Acute respiratory distress syndrome

Pathophysiology - The Leaky Lung

• Insult (e.g., sepsis, trauma, pancreatitis) triggers a massive pulmonary inflammatory cascade.
• Key Mediators: Activated neutrophils release proteases and reactive oxygen species, fueled by cytokines (TNF-α, IL-1, IL-6).
• Core Injury: Diffuse alveolar damage (DAD) to both the capillary endothelium and alveolar epithelium.
  • This breakdown of the alveolar-capillary barrier leads to ↑ permeability.
  • Damage to Type II pneumocytes causes ↓ surfactant, leading to alveolar collapse (atelectasis).

⭐ The hallmark is non-cardiogenic pulmonary edema. This is confirmed by a normal or low Pulmonary Capillary Wedge Pressure (PCWP) of <18 mmHg, distinguishing it from heart failure.

Etiology - The Usual Suspects

• Direct Lung Injury (Insult directly to the lungs)

  • Pneumonia: Viral or bacterial.
  • Aspiration of gastric contents.
  • Pulmonary contusion or fat embolism.
  • Near-drowning.

• Indirect Lung Injury (Systemic inflammation affecting lungs)

  • Sepsis: The #1 overall cause.
  • Severe Trauma with shock.
  • Acute Pancreatitis.
  • Transfusion-Related Acute Lung Injury (TRALI).

⭐ Sepsis is the single most common trigger for the development of ARDS, accounting for approximately one-third of all cases.

Diagnosis - Berlin's Big Criteria

📌 BERLIN Criteria for ARDS diagnosis:

• Bilateral Opacities: On chest imaging (X-ray/CT), not fully explained by other causes (e.g., effusion, collapse).
  • 
• Edema Origin: Respiratory failure not primarily from cardiac failure or fluid overload.
  • • Objective assessment (e.g., echo) needed if no ARDS risk factor.
• Respiratory Timing: Acute onset within 1 week of a known insult or new/worsening symptoms.
• Low Oxygenation (Hypoxemia): PaO₂/FiO₂ ratio (P/F ratio) on PEEP ≥ 5 cmH₂O defines severity.
  • • Mild: P/F 201-300 mmHg
  • • Moderate: P/F 101-200 mmHg
  • • Severe: P/F ≤ 100 mmHg

⭐ The PaO₂/FiO₂ ratio is a key prognostic indicator. A lower ratio signifies more severe hypoxemia and is associated with higher mortality.

Management - Lungs Under Pressure

Primary Goal: Treat the underlying cause + supportive care with lung-protective ventilation.

• Low Tidal Volume (LTV) Ventilation:
  • Tidal Volume (V_T): $4-8 \text{ mL/kg}$ of ideal body weight.
  • Plateau Pressure (P_plat): Keep <30 cm H₂O to minimize barotrauma.
  • Permissive Hypercapnia: Tolerate ↑PaCO₂ and mild acidosis as a trade-off for LTV.
• Positive End-Expiratory Pressure (PEEP):
  • Use high PEEP (>5 cm H₂O) to recruit collapsed alveoli and improve oxygenation.
• Prone Positioning:
  • For moderate-to-severe ARDS (P/F ratio <150).
  • Improves ventilation-perfusion (V/Q) matching; done for >12 hours/day.
• Conservative Fluid Management:
  • Diuresis or restricted fluids after shock resolves to reduce pulmonary edema.

⭐ High-Yield: Low tidal volume ventilation is the cornerstone intervention shown to decrease mortality in ARDS by reducing ventilator-induced lung injury (VILI).

• ARDS is non-cardiogenic pulmonary edema from alveolar-capillary damage, not heart failure.
• Key triggers include sepsis (most common), pneumonia, trauma, and pancreatitis.
• Presents with rapid-onset, severe hypoxemia refractory to supplemental oxygen.
• CXR shows bilateral, diffuse pulmonary infiltrates resembling a "white-out."
• PaO₂/FiO₂ ratio ≤ 300 mmHg is a hallmark diagnostic criterion.
• Pulmonary capillary wedge pressure (PCWP) is normal (≤ 18 mmHg), ruling out cardiogenic causes.
• Histology classically shows diffuse alveolar damage (DAD) with hyaline membranes.