapid breathing, respiratory rate > 60/min.;
• dyspnea = labored breathing, manifested by retraction of the intercostal spaces and the attachment of the diaphragm during inspiration and elevation of the nasal wings ("alar movement");
• grunting = "gruntling", a sound phenomenon caused by exhalation against a closed glottis, helps to maintain positive pressure in the airways, i.e. to maintain functional residual capacity (FRC).

Tachycardia – heart rate > 160/min).

Central cyanosis, decreased saturation value on pulse oximetry.

Examination

• ABR: hypoxemia, hypercapnia, mixed acidosis;
• Chest X-ray: typical picture of RDS – reticulogranular pattern and reduced transparency up to complete lung obscuration (“white lung”).
• Examination of blood count and inflammatory parameters to exclude sepsis.
• Glycemia – hypoglycemia may be accompanied by tachypnea and symptoms of respiratory distress.

Complications

• septicemia, pulmonary interstitial emphysema, pneumothorax, pneumomediastinum, pneumoperitoneum, pneumopericardium, pulmonary apoplexy, apnea/bradycardia, bronchopulmonary dysplasia (BPD), patent ductus arteriosus (PDA), persistent pulmonary hypertension of the newborn, necrotizing enterocolitis (NEC), retinopathy of prematurity (ROP), hypertension, failure to thrive, intracranial hemorrhage, periventricular leukomalacia (PVL).

Treatment

• symptomatic: oxygen therapy (humidified heated oxygen), possibly ventilation support (nasal CPAP, artificial pulmonary ventilation), infusion therapy;
• causal: intratracheal administration of surfactant;
  • in extremely immature newborns, prophylactic administration of surfactant is recommended immediately after birth, especially if pulmonary maturity induction has not been performed and if they require intubation in the delivery room;
• antibiotic therapy if infection is suspected, circulatory support (volume expansion, catecholamines) if there are signs of circulatory failure;
• prevention: pulmonary maturity induction in utero - by administering corticosteroids (e.g. Diprophos, Dexona) to pregnant women before delivery.

Links

Related articles

• Neonatal Pneumopathies

External links

• V. Vobruba: Novorozenecké pneumopatie
• European Consensus Guidelines on the Management of Respiratory Distress Syndrome - 2019 Update
• Clinical picture: "Recognizing Respiratory Distress" by Monica Kleinman, MD for OPENPediatrics

Links

Related articles

• Shock
• Respiratory distress syndrome (pediatrics)
• Pneumonia (pediatrics) | Pneumonia without typical X-ray findings | Pneumonia in infants

External links

• Wikipedia:ARDS

Source

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