Introduction Acute Respiratory Distress Syndrome (ARDS) results from acute lung injury that leads to non-cardiogenic pulmonary edema respiratory distress refractory hypoxemia decreased lung compliance Etiology acute endothelial damage resulting from aspiration infection pancreatitis multiple blood transfusions lung injury sepsis or shock major trauma large surface area burns fat emboli thromboembolism multi-system organ failure Prognosis high mortality rate (50% overall) is associated with ARDS even in setting of ICU Classification ARDS is represented by three phases Exudative phase initially hyaline membrane comprised of fibrin form Proliferative phase 3 days alveolar exudate resolves or organizes Fibrotic phase 3-4 weeks alveolar ducts and spaces undergo fibrosis Presentation Symptoms acute onset (12-48 hours) of dyspnea fever mottled or cyanotic skin Physical exam resistant hypoxia intercostal retractions rales/crackles and ronchi tachypnea Evaluation Hypoxemia is refractory to O2 3 different categories of ARDS based on degree of hypoxemia PaO2 / FIO2 ratio < 300 mm Hg= mild PaO2 / FIO2 ratio < 200 mm Hg= moderate PaO2 / FIO2 ratio < 100 mm Hg= severe Chest xray shows patchy pulmonary edema (air space disease) diffuse bilateral pulmonary infiltrates normal sized heart makes CHF less likely Respiratory compliance (<40 mL/cm H20) Positive end-expiratory pressure (>10cm H20) Corrected expired volume per minute (>10L/min) Differential Cardiogenic pulmonary edema (i.e. CHF or MI), bilateral pneumonia, SARS Treatment Nonoperative PEEP ventilation and steroids treat the underlying pathology/disease Operative early stabilization of long bone fractures (femur) Prevention closely monitor PEEP in patients at-risk of ARDS serial X-rays in concerning patients can assist in early identification and intervention Complications Pneumothorax secondary to ventilator with high PEEP
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