Acute Respiratory Distress Syndrome

Chapter: Acute Respiratory Distress Syndrome
McMaster Section Editor(s): Paul M. O’Byrne
Section Editor(s) in Interna Szczeklika: Ewa Niżankowska-Mogilnicka, Filip Mejza
McMaster Author(s): Maureen O. Meade, Tim Karachi
Author(s) in Interna Szczeklika: Wiesław Królikowski, Miłosz Jankowski
Additional Information

Definition, Etiology, Pathogenesis Top

1. According to the 2012 Berlin Definition, Acute respiratory distress syndrome (ARDS) is characterized by the following:

1) Acuity of onset or new or worsening respiratory symptoms within 1 week of a known clinical insult.

2) Chest imaging abnormalities: Bilateral opacities on plain radiographs or computed tomography (CT) scans not fully explained by effusions, lobar or lung collapse, or nodules.

3) Origin of pulmonary edema: Respiratory failure not fully explained by congestive heart failure or fluid overload. Patients with no risk factors for ARDS (see below) may require objective assessment (eg, echocardiography) to exclude hydrostatic edema.

4) Hypoxemia, as assessed in a ventilated patient by a ratio of PaO2 to FiO2 (in a healthy person breathing atmospheric air: PaO2 = 97 mm Hg; FiO2 = 0.21; PaO2/FiO2 = 470 mm Hg; at altitudes >1000 meters above the sea level use the formula: PaO2/FiO2 × atmospheric pressure in mm Hg/760). Based on this, ARDS is classified as one of the following:

a) Mild ARDS: 200 mm Hg <PaO2/FiO2 ≤300 mm Hg with positive end-expiratory pressure (PEEP) or noninvasive continuous positive airway pressure (CPAP) ≥5 cm H2O.

b) Moderate ARDS: 100 mm Hg <PaO2/FiO2 ≤200 mm Hg with PEEP ≥5 cm H2O.

c) Severe ARDS: PaO2/FiO2 ≤100 mm Hg with PEEP ≥5 cm H2O.

2. Causes (risk factors) of ARDS:

1) Pulmonary: A direct insult to the lungs as a result of aspiration of gastric contents, pneumonia, pulmonary contusion, toxic inhalation, thoracic irradiation, drowning.

2) Extrapulmonary: An indirect insult to the lungs as a result of a systemic inflammatory response as seen in sepsis, shock, acute necrotic pancreatitis, multiple long bone fractures (fat embolism), extensive burn injury, multiple transfusions, transfusion-related acute lung injury (TRALI), complications of pregnancy (eclampsia, amniotic fluid embolism), tumor lysis syndrome, prolonged cardiopulmonary bypass, adverse drug reactions, drug poisoning.

3. Pathogenesis of ARDS: An uncontrolled inflammatory process causing damage to the alveolar-capillary membrane with transfer of protein-rich fluid and cells from the vessels to the alveoli, destruction and impaired production of surfactant, collapse and edema of the alveoli (exudative phase); destruction of the alveolar septa by inflammatory cell infiltration, impaired gas exchange, reduced lung compliance, and eventually respiratory failure (with dominant hypoxemia) and (acute) pulmonary hypertension. Reparative processes begin within 2 to 3 weeks (proliferative phase) and regeneration of damaged cells or production of collagen by fibroblasts is possible at later stages (fibrotic phase).

Diagnosis Top

See Acute Respiratory Failure.

Diagnostic Criteria

See Definition, Etiology, Pathogenesis, above.

Treatment Top

See Acute Respiratory Failure.

The initial treatment of patients with ARDS is the same as for other causes of acute respiratory failure. Two elements fundamental to the management of ARDS are treatment of the underlying disorder and supportive care, the mainstay of which is mechanical ventilation. Noninvasive ventilation may be considered in mild ARDS; in other cases, use invasive treatment. A lung-protective ventilation strategy that targets tidal volumes in the range of 4 to 8 mL/kg predicted body weight is associated with higher survival rates than traditional tidal volumes in the range of 10 to 15 mL/kg.Evidence 1Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). Moderate Quality of Evidence (moderate confidence that we know true effects of intervention). Quality of Evidence lowered due to some inconsistency across trials for a critical outcome, mortality. However, the finding of reduced mortality was statistically significant. Burns KE, Adhikari NK, Slutsky AS, et al. Pressure and volume limited ventilation for the ventilatory management of patients with acute lung injury: a systematic review and meta-analysis. PLoS One. 2011 Jan 28;6(1):e14623. doi: 10.1371/journal.pone.0014623. Review. PubMed PMID: 21298026; PubMed Central PMCID: PMC3030554. The relative benefit of a high PEEP versus a low PEEP strategy is not altogether clear; a higher PEEP strategy does not appear to be harmful and may improve survival in patients with moderate to severe ARDSEvidence 2Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). Moderate Quality of Evidence (moderate confidence that we know true effects of intervention). Quality of Evidence from this individual patient data meta-analysis lowered due to the fact that high-PEEP treatment strategies varied in the studies of the review, the direction of survival effect was not consistent across the 3 major trials (one suggested possible harm), and the statistically significant finding was limited to a subgroup analysis (which met all criteria for credibility). Briel M, Meade M, Mercat A, et al. Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis. JAMA. 2010 Mar 3;303(9):865-73. doi: 10.1001/jama.2010.218. Review. PubMed PMID: 20197533. (Table. Strategies of PEEP/FiO2 adjustment in…). In the most severe cases of ARDS with hypoxemia, hypercapnia refractory to mechanical ventilation, or both, extracorporeal gas exchange techniques are sometimes used in experienced centers (best results in influenza-associated severe ARDS in relatively young patients).

TablesTop

Table. Strategies of PEEP/FiO2 adjustment in patients with acute respiratory distress syndrome

Lower PEEP strategy

FiO2

0.3-0.4

0.4-0.5

0.5-0.6

0.6-0.7

PEEP (cm H2O)

5

5-8

8-10

8-10

FiO2

0.7-0.8

0.8-0.9

0.9-1.0

1.0

PEEP (cm H2O)

10-14

14

14-18

18-24

Higher PEEP strategy

FiO2

0.3-0.4

0.4-0.5

0.5

0.5-0.8

PEEP (cm H2O)

5-14

14-16

16-18

18-20

FiO2

0.8-1.0

1.0

 

 

PEEP (cm H2O)

22

24

 

 

Adapted from: ARDS Clinical Network. Mechanical ventilation protocol summary of low tidal volume used in the ALVEOLI study. http://www.ardsnet.org/files/ventilator_protocol_2008-07.pdf.

FiO2, fraction of oxygen in the inspired air; PEEP, positive end-expiratory pressure.

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