Initial Pathogenetic Link
The key triggering factor of the disease is a deficiency of pulmonary surfactant or a critical decrease in its physiological effects. There are four main causes of this condition:
- Immaturity of lung tissue, which leads to an absolute deficiency in surfactant production, up to the complete cessation of its synthesis.
- Anomalies in physicochemical characteristics — a situation where surfactant is produced in optimal amounts, but its structure is impaired.
- Insufficiency of effects of normal surfactant composition and volume.
- Accelerated destruction of surfactant under the influence of pathological factors.
The main consequence of this deficiency is the progressive collapse of alveoli, known as atelectasis. As a result, there is a progressive decrease in total lung capacity, making adequate gas exchange impossible.
Formation of Hyaline Membranes
Further development of the pathology is associated with morphological changes in the airways. A pathological exudate, high in protein and leukocytes, begins to actively form and accumulate within them.
In parallel with this process, there is an accumulation of debris—breakdown products of damaged pulmonary epithelial cells. Upon microscopic examination, this stained cellular and proteinaceous debris visually resembles dense sheets. It is this specific morphological picture that historically gave rise to the term "hyaline membrane disease," which is used today as a full-fledged synonym for the primary diagnosis.
Cascade of Systemic Alterations
The pathogenesis of the syndrome is not limited to alveolar collapse alone. It triggers a complex cascade of reactions affecting the entire body:
- Inflammatory response. The content of blood formed elements (neutrophils, platelets, and erythrocytes) in the pulmonary microvessels sharply increases. An imbalance of biologically active substances occurs: cytokines, hormones, and reactive oxygen species are released in excess. All of this potentiates a powerful local and systemic inflammation.
- Vascular and hemostatic disorders. Damage to the microvascular endothelium occurs, leading to endothelial dysfunction. The logical outcome is hemostatic disorders and the development of thrombohemorrhagic syndrome. Microcirculatory disturbances affect the intravascular, transmural, and extravascular beds both in the lungs and in other organs.
- Gas exchange and hemodynamic disorders. Pathological blood shunting (right-to-left shunt) forms. This causes acute respiratory failure and generalized respiratory-type hypoxia. Subsequently, systemic circulatory failure, secondary pulmonary hypertension, heart failure, and arterial hypotension join in.
Principles of Therapy
Therapeutic tactics for neonatal RDS are based on two fundamental principles: etiotropic and pathogenetic.
The etiotropic principle aims at eliminating the root cause and providing emergency assistance. It addresses the following tasks:
- Emergency respiratory support: within the first 2–3 minutes after birth, clinicians must provide the newborn with an adequate ventilation volume.
- Surfactant therapy: simultaneous administration of a surfactant preparation directly into the airways.
- Oxygen therapy: targeted, strictly dosed oxygen therapy based on indications.
The pathogenetic principle aims to block the key links of disease development described above (combating inflammation, vascular catastrophes, and hemodynamic shifts).