A 27-year-old woman is admitted to the hospital urgently for labor. The patient has had no prenatal care. Delivery is complicated by premature rupture of membranes and prolonged labor. On day 3 of hospitalization, she develops fever, chills, lower abdominal pain, and hypotension. Postpartum endometritis is suspected. The patient is prescribed broad-spectrum antibiotics and intravenous fluids. Over the next 24 hours, she develops increasing shortness of breath. The patient receives a total of 5 L of normal saline to treat the hypotension. Temperature is 38.5 C (101.3 F), blood pressure is 110/66 mm Hg, pulse is 110/min, and respirations are 24/min. BMI is 34 kg/m². Pulse oximetry is 80% on a 100% nonrebreather mask, and the decision is made to intubate. There is no evidence of jugular venous distension. Cardiac examination is normal except for tachycardia. Lung auscultation reveals diffuse bilateral crackles. Mild bilateral pitting edema is present in the lower extremities. Chest x-rays 24 hours earlier (left) and at intubation (right) are shown in the images below: After intubation, an arterial blood gas test shows a PaO₂ of 60 mm Hg on 100% oxygen and a PaCO₂ of 34 mm Hg. Which of the following best explains this patient's respiratory symptoms?

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11ec25c8_d30a_7f18_bc81_27cc8d6afa3b_MD0003_00 This patient with sepsis (ie, fever, chills, hypotension) from postpartum endometritis has rapidly progressive dyspnea, diffuse crackles, bilateral lung infiltrates, and acute hypoxemic respiratory failure. FiO₂ is 100% (1.0) and PaO₂ is 60 mm Hg, resulting in a PaO₂/FiO₂ ratio of 60/1.0 = 60. This presentation is most consistent with acute respiratory distress syndrome (ARDS) due to sepsis. ARDS develops in the setting of direct (eg, pneumonia, aspiration) or indirect (eg, sepsis, pancreatitis) lung injury. Sepsis is a dysregulated host inflammatory response to infection (eg, endometritis), which promotes increased alveolar capillary permeability, exudation of proteinaceous fluid into the airspaces, and recruitment of leukocytes and cytokines into the lung. Gas exchange is impaired due to severe ventilation-perfusion mismatch owing to intrapulmonary shunt effect (perfusion of flooded, gasless alveoli). Lung compliance is reduced due to pulmonary edema and loss of surfactant. Bilateral infiltrates (noncardiogenic diffuse pulmonary edema) are seen on chest imaging. Mechanical ventilation is often required to support patients with severe respiratory failure. Increased FiO₂ is required to maintain an adequate PaO₂ (PaO₂/FiO₂ ≤300 is a diagnostic requirement for ARDS). Bilateral infiltrates (Choice B) Diffuse alveolar hemorrhage can cause respiratory distress and diffuse bilateral infiltrates (blood within the alveoli). It is usually associated with specific drugs (eg, crack cocaine) or rheumatologic conditions (eg, antineutrophilic cytoplasmic antibody vasculitides) and is an unlikely complication of sepsis. (Choice C) Hospital-acquired pneumonia presents with fever and purulent cough (bacterial infection). Although it may sometimes progress to ARDS, the pneumonia is usually lobar/focal, rather than diffuse, in onset and does not cause rapidly progressive hypoxemic respiratory failure. (Choices D and E) Iatrogenic volume overload is rare in the absence of cardiac dysfunction. Postpartum cardiomyopathy can occur from the last month of gestation to 5 months after delivery; however, it is unlikely in this patient with no jugular venous distension, S3, or cardiomegaly on chest x-ray. Her mild edema of the lower extremities is likely due to pregnancy. (Choice F) Pulmonary thromboembolism can cause respiratory distress, but chest x-ray is typically clear (no alveolar opacities). Wedge-shaped areas of infarction (Hampton hump) or peripheral lucency (Westermark sign) due to reduced blood flow may be present occasionally. Educational objective: Findings of acute respiratory distress syndrome (ARDS) include respiratory distress, severe hypoxemia, and bilateral alveolar infiltrates on chest imaging, which are not explained by volume overload. Sepsis is a pathologic host inflammatory response to infection and a leading etiology of ARDS. References: The acute respiratory distress syndrome. (http://www.ncbi.nlm.nih.gov/pubmed/25829644) Approach to the patient with the acute respiratory distress syndrome. (http://www.ncbi.nlm.nih.gov/pubmed/25453418) Sepsis and acute respiratory distress syndrome: recent update. (http://www.ncbi.nlm.nih.gov/pubmed/27066082)

A 27-Year-Old Woman Is Admitted to the Hospital Urgently for Labor