![]() ![]() History of needing water rescue, hypothermia History of institutionalization, patient with developmental disabilities, or decreased Glasgow Coma Scale score History of drug abuse, especially inhalational Productive cough, fever, pleuritic chest painīruising over the chest wall, associated injuries, history of motor vehicle crash or fall from a heightįacial burns, singed eyebrows, carbonaceous sputum, history of working near organic solvents or toxic chemicalsįever, rhinorrhea, cough, history of prematurity or congenital heart disease Organ hypoperfusion, low mean arterial pressure, oliguria, altered mental status, elevated lactate level Infection plus some of the following findings: temperature > 100.9☏ (38.3☌) or 90 beats per minute tachypnea altered mental status elevated C-reactive protein level arterial hypotension acute oliguria hyperlactatemia white blood cell count > 12,000 per mm 3 (12 × 10 9 per L), 10% immature forms 5 – 7 Chest radiography may show changes from air space opacification to coarse reticular opacification during this phase 8 (Figure 1). The end result of these changes is pulmonary edema, loss of surfactant, and deposition of dead cells and debris along the alveoli (hyaline membranes), which decrease pulmonary compliance and make gas exchange difficult. Intravascular coagulation in the alveolar capillaries leads to micro-thrombi. Inflammatory cells migrate across the vascular endothelial and alveolar epithelial surfaces and proinflammatory mediators and chemokines are released, leading to pathologic vascular permeability, gaps in the alveolar epithelial barrier, and necrosis of types I and II alveolar cells. This accumulation, in combination with neutrophil and alveolar epithelial cell activation, leads to tissue injury. ![]() In the exudative phase, which may last seven to 10 days, alveolar macrophages secrete mediators that lead to accumulation of inflammatory cells in the lung. 28, 52, 53ĪRDS progresses through several phases after a direct pulmonary or indirect extrapulmonary insult. Spontaneous breathing trials guided by a ventilator liberation (weaning) protocol should be initiated once a patient with ARDS begins to improve. 41Įnteral feeding should be initiated if a patient is anticipated to be on a ventilator for 72 hours or more. Prophylaxis for venous thromboembolism should be given to all patients hospitalized with ARDS. Prone positioning for 12 to 16 hours per day is recommended for patients with severe ARDS. Higher positive end-expiratory pressure values (12 cm H 2O) should be considered for initial mechanical ventilation in patients with ARDS. Randomized controlled trial, Cochrane review, and expert guidelines When mechanical ventilation is required, patients with ARDS should be started at lower tidal volumes (6 mL per kg) instead of at traditional volumes (10 to 15 mL per kg). Patients who survive ARDS are at risk of diminished functional capacity, mental illness, and decreased quality of life ongoing care by a primary care physician is beneficial for these patients. As patients with ARDS improve and the underlying illness resolves, a spontaneous breathing trial is indicated to assess eligibility for ventilator weaning. Prone positioning is recommended for some moderate and all severe cases. Low tidal volume and high positive end-expiratory pressure improve outcomes. Treatment of ARDS is supportive and includes mechanical ventilation, prophylaxis for stress ulcers and venous thromboembolism, nutritional support, and treatment of the underlying injury. ARDS often must be differentiated from pneumonia and congestive heart failure, which typically has signs of fluid overload. In-hospital mortality for patients with severe ARDS ranges from 46% to 60%. ARDS is responsible for one in 10 admissions to intensive care units and one in four mechanical ventilations. Most cases are associated with pneumonia or sepsis. Inflammatory cells damage the vascular endothelium and alveolar epithelium, leading to pulmonary edema, hyaline membrane formation, decreased lung compliance, and decreased gas exchange. ARDS is thought to occur when a pulmonary or extrapulmonary insult causes the release of inflammatory mediators, promoting inflammatory cell accumulation in the alveoli and microcirculation of the lung. Diagnostic criteria include onset within one week of a known insult or new or worsening respiratory symptoms, profound hypoxemia, bilateral pulmonary opacities on radiography, and inability to explain respiratory failure by cardiac failure or fluid overload. Acute respiratory distress syndrome (ARDS) is noncardiogenic pulmonary edema that manifests as rapidly progressive dyspnea, tachypnea, and hypoxemia. ![]()
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