Acute respiratory distress syndrome

Adult respiratory distress syndrome (ARDS) occurs as a result of severe pulmonary injury that cause alveolar damage heterogeneously throughout the lung ¹. It can either result from a direct pulmonary source or as a response to systemic injury.

Pathology

Lung damage results in leakage of fluid into alveoli, leading to non cardiogenic pulmonary oedema and decreased arterial oxygenation.

The diagnosis is based on mainly clinical criteria set forth by the American-European Consensus Conference ⁴. ARDS is characterised by the following criteria ⁷:

• lung injury of acute onset, within one week of an apparent clinical insult and with progression of respiratory symptoms
• bilateral opacities on chest imaging not explained by other pulmonary pathology (e.g. pleural effusion, pneumothorax, or nodules)
• respiratory failure not explained by heart failure or volume overload
• decreased arterial PaO2/FiO2 ratio
  • mild ARDS: ratio is 201-300 mmHg (≤ 39≤39.9 kPa)
  • moderate ARDS: 101-200 mmHg (≤ 26≤26.6 kPa)
  • severe ARDS: ≤100 mmHg (≤ 13≤13.3 kPa)

It is of note that the clinical diagnosis of ARDS using internationally accepted guidelines and plain film imageschest radiographs, has been demonstrated to correlate poorly with histopathological diagnosis at autopsy.^{8, 9}

Causes

• trauma
• septicaemia
• hypovolaemic shock
• fat embolism
• near-drowning
• burns
• viral pneumonia
• pancreatitis
• oxygen toxicity
• smoke inhalation
• disseminated intravascular coagulopathy
• transfusion reaction
• aspiration of gastric contents
• head injury

Radiographic features

Plain filmChest radiograph

Chest radiographic findings of ARDS are non-specificnonspecific and resemble those of typical pulmonary oedema or pulmonary haemorrhage. There are diffuse bilateral coalescent opacities (the only radiologic criterion defined by the Consensus Conference). The time course of ARDS may help in differentiating it from typical pulmonary edema.

Chest x-ray features usually develop 12-24 hours after initial lung insult as a result of proteinaceous interstitial oedema. Within one week, alveolar pulmonary oedema (hyaline membrane) occurs due to type 1 pneumocyte damage.

In contrast to cardiogenic pulmonary oedema, which clears in response to diuretic therapy, ARDS persists for days to weeks. In addition, as the initial radiographic findings of ARDS clear, the underlying lung appears to have a reticular pattern secondary to type 2 pneumocyte proliferation and fibrosis ⁴.

Treatment and prognosis

ARDS carries a high mortality of around 50% ² and many survivors develop chronic lung disease, with damaged lung healing by fibrosis. A minority recover fully.