Chest ImagingAdult respiratory distress syndrome
(ARDS), first defined in 1992, by the American/European Consensus Committee, as acute and persistent severe hypoxia (P
aO
2/F
IO
2
£ 300 mm Hg, where PaO
2 is the partial pressure of oxygen gas measured within the arterial blood, and F
IO
2 is the fraction of oxygen gas witin the inspired air (dry air)), bilateral
radiographic lung infiltrates, and no evidence of congestive heart failure. Patients with lesser degrees of hypoxia (P
aO
2/F
IO
2
£ 200 mm Hg) are classified as having acute lung injury. ARDS is not a disease but a syndrome that may be due to direct parenchymal injury (
trauma, pneumonia, aspiration) or due to capillary leak oedema from systemic
inflammation (sepsis,
hypotension) (Table 1). Traditionally, the clinical approach to and
radiographic understanding of ARDS has assumed that the type of underlying injury was not relevant to life support strategies and imaging interpretation. However, recent evidence suggests that lung mechanics and
radiographic appearance may be different in those with ARDS due to
pulmonary causes (ARDSp) and those with ARDS due to extrapulmonary causes (ARDSexp).
The classical radiographic description generally describes ARDS due to systemic insult. The classical radiographic descriptions of ARDS are as follows:
During the first 12-24 hours after a systemic insult, the chest radiograph is normal or it shows mild generalized atelectasis. Over the next 48 hours, there is a rapid increase in density throughout the lungs and often diffuse ground-glass to alveolar consolidation symmetrically distributed (Fig.1). The appearance then stabilizes for several days. Toward the end of the first week, the consolidation becomes less dense, eventually forming a fibrotic pattern.
This description is true for many but not all patients. Many have asymmetrical disease, focal areas of dense consolidation, or dense consolidation alternating with ground-glass opacification. These differences may relate, in part, to the underlying aetiology. In ARDSexp, the systemic insult, most often bloodborne, distributes itself diffusely and causes oedema, haemorrhage and atelectasis (Fig.2). Contrast this with ARDSp due to bacterial pneumonia, aspiration or direct lung trauma where only a portion of the lung parenchyma is affected. The early radiographs are more likely to show rapidly progressive focal alveolar consolidation mixed with normal areas. Eventually, ground-glass opacification may appear in remote areas (Fig.3). The latter may be due to atelectasis, lesser effects of the initial disease, or systemic effects of the lung disease reaching the remaining lung haematogenously.
Nosocomial infection is common in the intubated ARDS patient but whether an ARDS patient also has nosocomial infection is extremely difficult to diagnose both clinically and radiographically. The usual clinical markers of infection such as fever, leukocytosis and malaise have many other possible causes in the Intensive Care Unit (ICU) and bacteria frequently colonize the tracheobronchial secretions in the absence of pneumonia. When ARDS shows the classical pattern of symmetrical ground glass infiltrate, pneumonia is uncommon. Conversely, however, progressive, asymmetrical or focal infiltrates do not reliably predict the presence of pneumonia.
During the second and third week, fibrosis and repair begin. Regardless of the aetiology, the radiograph or CT shows less ground-glass and less consolidation. This is replaced with a coarser reticular pattern. Lung distorsion appears as fibrosis progresses. Barotrauma may cause interstitial emphysema leading to pneumomediastinum and pneumothorax, and pneumatocoeles. In survivors, lung remodelling is often remarkable. The chest radiograph often returns to normal, or near normal, and CT often shows modest areas of interstitial fibrosis.
Adult respiratory distress syndrome, Table 1. ARDS - Aetiology.
P
PG
LG - NK