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In 1967, Ashbaugh and colleagues reported a case series of 12 patients with lung disease, acute onset of shortness of breath, and hypoxemia.[1-5] They were the first to describe what came to be known as acute respiratory distress syndrome (ARDS) (shown), in which oxygen transfer from the alveoli to the pulmonary capillaries is severely impaired.[1,2,5,6] (The initial term "adult respiratory distress syndrome" was revised to "acute respiratory distress syndrome," because the syndrome occurs in adults and children.) However, although it has been nearly 50 years since the initial description, the optimal definition of ARDS remains controversial.[2,3,5]
In 1994, the American-European Consensus Conference (AECC) developed a definition of ARDS[2-5,7] by introducing and defining the term "acute lung injury" (ALI) with the following criteria[5-7]:
The AECC criteria for ARDS was the same as those for ALI, except the PaO2/FiO2 ratio was lowered to 200 mm Hg or less[3,5]; thus, the degree of hypoxemia separated ARDS from ALI.
Image courtesy of Wikimedia Commons/James Heilman, MD.
Following introduction of the new AECC definition, there was confusion among clinicians regarding issues that were not described or addressed, such as the timeframe for defining "acute," the cause of the lung injury and the different mechanisms for such injury, the PEEP level used, and the nonspecificity of the imaging criterion.[8] In response, in 2011, the European Society of Intensive Care Medicine (ESICM), with the support of the American Thoracic Society (ATS), convened an international panel in Berlin and developed the Berlin definition for ARDS ("Berlin criteria," "Berlin definition"), with a focus on the feasibility, reliability, validity, and objective evaluation of its performance.[3,9]
The essential aspects of the new Berlin Criteria (shown) are as follows[5,8-10]:
The important values to note are "100" and "200." Severe ARDS has a PaO2/FIO2 ratio lower than 100, whereas mild ARDS has a PaO2/FIO2 ratio above 200.
Adapted table courtesy of the World Health Organization (WHO).[11]
Lung epithelial injury causes ARDS.[12] Whereas lung endothelial injury is a prerequisite for the development of protein-rich pulmonary edema in ARDS, injury to the lung endothelium alone is usually not sufficient to cause ARDS in the absence of some degree of injury to the lung epithelium.[12]
Lung epithelial injury progresses through three phases. In the first phase, the acute or exudative phase (shown), alveolar flooding occurs[6] and is characterized by inflammation, pulmonary edema, and capillary leak. This results in refractory hypoxemia and decreased lung compliance. In some patients, this phase resolves in 4-7 days. Other patients may progress to the second phase, in which fibrosing alveolitis occurs and is characterized by continued hypoxemia. This causes worsening pulmonary compliance and pulmonary hypertension and lasts about 1-2 weeks. In the third phase, recovery is noted, with improvement in hypoxemia, full resolution of radiologic abnormalities, and return of the normal pulmonary function for many survivors.[4,6,12]
The photomicrograph shows the early proliferative stage of ARDS. Note the type 2 pneumocyte proliferation, with widening of the septae and proliferation of interstitial fibroblasts.
Image courtesy of Medscape.
The exact incidence and prevalence of ARDS is unclear, owing in large part to variations in how it is defined, as well as to differences in the regions and populations studied. In the United States, the incidence of ARDS may be rising, and the hospital mortality (38.5%) has not significantly improved over the past several decades.[4,6,12,13] Trends in 60-day mortality have shown some change over time. Trial data from the National Heart, Lung, and Blood Institute (NHLBI) ARDS Network (ARDSNet) note a decline in 60-day mortality from 1996-1997 (36%) to 2004-2005 (26%).[10] More recent ARDSNet data have reported a 60-day mortality of 22% in adult patients.
The most common risk factor for the development of ARDS is severe sepsis (79%), with either a pulmonary or nonpulmonary source.[13] Other risk factors include aspiration, toxic inhalation, lung contusion, and acute pancreatitis.[2,13] Environmental and genetic factors that contribute to a patient's susceptibility and the severity of ARDS have emerged as a major research focus; these include the chronic use of alcohol, exposure to cigarettes,[10] diabetes mellitus, and prehospital antiplatelet therapy.[2] In addition, clinical risk factors for mortality are advanced age, immunosuppression, the severity of illness, and the presence of sepsis.[2,14]
The chest radiograph demonstrates ARDS in a patient with murine typhus.
