Acute respiratory distress syndrome (ARDS)

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Acute respiratory distress syndrome:
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).
Clinical presentation — The clinical features of ARDS usually appear within 6 to 72 hours of an inciting event and worsen rapidly. 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.
Arterial blood gases reveal hypoxemia, which is often accompanied by acute respiratory alkalosis and an elevated alveolar-arterial oxygen gradient. High concentrations of supplemental oxygen are generally required to maintain adequate oxygenation.
The initial chest radiograph typically has bilateral alveolar infiltrates, while computed tomography (CT) usually reveals widespread patchy or coalescent airspace opacities that are usually more apparent in the dependent lung zones. The infiltrates do not have to be diffuse or severe, as bilateral infiltrates of any severity are sufficient.
Clinical findings related to the precipitant may also exist at presentation. As an example, in patients with ARDS due to sepsis, there may be fever, hypotension, leukocytosis, lactic acidosis, and disseminated intravascular coagulation (DIC).

This Tutorial Covers:
— Noncargiogenic Pulmonary Edema
— Large Insult

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