Acute respiratory distress syndrome (ARDS) is a life-threatening lung injury that allows fluid to leak into the lungs. Breathing becomes difficult and oxygen cannot get into the body. Most people who get ARDS are already at the hospital for trauma or illness.
The acute respiratory distress syndrome (ARDS) is a common cause of respiratory failure in critically ill patients and is defined by the acute onset of noncardiogenic pulmonary oedema, hypoxaemia and the need for mechanical ventilation. ARDS occurs most often in the setting of pneumonia, sepsis, aspiration of gastric contents or severe trauma and is present in ~10% of all patients in intensive care units worldwide. Despite some improvements, mortality remains high at 30-40% in most studies. Pathological specimens from patients with ARDS frequently reveal diffuse alveolar damage, and laboratory studies have demonstrated both alveolar epithelial and lung endothelial injury, resulting in accumulation of protein-rich inflammatory oedematous fluid in the alveolar space. Diagnosis is based on consensus syndromic criteria, with modifications for under-resourced settings and in paediatric patients. Treatment focuses on lung-protective ventilation; no specific pharmacotherapies have been identified. Long-term outcomes of patients with ARDS are increasingly recognized as important research targets, as many patients survive ARDS only to have ongoing functional and/or psychological sequelae. Future directions include efforts to facilitate earlier recognition of ARDS, identifying responsive subsets of patients and ongoing efforts to understand fundamental mechanisms of lung injury to design specific treatments.
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aPEEP may be delivered non-invasively if the criteria are in the mild category. bThe Kigali definition was not directly compared with the Berlin definition in the original publication; patients in the Kigali study were not receiving mechanical ventilation. ARDS, acute respiratory distress syndrome; FiO2, fraction of inspired oxygen; PaO2, partial pressure of arterial oxygen; PEEP, positive end-expiratory pressure; SpO2, peripheral capillary oxygen saturation.
Selected on the basis of several clinical studies that were focused on the pathogenesis and prognosis of ARDS. ARDS, acute respiratory distress syndrome; FAS, tumour necrosis factor receptor superfamily member 6; FasL, tumour necrosis factor ligand superfamily member 6.
Most patients who present with the early phase of acute lung injury complain of feeling short of breath. If pneumonia is the cause, they will often have a cough that produces purulent sputum. On physical examination, they appear to be in moderate or severe respiratory distress with an elevated respiratory rate and tachycardia and they usually are working harder than normal to breathe. Hypoxaemia may manifest with evidence of cyanosis in their fingernail beds. Oxygen saturation on room air will be decreased. Respiratory deterioration in ARDS may be hyper-acute (for example, in the case of TRALI, in which respiratory failure is often fulminant) or may develop slowly over a period of hours to days.
Similarities in the chest radiographs from a patient with acute respiratory distress syndrome (ARDS) from influenza pneumonia (panel a) and a patient with pulmonary oedema due to cardiac failure (panel b) reflect the difficulty in identifying ARDS. In both cases, diffuse bilateral parenchymal opacities are consistent with alveolar filling. The cardiac silhouette (panel b) is slightly more globular, consistent with heart failure; however, this feature is not reliable for distinguishing ARDS from cardiogenic pulmonary oedema.
When evaluating a patient with suspected ARDS for the likely causative pathogen or pathogens, several factors should be taken into consideration. Whether infection is community-acquired or healthcare-associated is an important determinant of the potential pathogens (Fig. 7). Other important factors include age and the presence of comorbid conditions, exposure history and vaccination status. In addition to commonly isolated organisms, physicians should consider other uncommon but important pathogens that are linked to travel or residence in certain geographic distributions or to specific exposures. Examples include the Middle East respiratory syndrome coronavirus (MERS-CoV), avian influenza H5N1 and H7N9 viruses, hantavirus, human adenovirus subtype-55 (HAdV-55), Plasmodium species, Blastomyces dermatitidis, Coxiella burnetti, coccidioidomycosis, histoplasmosis, Mycobacterium tuberculosis and Yersinia pestis (Fig. 7). For instance, patients who have travelled to Saudi Arabia and have been exposed to camels have a higher risk of developing MERS-CoV; patients who live in the central valley of California have a higher risk of developing coccidioidomycosis.
