Hypoxia/ARDS 1. the Intervention Most Likely to Reduce the Duration Of

1. The intervention most likely to reduce the duration of this patient's mechanical ventilation is scheduled doses of furosemide. Although this patient's hypoxemia is due to acute respiratory distress syndrome (ARDS) rather than cardiogenic edema, diuresis can shorten the duration of mechanical ventilation. A large study of patients with ARDS and normal blood pressure and kidney function found that patients treated with aggressive diuresis spent less time on a ventilator without increased risk of nonpulmonary organ failure compared with patients who were given usual care. This patient's weight gain, peripheral edema, pleural effusions, and relatively elevated central venous pressure suggest she will respond well to furosemide. The early use of paralytic agents such as cisatracurium in patients with severe lung injury (arterial PO2/FIO2 <120 mm Hg [16.0 kPa]) has been shown to improve mortality and shorten the duration of mechanical ventilation, but this strategy has not yet been widely adopted. This patient is already 6 days into her illness and does not have severe hypoxemia. Prone positioning improves oxygenation in most patients with ARDS, primarily by facilitating the recruitment of flooded and collapsed alveoli in posterior, dependent regions of the lung. Although previous trials did not demonstrate improved mortality, a recent meta-analysis suggests prone positioning may improve survival in the most severely affected patients. Prone positioning is not indicated in the current scenario given this patient's relatively mild hypoxemia and readiness for ventilator weaning. Previous trials of inhaled nitric oxide in ARDS demonstrated improved oxygenation but no mortality benefit.

2. The most likely cause of this patient's hypoxemia is acute respiratory distress syndrome (ARDS). This patient has septic shock owing to a bladder infection that has triggered ARDS. Sepsis is one of the most common causes of ARDS, and onset within 48 to 72 hours after risk factor exposure is typical. The diagnosis of ARDS is most often made from clinical criteria that have recently changed. The 2012 Berlin consensus definition for ARDS updated the diagnostic criteria, classified the severity, and eliminated the term acute lung injury (ALI). The need for objective assessment (echocardiogram or pulmonary arterial wedge pressure) to exclude cardiogenic edema as a cause for ARDS is no longer required in patients with a known ARDS risk factor. Acuity of onset is now defined as 1 week, and chest CT is an accepted imaging modality to recognize bilateral alveolar opacities. ARDS is now classified into mild, moderate, and severe based on the severity of hypoxemia, and the term ALI is no longer used. Escherichia coli pneumonia is unlikely because hematogenous spread of infection to the lungs is unusual even in bacteremic patients. Sepsis-induced ARDS is much more likely. Heart failure should be clinically excluded as the cause of acute bilateral alveolar infiltrates in patients being evaluated for ARDS. This patient's young age, normal central venous pressure, and absence of cardiomegaly on chest radiograph all make heart failure unlikely. Idiopathic acute eosinophilic pneumonia is characterized by infiltration of the lung parenchyma by eosinophils. Patients present with fever, nonproductive cough, dyspnea, and bilateral infiltrates. Peripheral eosinophilia may not be present early in the course of illness, but prominent eosinophilia is present in bronchoalveolar lavage fluid. Idiopathic acute eosinophilic pneumonia, however, is rare and would be unlikely in a patient presenting with gram-negative infection and sepsis.

3. The most appropriate next step in treatment is intubation and mechanical ventilation. This patient has cardiogenic shock and acute pulmonary edema due to acute decompensated heart failure. Her severe hypoxemia and respiratory distress are the first priority in stabilizing this patient, and therefore the next step in management should be endotracheal intubation and invasive mechanical ventilation. This patient is not a candidate for noninvasive mechanical ventilation. Contraindications to noninvasive ventilation include respiratory arrest, cardiovascular instability (hypotension, arrhythmias, myocardial infarction), change in mental status (lack of cooperation), high aspiration risk, viscous or copious secretions, recent facial or gastroesophageal surgery, craniofacial trauma, fixed nasopharyngeal abnormalities, burns, and extreme obesity. Early trials indicated that noninvasive positive pressure ventilation (NPPV) reduced the need for intubation in the setting of acute cardiogenic pulmonary edema. However, a recently published study found similar outcomes among patients with acute heart failure managed with continuous positive airway pressure, NPPV, and standard oxygen therapy alone, although the discordance with previous studies may be related to study population and design. Nitroglycerin infusion is commonly used in managing acute decompensated heart failure, but in this instance its use could worsen the patient's hypotension and multiorgan failure. Regardless, stabilizing this patient's respiratory status is a higher priority. Placement of a pulmonary artery catheter in selected patients can assist in addressing hemodynamic derangements; however, use of a pulmonary artery catheter does not ultimately appear to affect survival in critically ill patients or those with decompensated heart failure and should never take precedence over managing respiratory failure.

4. The most appropriate next step in management is continuous positive airway pressure (CPAP). This patient's presentation is most consistent with hypoxemia due to postoperative atelectasis. Obesity, which reduces end-expiratory lung volumes, coupled with curtailed diaphragmatic excursion from upper abdominal surgery, places patients undergoing bariatric surgery at increased risk of postoperative atelectasis. The diminished basilar breath sounds on examination correlate with the low lung volumes noted on chest radiograph, which also revealed linear opacities consistent with platelike atelectasis. Previous trials found that CPAP reduces the need for intubation and risk of pneumonia in patients with hypoxemia complicating abdominal surgery and lung resection. Bronchoscopy can be useful in the evaluation and management of postoperative lobar or complete-lung atelectasis, which is typically caused by mucus plugging. Generally, chest physiotherapy is considered first-line treatment with bronchoscopy reserved for refractory cases. However, this patient's basilar, platelike atelectasis is due to shallow inspiration with collapse of distal airways rather than mucus plugging and would not be amenable to bronchoscopic intervention. Administering continuous albuterol by nebulizer would be appropriate if this patient were having an asthma exacerbation; however, the absence of wheezes and accessory muscle use on examination and the presence of atelectasis rather than hyperinflation on chest radiograph make it much less likely that asthma is the cause of this patient's hypoxemia. Naloxone might be appropriate if this patient's hypoxemia were due to hypoventilation from the residual sedating effects of operative sedation and analgesia. However, this patient is alert, and his arterial blood gas studies indicate acute hypoxemic rather than hypercapnic failure.