Why does RDS occur?
Respiratory distress syndrome is not an independent nosological entity. It is a consequence of pulmonary or extrapulmonary pathologies that develop against the background of the infant's high anatomical and physiological vulnerability.
Key prerequisites for the development of RDS:
- Immaturity of the respiratory system, especially the surfactant production system—a substance that prevents alveoli from collapsing upon expiration.
- Immaturity of the central regulation of respiration.
- Biomechanics characteristics: small size of the alveoli combined with high chest wall compliance.
Problems with surfactant can manifest as its complete absence (absolute deficiency), qualitative inferiority (production defect), or accelerated destruction in the alveoli.
Dispersed pulmonary atelectasis
Atelectasis refers to areas of collapsed lung tissue. They can be small (dispersed) or large (involving one or more lung segments). The pathology is most characteristic of premature infants.
Pathism / Mechanism of development:
- The triggering factor is intrauterine or postnatal hypoxia.
- It inhibits the maturation of the alveolar epithelium and disrupts surfactant production.
- Due to the lack of surfactant, the distensibility of lung tissue drops sharply.
- The result is the development of hypoventilation and local oxygen deprivation (hypoxemia).
Symptomatology The clinical picture consists of three blocks:
- Respiratory syndrome: rapid breathing (tachypnea), breathing pauses (apnea), grunting expiration, retraction of compliant chest areas due to the work of accessory muscles. Wet rales and weakened breathing are auscultated in the lungs.
- Cardiovascular syndrome: cyanosis of the nasolabial triangle, tachycardia, muffled heart sounds.
- Neurological status: CNS depression syndrome (decreased muscle tone, reflexes, and spontaneous activity).
The radiograph shows a specific «mosaic» pattern: alternating dark areas of normal tissue with light areas of atelectasis. The prognosis is usually favorable—the lungs expand within a month.
Hyaline membrane disease (HMD)
In hyaline membrane disease, vascular disorders play a leading role. Due to vascular spasm and the operation of fetal shunts, capillary permeability increases. Plasma transudates into the alveoli, forming dense membranes there.
Symptoms usually appear with a delay of 1–2 hours after birth:
- Shallow, rapid breathing.
- Marked retraction of the sternum and intercostal spaces.
- Weakened breathing in the lower lobes.
- Generalized (diffuse) cyanosis and severe CNS depression.
Radiological stages of HMD
| Phase | Time | X-ray picture |
|---|---|---|
| 1. Nodular-reticular mesh | First day | Interstitial compaction, microatelectasis, overexpansion of bronchioles |
| 2. Air bronchogram | - | Contrast display of air-filled bronchi against the background of collapsed alveoli |
| 3. «White lungs» | - | Massive atelectasis with edema. Lung fields are gray, heart and diaphragm contours are blurred |
The prognosis for HMD is serious: the peak of severity is observed on the second day, mortality can reach 50%. With a favorable outcome, improvement occurs on days 4–5.
Class and exam questions
What triggers the formation of hyaline membranes?
HMD is based on hemodynamic disorders: vascular spasm and increased permeability of their walls lead to the escape of plasma into the alveoli and the formation of membranes. In atelectasis, the leading cause is surfactant deficiency against the background of hypoxia.
Who suffers most frequently from respiratory distress syndrome?
The pathology is most characteristic of premature newborns, as their respiratory system and surfactant production mechanisms are not yet matured.
What does HMD look like on an X-ray in the most severe stage?
In the third stage, the picture of «white lungs» develops: the lung fields appear pale gray due to massive edematous atelectasis, and the contours of the mediastinum and diaphragm are indistinguishable (silhouette sign).
What else to study on this topic
- Composition and functions of pulmonary surfactant
- Mechanisms of central respiratory regulation in newborns
- Influence of fetal shunts on infant hemodynamics
- Principles of therapy and oxygen support in RDS
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