Etiology and Mortality Statistics
ARDS is not an independent disease; it develops as a severe complication of other pathological processes. Clinically and morphologically, this syndrome is analogous to infant respiratory distress syndrome.
The main causes of shock lung include:
- Aspiration of gastric contents (has the highest mortality rate at 93.8%).
- Infectious lung diseases, primarily severe pneumonia (mortality around 60%).
- Various types of shock (including endotoxic shock) and sepsis (mortality 77.8%).
- Disseminated intravascular coagulation (DIC).
- Inhalation of toxic substances, including excess oxygen.
- Drug overdose.
- Radiation exposure.
- Open-heart surgery using extracorporeal circulation.
Overall, the mortality rate for this syndrome exceeds 60–65%.
Pathogenesis and Biochemical Mechanisms
The core mechanism of pathogenesis is direct damage to the capillary endothelium and type I pneumocytes, which form the blood-air barrier. This inevitably leads to acute respiratory failure.
In the early phase, key roles are played by polymorphonuclear leukocytes (neutrophils), alveolar macrophages, and the endothelium itself. Their activation triggers a cascade of damaging factors:
- Proteolytic lysosomal enzymes.
- Free oxygen radicals.
- Nitric oxide.
- Arachidonic acid derivatives (leukotrienes and prostaglandins) that activate phospholipase A.
Simultaneously, platelets become involved. Stimulated by platelet-activating factor, they aggregate and sequester within the pulmonary vasculature (clinically manifested as thrombocytopenia). Platelets begin to produce platelet-derived growth factor (PDGF), which powerfully stimulates sclerotic processes.
- Furthermore, damage to type II pneumocytes impairs surfactant synthesis. Deprived of this surface-active agent, the alveoli collapse, leading to multiple atelectases.
Morphological Stages
The morphogenesis of acute respiratory distress syndrome is typically divided into three sequential stages:
- Preclinical stage: Characterized by initial morphological signs of capillary damage in the alveolar septa. There are no prominent clinical manifestations yet.
- Acute stage: Develops within the first week following exposure to the injurious factor. During this period, interstitial and intra-alveolar edema increases. Microscopy reveals a large amount of fibrin and polymorphonuclear leukocytes within the exudate and infiltrates. Characteristic hyaline membranes form on the inner surfaces of the alveoli, and areas of atelectasis appear.
- Stage of exudate organization and proliferation: Organization processes begin very early—as soon as days 2–3 of the disease. Type II pneumocytes actively proliferate, and the exudate is replaced by connective tissue. The outcome of this stage is the development of interstitial fibrosis.
Clinical Presentation and Outcomes
Clinically, ARDS manifests as refractory hypoxemia—a critical drop in blood oxygen levels that cannot be corrected even by increasing the fraction of inspired oxygen. The patient's vital capacity (VC) is significantly reduced.
Radiological studies show signs of pronounced pulmonary edema. However, there is a crucial differential feature: unlike cardiogenic edema, intracapillary and oncotic pressures are normal in ARDS.
As the disease progresses, total interstitial pulmonary fibrosis develops. The proliferation of connective tissue and the obliteration of the vascular bed create insurmountable resistance for the right ventricle. Consequently, the direct cause of death in such patients is cor pulmonale (right-sided heart failure).