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Syndrome of (1) acute respiratory failure - PaO2 < 8: FiO2 > 0.6 with (2) non-cardiogenic pulmonary oedema

Leads to: reduced lung compliance, hypoxaemia
50-60% mortality.

1. PaO2:FiO2 ratio < 26.6kPa (200mmHg)
2. Pulmonary artery wedge pressure < 16mmHg
3. Bilateral pulmonary infiltrates

Acute lung injury - similar to above except PaO2:FiO2 <300mmHg

Causes

1. Direct lung injury
   • Pneumonia / pneumonitis / aspiration
   • Smoke inhalation / burns
   • Trauma
2. Indirect lung injury (cytokine mediated)
   • Multiple trauma
   • Transfusion reaction
   • DIC
   • Pancreatitis
   • Cardio-pulmonary bypass

Pathophysiology

1. Inflammatory phase: (1) neutrophils/MPs release free radicals, proteases, PGs, ILs, TNF, activate complement (2) Kills type 2 pneumocytes, loss of surfactant (and lung compliance) (3) get lots of lung oedema
2. Proliferative phase: proliferation of type 2 pneumocytes, increase in fibroblasts
3. Fibrotic phase (1) odema/secretions reduce compliance and cause atelectasis (2) resulting shunt and hypoxic vasoconstriction and pulmonary hypertension (3)  persisting fibrosis

Principles of Management

1. Treat insult
2. Fluid restriction/control to prevent worsening oedema
3. Nutrition
4. Mechanical ventilation - High PEEP to hold alveoli open; small tidal volumes; Inverse-ratio ventilation; prone ventilation
5. Treat pulmonary vasoconstriction/hypertension - nitric oxide, inhaled prostacyclin, phosphodiesterase inhibition (viagra)
6. Treat pulmonary fibrosis - steroids