ARDS is a type of acute diffuse inflammatory lung injury,
characterized by increased permeability of the alveolar–capillary membrane with edema,
loss of aerated lung tissue,
increased work of breathing and impaired gas exchange.
The annual incidence of ARDS is estimated approximately at 80 per 100.000/year. According to new Berlin definition the diagnosis is based on the onset of hypoxaemia and of bilateral chest opacities within 1 week of a known risk factor.
From the radiological point of view,
the presence of bilateral opacities remains one of the hallmarks for diagnosis; these findings could be detected by computed tomography (CT) instead of radiography.
ALI’s definition was eliminated and replaced by assigning a scale of gravity to ARDS.
THE BERLIN ARDS DEFINITION (2012)
- The onset of ARDS is identified within 7 days of a known clinical insult or new/worsening respiratory symptoms.
- Bilateral opacities consistent with pulmonary edema that are not fully explained by effusions,
lobar/lung collapse or nodules/masses on chest radiograph.
- Respiratory failure not fully explained by cardiac failure or fluid overload; need objective assessment (e.g.,
echocardiography) to exclude hydrostatic edema if no risk factor present.
- The term acute lung injury (ALI) was removed from the ARDS definition.
- ARDS mild: 200 < PaO2/FiO2 ≤ 300 with PEEP or CPAP > 5 cm H2O
- ARDS moderate: 100 < PaO2/FiO2 ≤ 200 with PEEP > 5 cm H2O
- ARDS severe: PaO2/FiO2 ≤ 100 with PEEP > 5 cm H2O
Legend: PaO2 partial pressure of arterial oxygen,
FiO2 fraction of inspired oxygen,
PEEP positive end-expiratory pressure,
CPAP continuous positive airway pressure.
![](https://epos.myesr.org/posterimage/esr/esti-escr2018/146010/media/778298?maxheight=300&maxwidth=300)
Fig. 1: There are two aetiological categories of ARDS: in the first lung injury is a consequence of a direct insult as exemplified by patients with severe pneumonia or aspiration. Instead indirect injury most commonly occurs in the context of systemic sepsis, severe non thoracic trauma, transfusions, pancreatitis and others.
References: Radiology, University Hospital of Chieti - Chieti/IT
ALVEOLAR EPITHELIAL INJURY
![](https://epos.myesr.org/posterimage/esr/esti-escr2018/146010/media/778299?maxheight=300&maxwidth=300)
Fig. 2: Microscopically, lungs from afflicted individuals in the early stages show diffuse alveolar damage with alveolar flooding by proteinaceous fluid, neutrophil influx into the alveolar space, loss of alveolar epithelial cells, deposition of hyaline membranes on the denuded basement membrane and formation of microthrombi.
References: Radiology, University Hospital of Chieti - Chieti/IT
DIFFERENTIAL DIAGNOSIS: CARDIOGENIC EDEMA VERSUS ARDS
The main differential diagnosis is still between ARDS and cardiogenic edema,
especially in the acute phase.
The differential diagnosis between ARDS and cardiogenic edema can be assessed on chest radiograph in typical cases.
![](https://epos.myesr.org/posterimage/esr/esti-escr2018/146010/media/778305?maxheight=300&maxwidth=300)
Fig. 3: Cardiogenic edema is usually characterized in its first stage by septal lines (more visible in the costophrenic angles), prominence of the upper lobe vessels, peribronchovascular haze and cuffing, widened vascular pedicle of the mediastinum and pleural effusion. If an alveolar edema occurs, it appears as an airspace opacity with gravitational or perihilar distribution. Acute (‘‘flash’’) congestive cardiac failure with edema generally produces a radiographic pattern of patchy or ‘‘bat wing’’ alveolar opacities with peripheral sparing. The clinical evolution, in addition to the absence of heart enlargement, septal lines or pleural effusion and the abrupt appearance of alveolar opacities, all favour ARDS. However a reliable method to distinguish cardiac from ARDS edema or to evaluate the hydrostatic component in ARDS patients still does not exist.
References: Radiology, University Hospital of Chieti - Chieti/IT
CLINICAL PRESENTATION
Signs and symptoms are not specific (mainly dyspnoea,
cyanosis,
tachypnea and hypoxaemia) and mimic those of pulmonary edema.
Pathologically,
ARDS is characterized by diffuse alveolar damage (DAD) and evolves over 2 or 3 weeks through exudative,
proliferative and fibrotic phases.
- THE EXUDATIVE PHASE (1-7 days): injury to the endothelium results in increased capillary permeability and the influx of protein-rich fluid into the alveolar space and interstitium,
which promotes pulmonary edema.
- THE PROLIFERATIVE PHASE (8-15 days): there is proliferation of fibroblasts and type II pneumocytes.
There may be extensive alveolar consolidation (primarily due to inflammation and haemorrhage) which can persist for a variable time.
- THE FIBROTIC PHASE (>15 days): in surviving patients there is deposition of collagen.
![](https://epos.myesr.org/posterimage/esr/esti-escr2018/146010/media/778310?maxheight=300&maxwidth=300)
Fig. 4: Illustration of the temporal evolution and resolution of the ARDS.
References: Radiology, University Hospital of Chieti - Chieti/IT