title: Fluid flux and clearance in acute lung injury.
abstract: Acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome (ARDS), were presciently described nearly two centuries ago by René Laennec, later to be described clinically in the 1950s and 1960s. Substantial advances have been made in understanding the pathogenesis of these forms of permeability pulmonary edema, including Starling forces and cellular transport mechanisms involved in the generation and resolution of this form of lung injury. Functional animal models and clinically applicable case definitions for ALI and ARDS were instrumental in gaining these new insights. Although no specific pharmacological therapies for ALI and ARDS yet exist, outcomes have improved with advancements in respiratory and fluid-based supportive therapies, and methods to prevent the development or exacerbation of lung injury. Newer targeted therapies continue to be tested for efficacy in this condition where mortality rates frequently exceed 30%. In this article, we review the history of the pathophysiology of lung fluid and solute movement and the seminal clinical observations that brought that history to clinical relevance. We review the relevant lung structure and function and the dynamics of edema formation and resolution, and we describe the related clinical syndromes and the current treatment modalities.
authors.affiliation: Division of Pulmonary, Allergy and Critical Care, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, USA.
authors.forename: Greg S
authors.initials: GS
authors.lastname: Martin
authors.forename: Kenneth L
authors.initials: KL
authors.lastname: Brigham
mesh_terms: D055371:Acute Lung Injury / Q000209:etiology / Q000266:history / Q000503:physiopathology* / Q000628:therapy; D000222:Adaptation, Physiological; D000818:Animals; D002199:Capillary Permeability / Q000502:physiology; D004195:Disease Models, Animal; D015633:Extravascular Lung Water / Q000378:metabolism; D049673:History, 20th Century; D006801:Humans; D011650:Pulmonary Alveoli / Q000473:pathology / Q000503:physiopathology; D011654:Pulmonary Edema / Q000209:etiology / Q000503:physiopathology; D012128:Respiratory Distress Syndrome / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D013577:Syndrome