Which finding is a hallmark signs and symptoms that the patient is developing ARDS?
IntroductionFive decades ago, Ashbaugh and colleagues first used the term “syndrome of acute respiratory distress” (ARDS) to describe 12 patients with respiratory failure [1]. The hallmarks of the syndrome were hypoxemia refractory to supplemental oxygen, diffuse radiographic opacities, and histologic evidence of diffuse alveolar damage (DAD) in most but not all fatal cases. Over three decades later, the widely adopted American–European Consensus Conference (AECC) definition of ARDS facilitated research and aided cross-study comparison and translation of research findings to clinical practice [2]. The new Berlin definition refined the AECC definition by explicitly defining acute onset. Since the majority of patients destined to develop ARDS do so within the first 72 h after recognition of a clinical risk factor, with the rest progressing within a week, the Berlin definition explicitly defined “acute onset” as 7 days [3]. It defined mild, moderate, and severe ARDS with explicit ranges of PaO2/FiO2. It also attempted to improve the poor interobserver agreement on the AECC radiographic criteria by explicitly describing qualifying opacities and providing example radiographs [4, 5]. As left atrial hypertension and ARDS may coexist, the Berlin definition abandoned the pulmonary artery occlusion pressures exclusion [6]. Finally, the Berlin definition added the requirement for a known clinical risk factor (e.g., pneumonia, sepsis, trauma, etc.), and if none is apparent then additional testing is recommended to exclude congestive heart failure. Both the AECC and the Berlin definition retain the central elements of Ashbaugh’s original description. However, both the definitions have only moderate sensitivity and specificity for identifying patients who have DAD on post mortem examination, even in the severe subgroup of the Berlin definition [7, 8]. Moreover, lung biopsy findings in patients with what is assumed to be unresolving ARDS frequently show a number of pathologic entities other than DAD. From our clinical experience, we discuss ten of these clinical entities that may be mistaken for ARDS. Show
Ten diseases that may be mistaken for ARDSTable 1 lists ten clinical entities that may be mistaken for ARDS. While it is beyond the scope of this brief report to outline a diagnostic approach to all of these entities, we offer a few observations from clinical experience. While some entities may present in an accelerated time course of several–many days, which would be consistent with the time course for ARDS, more typically they present with a longer time course. This should raise suspicion that the clinical problem is something other than ARDS. Another clinical clue is the absence of a known clinical risk factor for ARDS; or if a clinical risk factor has been identified and treated appropriately (for example, pneumonia), progression should stimulate consideration of other entities. Occasional signs and symptoms (e.g., hemoptysis, association with rheumatologic conditions, or with glomerulonephritis) may distinguish an entity from ARDS. There is substantial overlap in the radiographic findings between ARDS and these entities, but some findings may distinguish some entities from ARDS (e.g., honeycombing in pulmonary fibrosis and cavitary nodules in granulomatosis with polyangiitis) [9]. Some bronchoalveolar lavage findings may also help to distinguish some of these entities from ARDS as noted in Table 1 [10]. A single-center study suggested that open lung biopsy in patients with suspected ARDS may improve outcomes if it contributes to management [11]. In general, the combination of a careful history and physical examination, serologic testing for connective tissue disease and vasculitis, computed tomography (CT) scan, and bronchoscopy findings as presented in Table 1 should limit the need for open lung biopsy to establish a diagnosis in enigmatic cases that masquerade as ARDS. Table 1 Ten clinical entities that may be mistaken for acute respiratory distress syndrome Full size table Implications for treatmentIf a patient with one of these ten ARDS mimics requires mechanical ventilation, there may be a substantial risk of ventilator-induced lung injury because inflammatory processes increase the vulnerability of the lung parenchyma to mechanical stress. Moreover, the volume of aerated lung is reduced, making the aerated lung vulnerable to overdistension. Therefore, we recommend using a lung-protective approach, as in ARDS, with an initial tidal volume goal of approximately 6 ml/kg predicted body weight [12]. The optimal level of positive end-expiratory pressure (PEEP) in ARDS is still controversial, and we know of no data to guide us in the use of PEEP in patients with the entities described in Table 1. Whereas use of steroids in unresolving ARDS remains a matter of debate [13, 14], some of the disease entities in Table 1 should prompt clinicians to start steroids without delay. This holds true for systemic lupus, alveolar hemorrhage complicating polyangiitis and Goodpasture’s syndrome, acute eosinophilic pneumonia, and most patients with nonspecific interstitial pneumonitis. Other diagnoses will require additional therapies (such as plasmapheresis and immunosuppressive therapy for Goodpasture’s syndrome and additional immunosuppressive therapy for polyangiitis). Some require a careful search for an environmental or occupational exposure (hypersensitivity pneumonitis) or an offending drug exposure to prevent recurrence or progression and improve clinical outcomes. Close interaction with a pneumologist and/or a physician skilled in systemic diseases is often helpful to coordinate care. The distinction between ARDS and some of the other entities may have important prognostic implications. Although the mortality rate from ARDS is high, most patients recover from the acute process, and many return to productive lives. In contrast, idiopathic pulmonary fibrosis (IPF) progresses relentlessly, leading to irreversible respiratory failure. If the diagnosis of IPF can be established before onset of respiratory failure, patients can be counseled about their condition and make more informed decisions about end-of-life care. References
Download references Conflicts of interestOn behalf of all authors the corresponding author states that there is no conflict of interest related to this manuscript. Author informationAuthors and Affiliations
Authors
Corresponding authorCorrespondence to Claude Guérin. Rights and permissionsAbout this articleCite this articleGuérin, C., Thompson, T. & Brower, R. The ten diseases that look like ARDS. Intensive Care Med 41, 1099–1102 (2015). https://doi.org/10.1007/s00134-014-3608-x Download citation
Keywords
What are the 5 hallmark signs and symptoms of ARDS?The signs and symptoms of ARDS can vary in intensity, depending on its cause and severity, as well as the presence of underlying heart or lung disease.. Severe shortness of breath.. Labored and unusually rapid breathing.. Low blood pressure.. Confusion and extreme tiredness.. What is the hallmark of ARDS?Acute respiratory distress syndrome (ARDS) is a diffuse inflammatory reaction of the lung to an insult and is characterized by increased pulmonary capillary permeability, lung edema, and atelectasis. The histological hallmark of ARDS is diffuse alveolar damage and its pathognomonic hyaline membranes.
Which PAWP is one of the hallmark signs of ARDS?Increased capillary permeability is a pathophysiological hallmark of ARDS, and the severity of pulmonary edema is positively associated with the prognosis of ARDS [1].
Which is a classic finding for a patient with ARDS?Findings of ARDS — ARDS should be suspected in patients with progressive symptoms of dyspnea, an increasing requirement for oxygen, and alveolar infiltrates on chest imaging within 6 to 72 hours of an inciting event (table 1).
|
