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Acute respiratory distress syndrome: Clinical features and diagnosis in adults

Author
Mark D Siegel, MD
Section Editor
Polly E Parsons, MD
Deputy Editor
Geraldine Finlay, MD

INTRODUCTION

A distinct type of hypoxemic respiratory failure characterized by acute abnormality of both lungs was first recognized during the 1960s. Military clinicians working in surgical hospitals in Vietnam called it shock lung, while civilian clinicians referred to it as adult respiratory distress syndrome [1]. Subsequent recognition that individuals of any age could be afflicted led to the current term, acute respiratory distress syndrome (ARDS).

ARDS is an acute, diffuse, inflammatory lung injury that leads to increased pulmonary vascular permeability, increased lung weight, and a loss of aerated tissue [2]. Clinical hallmarks of ARDS are hypoxemia and bilateral radiographic opacities, while the pathological hallmark is diffuse alveolar damage (ie, alveolar edema with or without focal hemorrhage, acute inflammation of the alveolar walls, and hyaline membranes).

ARDS is associated with a variety of risk factors and etiologies. These conditions are grouped together under the term ARDS because the clinical, physiological features, pathological features, and management are similar regardless of the inciting event.

The clinical presentation, course, diagnostic evaluation, and diagnostic criteria of ARDS are reviewed here. The epidemiology, pathogenesis, etiology, and management of ARDS are discussed separately. (See "Acute respiratory distress syndrome: Epidemiology, pathophysiology, pathology, and etiology in adults" and "Acute respiratory distress syndrome: Prognosis and outcomes in adults" and "Mechanical ventilation of adults in acute respiratory distress syndrome" and "Acute respiratory distress syndrome: Supportive care and oxygenation in adults" and "Acute respiratory distress syndrome: Investigational or ineffective pharmacotherapy in adults".)

CLINICAL FEATURES

Clinical presentation — The clinical features of ARDS usually appear within 6 to 72 hours of an inciting event and worsen rapidly [3]. Patients typically present with dyspnea, cyanosis (ie, hypoxemia), and diffuse crackles. Respiratory distress is usually evident, including tachypnea, tachycardia, diaphoresis, and use of accessory muscles of respiration. A cough and chest pain may also exist.

                

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Literature review current through: Nov 2016. | This topic last updated: Tue Mar 15 00:00:00 GMT+00:00 2016.
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