A 45-year-old previously healthy man is brought to the emergency department after being hit by a car while cycling. The patient is hypotensive and tachycardic on arrival and has comminuted fractures of the pelvis and lower extremities. Volume resuscitation is performed with intravenous fluids and multiple units of packed red blood cells and plasma. Several hours later, the patient develops worsening dyspnea and hypoxia. Chest imaging reveals new bilateral infiltrates. Endotracheal intubation is performed for respiratory support. Despite aggressive resuscitation, the patient dies 24 hours later. Autopsy examination of the lungs shows protein-rich fluid within the alveolar airspaces. Breakdown of the barrier formed by which of the following cells most likely contributed to this patient's pulmonary pathology?

Question

A 45-year-old previously healthy man is brought to the emergency department after being hit by a car while cycling.  The patient is hypotensive and tachycardic on arrival and has comminuted fractures of the pelvis and lower extremities.  Volume resuscitation is performed with intravenous fluids and multiple units of packed red blood cells and plasma.  Several hours later, the patient develops worsening dyspnea and hypoxia.  Chest imaging reveals new bilateral infiltrates.  Endotracheal intubation is performed for respiratory support.  Despite aggressive resuscitation, the patient dies 24 hours later.  Autopsy examination of the lungs shows protein-rich fluid within the alveolar airspaces.  Breakdown of the barrier formed by which of the following cells most likely contributed to this patient's pulmonary pathology?

Quizplus · Accepted Answer

11ec160b_3b4d_0f5a_9249_63ab714f634e_MD0001_00 This patient who developed hypoxia, pulmonary edema (bilateral pulmonary infiltrates), and protein-rich fluid in the alveoli had acute respiratory distress syndrome (ARDS). ARDS is a severe inflammatory reaction that occurs in the lungs and results in respiratory failure with hypoxemia and noncardiogenic pulmonary edema. Risk factors include sepsis, severe trauma (eg, long-bone fractures with fat embolism, extensive tissue injury), and transfusion of blood products, all of which can initiate pulmonary injury and trigger a cascade of inflammation: In response to injury, alveolar macrophages release multiple proinflammatory cytokines that recruit neutrophils to the lungs (Choice A). Upon arrival to pulmonary tissue, the neutrophils release inflammatory mediators (eg, proteases, free radicals). This increases inflammation and leads to damage to the pulmonary endothelium and alveolar pneumocytes. The alveolar-capillary barrier, which is formed by the endothelial cells and type I pneumocytes, is then destroyed, allowing fluid and red blood cells to escape the vascular and interstitial spaces and pour into the alveoli. There, they combine with material from necrotic cells and form a thick proteinaceous fluid and a hyaline membrane. Destruction of type II pneumocytes, which normally produce surfactant and proliferate in response to injury, leads to alveolar collapse (but does not cause destruction of the alveolar capillary barrier) (Choice F). The net effect is impaired alveolar gas exchange and respiratory failure, with affected patients having a high mortality rate. (Choices B and D) Ciliated epithelium and goblet cells line the larger airways. Goblet cells secrete mucus that traps particulate matter (eg, dust, bacteria), while ciliated epithelial cells assist in its elimination by sweeping the mucus up the bronchi and trachea to the pharynx, where it is swallowed. These cells are not prominently involved in ARDS. (Choice C) Club cells (formerly called Clara cells) are nonciliated, secretory constituents of the terminal respiratory epithelium. They secrete protein and surfactant components and help detoxify inhaled substances (eg, tobacco smoke). They are not prominently involved in ARDS. Educational objective: Acute respiratory distress syndrome is a severe inflammatory reaction that occurs in the lungs and results in hypoxemia and noncardiogenic pulmonary edema. Pulmonary injury leads to an inflammatory response resulting in breakdown of the capillary-alveolar barrier (created by type I pneumocytes and endothelial cells), increased capillary permeability, intraalveolar fluid accumulation, and hyaline membrane formation.

A 45-Year-Old Previously Healthy Man Is Brought to the Emergency