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ARDS is marked by the rapid onset of profound dyspnea that usually occurs 12 48 hours after the initiating event
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No measures that effectively prevent ARDS have been identified; specifically, prophylactic use of PEEP in
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A large number of innovative therapeutic interventions to improve outcomes in ARDS patients have been or are being investigated Unfortunately, to date, none have consistently shown benefit in clinical trials Systemic corticosteroids have been studied extensively with variable and inconsistent results While recent studies suggest some specific improved outcomes when given within the first 2 weeks after the onset of ARDS, the routine use of corticosteroids is not recommended
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patients at risk for ARDS has not been shown to be effective Intravenous methylprednisolone does not prevent ARDS when given early to patients with sepsis syndrome or septic shock
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Treatment of ARDS must include identification and specific treatment of the underlying precipitating and secondary conditions (eg, sepsis) Meticulous supportive care must then be provided to compensate for the severe dysfunction of the respiratory system associated with ARDS and to prevent complications (see above) Treatment of the hypoxemia seen in ARDS usually requires tracheal intubation and positive-pressure mechanical ventilation The lowest levels of PEEP (used to recruit atelectatic alveoli) and supplemental oxygen required to maintain the PaO2 above 60 mm Hg or the SaO2 above 90% should be used Efforts should be made to decrease FIO2 to less than 60% as soon as possible in order to avoid oxygen toxicity PEEP can be increased as needed as long as cardiac output and oxygen delivery do not decrease and airway pressures do not increase excessively Prone positioning may transiently improve oxygenation in selected patients by helping recruit atelectatic alveoli; however, great care must be taken during the maneuver to avoid dislodging catheters and tubes A variety of mechanical ventilation strategies are available A multicenter study of 800 patients demonstrated that a protocol using volume-cycled ventilation with small tidal volumes (6 mL/kg of ideal body weight) resulted in a 10% absolute mortality reduction over standard therapy; this trial reported the lowest mortality (31%) of any intervention to date for ARDS Cardiac output that falls when PEEP is used may be improved by reducing the level of PEEP or by the judicious use of inotropic drugs (eg, norepinephrine); administering fluids to increase intravascular volume should be done only with great caution because increases in pulmonary capillary pressure worsen pulmonary edema in the presence of increased capillary permeability Therefore, the goal of fluid management is to maintain pulmonary capillary wedge pressure at the lowest level compatible with adequate cardiac output Crystalloid solutions should be used when intravascular volume expansion is necessary Diuretics should be used to reduce intravascular volume if pulmonary capillary wedge pressure is elevated Oxygen delivery can be increased in anemic patients by ensuring that hemoglobin concentrations are at least 7 g/dL; patients are not likely to benefit from higher levels Increasing oxygen delivery to supranormal levels through the use of inotropes and high hemoglobin concentrations is not clinically useful and may be harmful Strategies to decrease oxygen consumption include the appropriate use of sedatives, analgesics, and antipyretics
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The mortality rate associated with ARDS is 30 40% If ARDS is accompanied by sepsis, the mortality rate may reach 90% The major causes of death are the primary illness and secondary complications such as multiple organ system failure or sepsis Median survival is about 2 weeks Many patients who succumb to ARDS and its complications die after withdrawal of support (see Withdrawal of Support in 5) Most survivors of ARDS are left with some pulmonary symptoms (cough, dyspnea, sputum production), which tend to improve over time Mild abnormalities of oxygenation, diffusing capacity, and lung mechanics persist in some individuals
Adhikari N et al Pharmacologic therapies for adults with acute lung injury and acute respiratory distress syndrome Cochrane Database Syst Rev 2004 Oct 18;(4):CD004477 [PMID: 15495113] Bernard GR Acute respiratory distress syndrome: a historical perspective Am J Respir Crit Care Med 2005 Oct 1;172(7): 798 806 [PMID: 16020801] Hager DN et al Tidal volume reduction in patients with acute lung injury when plateau pressures are not high Am J Respir Crit Care Med 2005 Nov 15;172(10):1241 5 [PMID: 16081547] Matthay MA et al Acute lung injury and the acute respiratory distress syndrome: four decades of inquiry into pathogenesis and rational management Am J Respir Cell Mol Biol 2005 Oct;33(4):319 27 [PMID: 16172252] Rubenfeld GD et al Incidence and outcomes of acute lung injury N Engl J Med 2005 Oct 20;353(16):1685 93 [PMID: 16236739] Schwarz MI et al Imitators of the ARDS: implications for diagnosis and treatment Chest 2004 Apr;125(4):1530 5 [PMID: 15078770] Steinberg KP et al; National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network Efficacy and safety of corticosteroids for persistent acute respiratory distress syndrome N Engl J Med 2006 Apr 20;354(16):1671 84 [PMID: 16625008] Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome The Acute Respiratory Distress Syndrome Network N Engl J Med 2000 May 4;342(18): 1301 8 [PMID: 10793162] Wheeler AP et al; National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network Pulmonary-artery versus central venous catheter to guide treatment of acute lung injury N Engl J Med 2006 May 25;354(21): 2213 24 [PMID 16714768]
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