Although true prevention trials have been challenging to conduct because of the rapid development and low incidence of ARDS, an alternative approach has been to test the value of early treatment in patients with incipient acute hypoxaemic respiratory failure, which in many cases progresses to ARDS. A French trial illustrated the potential value of this approach, comparing high-flow nasal cannula to noninvasive ventilation and face-mask oxygen in 310 non-intubated patients with a PaO2/FiO2
QOL studies have consistently demonstrated a decrement in physical function domains among survivors of ARDS. Early reports postulated these decrements might be due to exercise limitation from residual pulmonary function abnormalities212,213,214. Later studies combined pulmonary and functional outcome measures with QOL assessments, observing that both pulmonary function and self-perceived overall health gradually improve through 6 months after the acute illness. However, the severity of disability was not wholly explained by changes in pulmonary function or respiratory symptoms215. The aetiology of this reported dysfunction was uncertain. A later study combined measures of pulmonary function with an evaluation of quality-adjusted life years using the Quality of Well-Being Scale (a general health questionnaire that measures well-being over the previous 3 days in terms of physical activities, social activities, mobility and symptoms) and found that ARDS survivors had poor quality-adjusted survival associated with an important illness burden. Again, the specific contributors to this dysfunction remained unclear216.
Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition that prevents enough oxygen from getting to the lungs and into the blood. Infants can also have respiratory distress syndrome.
Binnie A, Herridge MS, Lee WL. Acute respiratory distress syndrome. In: Broaddus VC, Ernst JD, King TE, et al, eds. Murray and Nadel's Textbook of Respiratory Medicine. 7th ed. Philadelphia, PA: Elsevier; 2022:chap 134.
Acute respiratory distress syndrome manifests as rapidly progressive dyspnea, tachypnea, and hypoxemia. Diagnostic criteria include acute onset, profound hypoxemia, bilateral pulmonary infiltrates, and the absence of left atrial hypertension. Acute respiratory distress syndrome is believed to occur when a pulmonary or extrapulmonary insult causes the release of inflammatory mediators, promoting neutrophil accumulation in the microcirculation of the lung. Neutrophils damage the vascular endothelium and alveolar epithelium, leading to pulmonary edema, hyaline membrane formation, decreased lung compliance, and difficult air exchange. Most cases of acute respiratory distress syndrome are associated with pneumonia or sepsis. It is estimated that 7.1 percent of all patients admitted to an intensive care unit and 16.1 percent of all patients on mechanical ventilation develop acute lung injury or acute respiratory distress syndrome. In-hospital mortality related to these conditions is between 34 and 55 percent, and most deaths are due to multiorgan failure. Acute respiratory distress syndrome often has to be differentiated from congestive heart failure, which usually has signs of fluid overload, and from pneumonia. Treatment of acute respiratory distress syndrome is supportive and includes mechanical ventilation, prophylaxis for stress ulcers and venous thromboembolism, nutritional support, and treatment of the underlying injury. Low tidal volume, high positive end-expiratory pressure, and conservative fluid therapy may improve outcomes. A spontaneous breathing trial is indicated as the patient improves and the underlying illness resolves. Patients who survive acute respiratory distress syndrome 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.
Acute respiratory distress syndrome (ARDS) is a rapidly progressive disorder that initially manifests as dyspnea, tachypnea, and hypoxemia, then quickly evolves into respiratory failure. The American-European Consensus Conference (AECC) has published diagnostic criteria for ARDS: acute onset; ratio of partial pressure of arterial oxygen to fraction of inspired oxygen (PaO2/FiO2) of 200 or less, regardless of positive end-expiratory pressure; bilateral infiltrates seen on frontal chest radiograph; and pulmonary artery wedge pressure of 18 mm Hg or less when measured, or no clinical evidence of left atrial hypertension.1 Acute lung injury is a slightly less severe syndrome characterized by less profound hypoxemia but otherwise similar diagnostic criteria to ARDS.1 Because more than one-half of intensive care units (ICUs) in the United States are not staffed with intensivists,2 many primary care physicians provide care for patients with ARDS or acute lung injury. SORT: KEY RECOMMENDATIONS FOR PRACTICEClinical recommendationEvidence ratingReferencesWhen 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).A21, 22 Higher positive end-expiratory pressure values (12 to 18 or more cm H2O) should be considered for initial mechanical ventilation in patients with ARDS.B23 Conservative fluid therapy (targeting lower central pressures) in patients with ARDS may be associated with decreased days on a ventilator and increased days outside the intensive care unit.B24 Pulmonary artery catheters should not be used for the routine management of ARDS.A25, 26 Surfactant therapy does not improve mortality in adults with ARDS.A27 17dc91bb1f
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