Image courtesy of van der Vaart TW, van Thiel PP, Juffermans NP, et al. Emerg Infect Dis. 2014;20(8):1375-7. [Open access.] PMID: 25062435, PMCID: PMC4111165.
A potential mechanism underlying the development of ARDS is the "multiple-hit model" (shown), in which a series of predisposing conditions combined with multiple hits (ie, modifying factors and treatments) triggers a chain reaction that causes progression from an initial lung injury to mild, moderate, or severe ARDS.[15]
Genetic risk factors for the development of ARDS have been not well investigated.[15]
Image courtesy of de Haro C, Martin-Loeches I, Torrents E, Artigas A. Ann Intensive Care. 2013;3(1):11. [Open source.] PMID: 23617961, PMCID: PMC3639084.
Clinically, patients with ARDS experience acute hypoxemic respiratory failure, which manifests as dyspnea, tachypnea, and tachycardia.[6] On chest auscultation, diffuse bibasilar crackles or wheezing may be present. Other features may include cyanosis and the presence of pulmonary hypertension and multiple organ dysfunction syndrome (MODS).[6]
The differential diagnosis of ARDS includes acute cardiogenic pulmonary edema, high altitude pulmonary edema, lymphangitic carcinomatosis, pulmonary veno-occlusive disease, pulmonary vasculitis, collagen vascular disease–associated interstitial lung diseases, acute hypersensitivity pneumonitis, and acute eosinophilic pneumonia.[17]
The radiographs demonstrate left lower lobe pneumonia (left) transitioning to ARDS (right) over an 18-hour period following airway intubation in a patient without cardiac disease.
Image courtesy of Marini JJ. Crit Care. 2013;17 suppl 1:S1. [Open access.] PMID: 23514222, PMCID: PMC3603465.
The diagnosis of ARDS requires excluding the presence of left atrial hypertension on the basis of clinical findings.[12] Thus, ARDS is a clinical diagnosis. No specific laboratory abnormalities are observed beyond the expected disturbances in gas exchange. As noted earlier, in ARDS, the PaO2/FIO2 ratio is 200 or less.[10]
To rule out cardiogenic pulmonary edema, it may be helpful to obtain levels of plasma B-type natriuretic peptide (BNP) (BNP level <100 pg/mL favors the diagnosis of ALI/ARDS vs cardiogenic pulmonary edema) as well as an echocardiogram.[17] In selected cases, invasive hemodynamic monitoring with a pulmonary artery (Swan-Ganz) catheter may also be helpful to distinguish cardiogenic from noncardiogenic pulmonary edema.[16,17] However, the use of the catheter is controversial, because it does not appear to improve survival in patients with suspected or confirmed ARDS.[16,17]
The chest sonogram on the left shows an area of normal lung ("spared area") surrounded by homogeneously distributed alveolar-interstitial syndrome (subpleural interlobular septal thickening). These features are more characteristic of ARDS. The chest sonogram on the right reveals a relatively solid "white lung" appearance, which is more typical for cardiogenic pulmonary edema.
Image courtesy of Copetti R, Soldati G, Copetti P. Cardiovasc Ultrasound. 2008;6:16. [Open access.] PMID: 18442425, PMCID: PMC2386861.
Clinical evaluation and routine chest radiography are sufficient in most cases of the patients presenting with ARDS. Chest radiographs reveal bilateral diffuse alveolar and interstitial infiltrates, which can be difficult to differentiate from congestive heart failure or fluid overload.[6]
In general, computed tomography (CT) scanning is not required to evaluate patients with suspected or confirmed ARDS. However, this imaging modality is more sensitive than plain chest radiography in the detection of pulmonary interstitial emphysema, pneumothorax, pneumomediastinum, pleural effusions, cavitation, and mediastinal lymphadenopathy.[17]
Patients with ARDS should undergo 2-dimensional (2-D) echocardiography to screen for potential cardiac abnormalities and/or cardiogenic causes of pulmonary edema.[17]
Consider bronchoscopy to evaluate for potential infection, alveolar hemorrhage, or acute eosinophilic pneumonia in acutely ill patients with bilateral pulmonary infiltrates on chest films.[17]
Histologic findings include diffuse alveolar damage,[2,17] alveolar atelectasis, hyperemia, interstitial and intra-alveolar damage, numerous alveolar macrophages, hyaline membrane formation, and diffuse interstitial hyperemia.[16,17]
The sonograms (A, B) demonstrate lung consolidations with air bronchograms in the posterior lung fields in a patient with ARDS.
