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A 45-year-old man is admitted to the neurologic intensive care unit (NeuroICU) after resection of a craniopharyngioma. Three days into his ICU admission, he has a witnessed aspiration event with subsequent respiratory distress and hypoxemia requiring invasive mechanical ventilation. Over the next 24 hours, his hypoxemic respiratory failure worsens despite increasing mechanical ventilatory support, deep sedation, neuromuscular blockade, and a trial of prone positioning. His chest radiograph demonstrates diffuse bilateral infiltrates. With the patient receiving a fraction of inspired oxygen of 1.0, a positive end-expiratory pressure of 15 cm H2O, a tidal volume of 6 mL/kg of predicted body weight, and a respiratory rate of 35 breaths per minute, arterial blood gas analysis reveals a pH of 7.14, a PaCO2 of 70 mm Hg, and a PaO2 of 50 mm Hg. Plateau airway pressure, measured at end inspiration, is 37 cm H2O.

What is the role of venovenous extracorporeal membrane oxygenation (ECMO) in the management of the acute respiratory distress syndrome (ARDS)?

The ARDS is characterized by the rapid onset of hypoxemia and bilateral pulmonary infiltrates consistent with pulmonary edema that cannot be fully attributed to cardiac failure or fluid overload.1,2 The definition of ARDS was recently revised, using the ratio of the partial pressure of oxygen (PaO2) to the fraction of inspired oxygen (FIO2) to classify ARDS into mild (200 < PaO2/FIO2 ≤ 300 mm Hg), moderate (100 < PaO2/FIO2 ≤ 200 mm Hg), and severe (PaO2/FIO2 ≤ 100 mm Hg) forms, with a minimum positive end-expiratory pressure (PEEP) of 5 cm H2O. There is evidence that mortality correlates with severity of illness, with the lowest PaO2 to FIO2 ratios resulting in the highest mortality rates; however, this association requires further validation.2,3

Pathologically, ARDS is characterized by injury to the lung epithelium and capillary endothelium, resulting in increased permeability of protein-rich fluid.4,5 The resulting pulmonary edema and disruption of surfactant production and function lead to decreased lung compliance and impaired gas exchange.6 This lung injury may be further exacerbated by positive-pressure ventilation, so-called ventilator-associated lung injury (VALI), through the over-distention of less affected lung regions and the repeated opening and closing of alveoli and small bronchioles.7 The mainstay of management in ARDS is treatment of the underlying disease process and minimization of VALI while supplying adequate gas exchange support.5

There are few strategies that have been demonstrated to reduce mortality in ARDS. The most widely accepted approach to the management of ARDS is a lung-protective ventilatory strategy targeting low tidal volumes and plateau airway pressures. In a landmark trial by the ARDS Network, 861 patients with ARDS were randomized to a tidal volume of 4 to 6 mL/kg predicted body weight ...

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