Acute respiratory distress syndrome (ARDS) is classically described as noncardiogenic pulmonary edema, thought to be secondary to increased pulmonary capillary permeability. This process may occur for a number of reasons, both pulmonary and systemic in origin. Common causes of ARDS include pulmonary or systemic infection, trauma, burns, pancreatitis, near-drowning, transfusion, medication overdose, and toxic inhalations.
Treatment of ARDS is evolving, with several recent large-scale studies that have altered standard practice:
- Low tidal volume ventilation (6mL/kg) improves absolute mortality 9% (ARDSNet, 2000)
- Restrictive fluid management strategies (initiated after hemodynamic stabilization) increases ventilation-free and ICU-free days, but has no effect on 60-day mortality (ARDSNet, 2006)
- High versus low levels of positive end-expiratory pressure (PEEP) has no effect on clinically relevant outcomes (Brower et al, 2004)
- No benefit, but increased complication rates when pulmonary arterial catheters are used to guide treatment (ARDSNet, 2006)
- Steroid therapy increases morbidity and possibly increases mortality, especially if initiated late (> 14 days) in ARDS course (Steinberg et al, 2006)
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