Image courtesy of Copetti R, Soldati G, Copetti P. Cardiovasc Ultrasound. 2008;6:16. [Open access.] PMID: 18442425, PMCID: PMC2386861.
The "baby lung" concept was introduced in the 1980s to describe the characteristic reduced lung volume and irregular distribution of regional atelectasis seen on CT scans (shown) in patients with ARDS (ie, comparable to the size of a baby's lung).[19] The volume of ventilated lung is greater superiorly, whereas the inferior lung is collapsed and not ventilated. Therefore, decreasing tidal volume is important to avoid overdistention of the aerated lung regions and to avoid causing further lung injury.
The CT scan shows the position of the esophagus in relation to the interface between open and closed lung units in a patient with early-stage ARDS.
Image courtesy of Marini JJ. Crit Care. 2013;17 suppl 1:S1. [Open access.] PMID: 23514222, PMCID: PMC3603465.
Management of ARDS is based on the early detection of sepsis and adequate therapy, which includes source control and early appropriate antimicrobial therapy.[2,15]
Lung protective mechanical ventilation is the main treatment for ARDS.[2,15,20,21] It reduces the accumulation of pulmonary edema by preserving the barrier properties of the alveolar endothelium and alveolar epithelium, as well as benefits nonpulmonary organ function.[10] However, mechanical ventilation can cause lung injury by mechanisms such as diffuse alveolar damage, pulmonary edema, and local production of mediators; these complications are known as ventilation-induced lung injury (VILI).[15,22]
Higher PEEP levels have not been associated with improved survival in patients with ARDS.[4,23,24] Moreover, data from the ARDS Network trial published in 2000 confirmed that mechanical ventilation with lower tidal volumes (eg, 6 mL/kg predicted body weight) resulted in an increase in the number of ventilator-free days as well as a reduction in in-hospital mortality.[4,10,15,23,25]
Image courtesy of Medscape/Ryland P Byrd, Jr, MD.
Prone positioning of the patient and the use of neuromuscular blockers reduced mortality in several studies.[4,13,23] However, adverse effects of prone positioning include pressure sores[21,31] and endotracheal tube displacement.[21,32] The number needed to treat (NNT) to save one life with prone positioning was six.[32]
Fluid balance is another important strategy in the management of patients with ARDS.[4,15,23] Its primary beneficial mechanism can be explained by a favorable effect on Starling forces. Thus, lower vascular pressures reduce transvascular fluid filtration, particularly in the presence of increased lung vascular permeability.[10]
Salvage therapies include nitric oxide[12] and extracorporeal membrane oxygenation (ECMO).[21,23]
Images courtesy of Dreamstime/Oocoskun (top right), Dreamstime/Phudui (left center), and Dora Izaguirre-Anariba, MD (bottom right).
ECMO (shown) is used to support oxygenation of patients with severe ARDS. It allows for the use of very low ventilator settings to reduce lung induce injury.[23] During the H1N1 influenza epidemic in 2009, the use of ECMO may have been key in the survival of many critically ill patients with ARDS.[26,27]
The single-site approach to venovenous ECMO cannulation involves the insertion of a dual-lumen cannula into the jugular vein and extended into the inferior vena cava.[28,29] Venous blood is drained through a lumen with ports in the superior and inferior vena cava; then, oxygenated blood is reinfused through the second lumen, exiting at the right atrium. The reinfusion port is positioned to direct oxygenated blood across the tricuspid valve and into the right ventricle, which, when correctly placed, allows a significant reduction in the recirculation of blood.[28,29] Echocardiography is used to confirm the placement.
Image courtesy of Wikimedia Commons/Cmenesesoliveira.
Prevention of ARDS may be its best treatment. Preventive strategies in critically ill patients include the following[30]:
Image courtesy of de Haro C, Martin-Loeches I, Torrents E, Artigas A. Ann Intensive Care. 2013;3(1):11. [Open source.] PMID: 23617961, PMCID: PMC3639084.
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