Respiratory Distress Syndrome, Acute (ARDS)
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- Acute respiratory distress syndrome is defined as onset of acute hypoxemia within 7 days of known clinical insult or new or worsening respiratory symptoms. On imaging, it appears as bilateral opacities consistent with pulmonary edema not fully explained by effusions, lung collapse or nodules. The respiratory failure is not explained by cardiac failure or fluid overload.
- Severity of ARDS depends on oxygenation of the blood. It is measured with ratio of partial pressure of arterial oxygen (PaO2) to fraction of inspired oxygen (FiO2) at positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) of at least 5 centimeter of water (cm H2O).
- Mild—200 mm Hg < PaO2/FiO2 ≤300 millimeter of mercury (mm Hg)
- Moderate—100 mm Hg < PaO2/FiO2 ≤200 mm Hg
- Severe—PaO2/FiO2 ≤100 mm Hg
- Synonym(s): acute lung injury; increased-permeability pulmonary edema; noncardiac pulmonary edema
- Systems affected—pulmonary, cardiovascular
Incidence of ARDS is very variable. Highest incidence rate was in United States of 78.9 per 100,000 person-years.
Etiology and Pathophysiology
- ARDS is a response to an injury to lung which can be direct or indirect.
- Aspiration of gastric contents
- Pneumonia (bacterial, viral, fungal or opportunistic infections)
- Air, fat, or amniotic fluid emboli
- Pulmonary contusion
- Inhalation injury
- Sepsis (nonpulmonary source)
- Major burn injury
- Nonthoracic trauma
- Drug overdose
- Pancreatitis, severe
- Cardiopulmonary bypass
- Reperfusion edema after lung transplant or embolectomy
- Progression of ARDS is divided into 3 phases.
- Exudative phase—It is the initial phase where alveolar macrophages are activated in high inflammatory stage due to lung injury which leads to complement activation, release of pro-inflammatory mediators, and activation of neutrophils. It causes epithelial–endothelial barrier disruption, leading to intra-alveolar and extra-alveolar flooding with fluid. It is followed by hyaline membrane formation leading to alveolar collapse.
- Proliferative phase—Fibroblasts, myofibroblasts, and alveolar epithelial cell (ACE) II mediate repair in this phase. Formation of new matrix, differentiation into ACE I, and formation of cellular junctions begin which leads to expression of aquaporin and ion channels. These help in reabsorption of fluid.
- Fibrotic phase—not seen in everyone; related to prolonged mechanical ventilation and increased mortality.
Good ICU practices like low tidal volumes in all mechanically ventilated patients, early resuscitation and antibiotics for sepsis, restrictive use of blood products, and intensivist involvement may help prevent nosocomial ARDS.
Commonly Associated Conditions
Pneumonia, sepsis, and aspiration of gastric contents lead to 85% cases of ARDS.