what are the pathogenesis of acute respiratory distress syndrome?

what are the pathogenesis of acute respiratory distress syndrome?

The pathogenesis of Acute Respiratory Distress Syndrome (ARDS) involves a complex series of events that begin with an injury to the alveolar-capillary membrane, leading to severe inflammation and impaired gas exchange. ARDS typically develops in response to direct or indirect insults to the lungs.

Here’s a step-by-step overview of the pathogenesis of ARDS:

1. Initial Injury

ARDS can be caused by:

  • Direct lung injury: pneumonia, aspiration, inhalation of toxic substances.

  • Indirect lung injury: sepsis, trauma, pancreatitis, massive transfusion.

2. Activation of Inflammatory Response

  • The initial injury activates alveolar macrophages.

  • These macrophages release pro-inflammatory cytokines such as

    • Tumor Necrosis Factor-alpha (TNF-α)

    • Interleukin-1 (IL-1)

    • Interleukin-6 (IL-6)

  • This causes recruitment of neutrophils to the lungs.

3. Neutrophil Activation and Injury

  • Neutrophils release:

    • Proteases

    • Reactive oxygen species (ROS)

    • More cytokines

  • These substances damage the alveolar-capillary membrane, increasing permeability.

4. Increased Vascular Permeability

  • Leads to non-cardiogenic pulmonary edema.

  • Protein-rich fluid leaks into the alveolar spaces, causing:

    • Alveolar flooding

    • Impaired gas exchange

    • Loss of surfactant (produced by type II pneumocytes)

5. Surfactant Dysfunction

  • Damage to type II alveolar cells reduces surfactant production.

  • Leads to alveolar collapse (atelectasis) and decreased lung compliance.

6. Formation of Hyaline Membranes

  • Dead epithelial cells and proteins accumulate in alveoli, forming hyaline membranes.

  • These further impair oxygen diffusion and gas exchange.

7. Fibrosis and Healing (Late Phase)

  • In some patients, the inflammatory process continues into a fibroproliferative phase.

  • This involves

    • Fibroblast proliferation

    • Collagen deposition

    • Pulmonary fibrosis (which may be irreversible)

Clinical Consequences

  • Severe hypoxemia (low blood oxygen)

  • Reduced lung compliance

  • Diffuse bilateral infiltrates on chest X-ray

  • Respiratory failure requiring mechanical ventilation

Summary

ARDS pathogenesis involves:

Alveolar injury → Inflammation → Neutrophil infiltration → Increased permeability → Edema → Surfactant loss → Alveolar collapse → Impaired gas exchange


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