Atelectasis and acute respiratory distress syndrome

A) Atelectasis

Definition

Atelectasis = collapse of a small or large area of lung tissue → inadequate expansion of airspaces → poorly oxygenated blood shunted from pulmonary artery to pulmonary veins → ventilation-perfusion imbalance and hypoxia.

3 Forms

1. Resorption atelectasis

• Cause: complete airway obstruction by mucus or mucopurulent plug
• Mechanism: obstruction → trapped air is gradually absorbed → alveolar collapse
• Associated with: bronchial asthma, chronic bronchitis, bronchiectasis, post-op states, foreign body aspiration

2. Compression atelectasis

• Cause: accumulation of fluid, blood, or air in the pleural cavity → mechanically collapses the lung
• Causes:
  • Congestive heart failure → pleural effusion
  • Pneumothorax → air leaks into pleural cavity
  • Ascites/bedridden patients → elevated diaphragm → basal atelectasis

3. Contraction atelectasis

• Cause: local or generalized fibrotic changes in the lung or pleura prevent full expansion

Key points

• Resorption and compression atelectasis: reversible
• Contraction atelectasis: irreversible
• Treat immediately to prevent hypoxemia and superimposed infection

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B) ARDS (Acute Respiratory Distress Syndrome)

Definition

• End result of acute alveolar injury caused by a variety of insults
• Initial injury: to capillary endothelium or alveolar epithelium (or both)
• Diffuse alveolar damage (DAD): histological term for structural lung changes in early ARDS

Pathogenesis

• Alveolar-capillary membrane is normally formed by two barriers: capillary endothelium + alveolar epithelium
• In ARDS: membrane is compromised → two consequences:
  1. Endothelial injury → ↑ capillary permeability → interstitial edema → alveolar edema → fibrin exudation → hyaline membrane formation
  2. Type II pneumocyte damage → loss of surfactant → alveoli unable to expand
• Underlying mechanism: pro-inflammatory/anti-inflammatory imbalance → shift to pro-inflammatory state → lung damage by endotoxins, neutrophils, macrophages

Morphology

Acute phase:

• Lungs: dark red, firm, airless, heavy
• Histology: capillary congestion, alveolar epithelial necrosis, interstitial and intra-alveolar hemorrhage, neutrophil accumulation
• Most characteristic: hyaline membrane (fibrin-rich edema fluid + necrotic epithelial cell remnants)

Organized phase:

• Type II pneumocyte proliferation → attempt to regenerate alveolar lining
• Organization of fibrin exudate → intra-alveolar fibrosis → thickening of alveolar septa

Clinical features

If patient survives acute phase, two outcomes:

1. Normal respiratory function returns within 6–12 months
2. Diffuse interstitial fibrosis → permanent impairment of respiratory function

💡 High-yield: Atelectasis types: resorption (mucus plug), compression (pleural effusion/pneumothorax), contraction (fibrosis; irreversible). ARDS = DAD; hyaline membrane = fibrin + necrotic cells; type II pneumocyte damage → no surfactant. Outcome: recovery OR interstitial fibrosis.