This is a plain film radiograph of the lung. There are patchy bilateral pulmonary infiltrates. In addition, the heart is of normal size. This in the context of the patients history of pancreatitis is consistent with acute respiratory distress syndrome.

These are a spectrum of disorders where acute respiratory distress syndrome is the most severe form. The spectrum is characterised by:

• Non cardiogenic pulmonary oedema seen as diffuse pulmonary infiltrates on a CXR
• Progressive hypoxaemia
• Reduced lung compliance

Causes of acute lung injury and acute respiratory distress syndrome can be remembered using the FAT HIPS:

• Fat embolus
• Aspiration pneumonia
• Trauma and burns
• Heart bypass
• DIC
• Pancreatitis
• Sepsis

Diagnostic criteria of acute lung injury and acute respiratory distress syndrome

• Acute onset
• Diffuse pulmonary infiltrates on CXR
• Pulmonary artery wedge pressure <18mmHg
• PaO2/FiO2 <40 = All
• PaO2/FiO2 <26.6 = ARDS

Inflammation/Exudation phase

• Onset is at 1-2 days
• Mediated by macrophages and neutrophils via release of cytokines, proteases and free radical formation.
• Interstitial alveolar oedema occurs
• Treatment is mainly supportive: Treat the cause of ARDS and consider using positive end expiratory ventilation

Proliferation phase

• Onset is at 1-2 weeks
• Proliferation of type II alveolar cells and fibroblasts. Granulation tissue is produced which narrows alveoli and blood vessels.
• Treatment: Inhaled NO may help improve V/Q mismatch.

Fibrosis phase

• Onset is at 2-4 weeks
• Pulmonary fibrosis
• Treatment: steroid can be given.

Lung compliance is decreased during acute respiratory distress syndrome. The decrease of lung compliance occurs due to the reduction of airspace volume due to alveoli collapse by inflammatory cells, fluid and superimposed pressure, along with impairment of surfactant function.