A 60-year-old woman with a history of poorly controlled type 2 diabetes mellitus comes to the emergency department due to worsening perianal pain. The patient is febrile, hypotensive, and tachycardic. Physical examination reveals tenderness and swelling in the perianal and gluteal region with dusky overlying skin and palpable crepitus. Leukocyte count is 27,000/mm³, and CT scan shows edema of the gluteal and perineal subcutaneous tissue with free gas. Intravenous fluids and antibiotics are initiated, and the patient undergoes urgent surgical debridement of the necrotic tissue. Several hours later, she experiences increasing dyspnea and hypoxemia. Chest x-ray reveals new bilateral lung infiltrates. Bedside echocardiography shows a hyperdynamic left ventricle with no significant valve disease. Which of the following best describes this patient's current pulmonary condition?

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11ec25c8_d936_8b10_bc81_83ccf139c5d8_MD0003_00 This patient with hypoxemia and bilateral lung infiltrates likely has acute respiratory distress syndrome (ARDS) due to sepsis from necrotizing fasciitis. ARDS involves an inflammatory response that leads to capillary leakage and diffuse pulmonary edema. Fluid from pulmonary edema fills the alveoli and facilitates alveolar collapse. Alveolar ventilation (V) is zero, which results in an extreme ventilation/perfusion (V/Q) mismatch (right-to-left intrapulmonary shunting), causing hypoxemia. Because diffuse pulmonary edema prevents air from reaching the alveoli throughout much of the lungs (eg, >50%), an increase in the fraction of inspired O₂ (FiO₂) does not correct the hypoxemia. Increased alveolar-arterial (A-a) gradient is another characteristic of pulmonary edema, as with any process causing V/Q mismatch or impaired diffusion across the A-a membrane. Finally, pulmonary edema also leads to fluid collection within the lung interstitium, resulting in stiffening of the lungs (decreased lung compliance). In contrast to hypoxemia due to diffuse pulmonary edema, hypoxemia due to localized intrapulmonary shunting (eg, lobar pneumonia, atelectasis, basilar pulmonary edema) typically does correct with increased FiO₂ because only a portion of the lungs is affected and the normally ventilated alveoli compensate via increased O₂ transfer. (Choices A and C) Interstitial lung disease involves stiffening of the alveolar walls and decreased lung compliance. Emphysema involves destruction of alveolar walls and increased lung compliance. In both, hypoxemia results largely from impaired diffusion of O₂ across the disrupted A-a membrane as well as some V/Q mismatching. Because alveolar ventilation is generally intact, increased FiO₂ usually improves the hypoxemia. (Choice B) Obesity hypoventilation syndrome involves decreased compliance of the chest wall with impaired lung expansion. Although ventilation is decreased, diffusion and V/Q matching are intact; therefore, the A-a gradient is normal and increased FiO₂ increases gas exchange and improves hypoxemia. (Choice E) Large-scale dead-space ventilation (eg, massive pulmonary embolism) is the other major cause of hypoxemia that does not correct with supplemental O₂. Although alveolar ventilation is normal, there is no perfusion of large portions of the lung (extreme V/Q mismatch), resulting in minimal gas exchange. Educational objective: Pulmonary edema causes hypoxemia due to right-to-left intrapulmonary shunting, an extreme ventilation/perfusion (V/Q) mismatch. When the edema is diffuse, alveolar ventilation is zero throughout much of the lungs and the hypoxemia does not correct with supplemental O₂. As with any type of V/Q mismatch, pulmonary edema leads to an increase in the alveolar-arterial O₂ gradient. It also causes stiffening of the lungs and decreased lung compliance. References: Gas exchange and ventilation-perfusion relationships in the lung. (http://www.ncbi.nlm.nih.gov/pubmed/25063240)

A 60-Year-Old Woman with a History of Poorly Controlled Type