A 34-year-old man is being evaluated for acute hypoxemic respiratory failure. Two days ago, the patient was brought to the emergency department due to opioid and alcohol intoxication. While unconscious, he vomited profusely and then rapidly developed hypoxia and shortness of breath that has continued to worsen. Today, temperature is 38.4 C (101.1 F), blood pressure is 108/74 mm Hg, pulse is 120/min, and respirations are 26/min. Diffuse crackles are heard on auscultation. The extremities are warm, well perfused, and without edema. Chest x-ray reveals bilateral alveolar opacities. The results of arterial blood gas analysis on room air are as follows: Which of the following pathologic processes is the primary contributor to this patient's lung findings?

Question

A 34-year-old man is being evaluated for acute hypoxemic respiratory failure.  Two days ago, the patient was brought to the emergency department due to opioid and alcohol intoxication.  While unconscious, he vomited profusely and then rapidly developed hypoxia and shortness of breath that has continued to worsen.  Today, temperature is 38.4 C (101.1 F), blood pressure is 108/74 mm Hg, pulse is 120/min, and respirations are 26/min.  Diffuse crackles are heard on auscultation.  The extremities are warm, well perfused, and without edema.  Chest x-ray reveals bilateral alveolar opacities.  The results of arterial blood gas analysis on room air are as follows:  Which of the following pathologic processes is the primary contributor to this patient's lung findings?

Quizplus · Accepted Answer

11ec160b_3b2b_5741_9249_49a064d49815_MD0001_00 This patient has acute hypoxemic respiratory failure following an episode of emesis while unconscious. He most likely developed acute respiratory distress syndrome (ARDS) due to the aspiration of gastric contents. Alveolar epithelial damage (eg, by gastric hydrochloric acid) causes release of damage-associated molecular patterns (DAMPs) (eg, mitochondrial DNA, extracellular histones) into the extracellular space. These DAMPs bind to pattern recognition receptors on innate immune cells, promoting the release of proinflammatory cytokines (eg, tumor necrosis factor-alpha, IL-1, IL-6) that recruit neutrophils to the alveoli. The activated neutrophils then release proteases and reactive oxygen species (ROS) that further damage the alveolar membrane. The cascade of lung damage leads to failure of alveolar tight junctions and exudation of fibrinous proteinaceous fluid into the airspaces, resulting in pulmonary edema. Therefore, the origin of pulmonary edema in ARDS is abnormal vascular permeability rather than hydrostatic congestion due to left ventricular dysfunction (ie, noncardiogenic). Surfactant is depleted and dysfunctional, leading to alveolar collapse (increased surface tension causes alveolar walls to cling together), further impairing lung inflation. The flooding and collapse of alveoli produce diffuse crackles on lung auscultation and bilateral infiltrates on chest x-ray. Several important clinical entities can mimic ARDS: diffuse alveolar hemorrhage (DAH), acute eosinophilic pneumonia (AEP), and acute hypersensitivity pneumonitis (HP). Like ARDS, these conditions present with acute severe hypoxemia, diffuse bilateral infiltrates, and fever. However, the pathophysiologic bases of these conditions are fundamentally different from that of ARDS. (Choice A) DAH is characterized by widespread alveolar bleeding due typically to small-vessel vasculitis, which can be driven by autoantibodies (eg, against basement membrane collagen [anti-GBM disease]) causing pulmonary capillary necrosis with subsequent hemorrhage. ARDS is an innate immune response driven primarily by neutrophils rather than autoantibodies. (Choice B) AEP is an idiopathic form of pneumonia caused by eosinophilic invasion of the lung tissue, often with hyaline membranes, a nonspecific finding of inflammatory fibrinous edema. ARDS also features prominent hyaline membranes, but the inflammation is driven by neutrophils rather than eosinophils. (Choice C) HP is characterized by lymphocyte-driven granuloma formation in response to extrinsic antigens (eg, mold, bird dander). ARDS is characterized by neutrophilic, rather than granulomatous, inflammation. Educational objective: Acute respiratory distress syndrome involves acute neutrophilic lung inflammation with widespread alveolar damage due to proteases and reactive oxygen species, leading to failure of the vascular barrier and exudative pulmonary edema.

A 34-Year-Old Man Is Being Evaluated for Acute Hypoxemic Respiratory