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)
Roy G Brower et al.
New England Journal of Medicine 2000 May 4, 342 (18): 1301-8
Herbert P Wiedemann et al.
New England Journal of Medicine 2006 June 15, 354 (24): 2564-75
Brower RG, et al.
New England Journal of Medicine 2004 July 22, 351 (4): 327-36
Arthur P Wheeler et al.
New England Journal of Medicine 2006 May 25, 354 (21): 2213-24
Steinberg KP et al.
New England Journal of Medicine 2006 April 20, 354 (16): 1671-84
The PaO₂:FiO₂ Ratio calculator is created by QxMD.