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Fibroproliferative ARDS in the Era of Low-Tidal-Volume VentilationFibroproliferative ARDS

Manu Jain, MD
Author and Funding Information

From the Division of Pulmonary Critical Care, Department of Medicine, Northwestern University.

CORRESPONDENCE TO: Manu Jain, MD, Northwestern University, 240 E Huron Ave, McGaw M-332, Chicago, IL 60611; e-mail: m-jain@northwestern.edu


FINANCIAL/NONFINANCIAL DISCLOSURES: The author has reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;146(5):1140-1142. doi:10.1378/chest.14-1210
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Though mortality in ARDS has been improving, in unselected populations, mortality may still be as high as 40%.1 Patients with ARDS infrequently die of refractory hypoxemia and more often die due to sepsis and multiorgan failure, both complications of prolonged mechanical ventilation (MV). Inability to discontinue MV likely reflects disordered lung repair which may in part be due to excessive fibroblast activation. Markers of fibroblast activation such as procollagen III2 and transforming growth factor-β are elevated early in ARDS3 and are associated with increased mortality. Factors that have contributed to better ARDS outcomes include less-injurious MV strategies, judicious fluid management, and generally improved supportive care.4,5 As more patients with ARDS are surviving their acute illness, long-term outcomes for these patients have garnered increased attention. It has been shown in multiple studies that survivors of ARDS continue to have reduced health-related quality of life (HRQoL) for years after their acute illness.6 The cause of reduced HRQoL has most often been attributed to neuromuscular and psychosocial dysfunction.6 The contributions of residual pulmonary dysfunction have received less attention and a National Institutes of Health-sponsored ARDS workshop failed to identify fibroproliferation as a significant contributor to morbidity and mortality in the era of low-tidal-volume ventilation.7

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