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A 63-year-old man with no past medical history presented with a 3-day history of productive cough, hemoptysis, fever, and shortness of breath. In the emergency department (ED) the patient was mildly hypotensive and in severe respiratory distress, which required immediate intubation and initiation of mechanical ventilation. His laboratory workup revealed leukocytosis, mild renal insufficiency, and elevated serum lactate. His chest radiograph revealed dense consolidation in the right lower lung field with bilateral patchy infiltrates. The patient continued to be profoundly hypoxemic despite incremental increases in the mechanical ventilation support.

This is unfortunately a common clinical scenario for severe community-acquired pneumonia with associated sepsis and acute respiratory distress syndrome. In this chapter we will:

  • Review the definitions, etiologies, and clinical aspects of acute respiratory distress syndrome (ARDS).

  • Describe ventilator-induced lung injury and how it can be minimized.

  • Review the role of steroid therapy and fluid management in ARDS.

  • Review rescue strategies that may be considered in selected patients with ARDS.

  • Describe outcome of ARDS survivors.

  • Review neurogenic pulmonary edema.

  • Review the effect of positive ventilation on cerebral perfusion.

How is the syndrome defined?

ARDS is an acute process of noncardiogenic pulmonary edema due to lung inflammation leading to hypoxemia. The American-European Consensus Conference (AECC)1 defines ARDS as (1) acute onset (< 7 days); (2) partial pressure of oxygen in arterial blood (Pao2)/fraction of inspired oxygen (Fio2) less than or equal to 200 mm Hg (regardless of positive end-expiratory pressure [PEEP] level); (3) diffuse bilateral infiltrates on frontal chest radiograph, consistent with pulmonary edema; and (4) pulmonary capillary arterial occlusion pressure (PAOP) less than or equal to 18 mm Hg if measured, or in the absence of capability to measure PAOP, no clinical evidence of left atrial hypertension.

Acute lung injury (ALI) carries the same definition except a lesser degree of hypoxemia (Pao2/Fio2 ≤ 300 mm Hg for ALI). The definitions of ARDS and ALI do not require mechanical ventilation and exclude chronic lung diseases.

Etiologies of ARDS are divided into primary (initial insult comes from alveolar side of lung interstitium) and secondary or extrapulmonary (insult comes from blood side of lung interstitium) (Table 37-1).2 The diagnosis of ARDS does not require a pulmonary artery (PA) catheter. Echocardiography, however, is often relied on in diagnosing systolic or diastolic dysfunction as the cause of pulmonary edema and in ruling out ALI/ARDS. Patients presenting with cardiogenic edema may have normal PAOP by the time a pulmonary artery catheter is placed (therapy had already been initiated).

Table 37-1.Common Causes of ALI/ARDS

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