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Essentials of Diagnosis
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Onset of respiratory distress, often progressing to respiratory failure, within 7 days of a clinical insult
New bilateral radiographic pulmonary opacities not explained by pleural effusion, atelectasis, or nodules
Respiratory failure not fully explained by heart failure or volume overload
Impaired oxygenation, with ratio of partial pressure of oxygen in arterial blood (PaO2) to fractional concentration of inspired oxygen (FIO2) < 300 mm Hg, with positive end-expiratory pressure (PEEP) ≥ 5 cm H2O
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General Considerations
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Damage to capillary endothelial cells and alveolar epithelial cells is common and results in increased vascular permeability and decreased production and activity of surfactant, leading to
Pro-inflammatory cytokines released from stimulated inflammatory cells appear to be pivotal in lung injury
Severity of ARDS is based on the level of oxygenation impairment
Mild: PaO2/FIO2 ratio of between 200 mm Hg and 300 mm Hg
Moderate: PaO2/FIO2 ratio between 100 mm Hg and 200 mm Hg
Severe: PaO2/FIO2 ratio < 100 mm Hg
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Systemic insults associated with ARDS
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Pulmonary insults associated with ARDS
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Aspiration of gastric contents
Near-drowning
Pneumonia, bacterial, viral, or fungal infection
Miliary tuberculosis
Toxic gas inhalation
Nitrogen dioxide
Chlorine
Sulfur dioxide
Ammonia
Smoke inhalation
Free-base cocaine smoking
Embolism of thrombus, fat, air, or amniotic fluid
Lung contusion
Acute eosinophilic pneumonia
Cryptogenic organizing pneumonia
Acute upper airway obstruction
Lung reexpansion or reperfusion
Radiation exposure
High-altitude exposure
Oxygen toxicity
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Rapid onset of profound dyspnea, usually 12–48 hours after the initiating event
Labored breathing, tachypnea, intercostal ...