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Background: Since publication of the 2012 Berlin definition of acute respiratory distress syndrome (ARDS), several developments have supported the need for an expansion of the definition, including the use of high-flow nasal oxygen, the expansion of the use of pulse oximetry in place of arterial blood gases, the use of ultrasound for chest imaging, and the need for applicability in resource-limited settings. Methods: A consensus conference of 32 critical care ARDS experts was convened, had six virtual meetings (June 2021 to March 2022), and subsequently obtained input from members of several critical care societies. The goal was to develop a definition that would 1 ) identify patients with the currently accepted conceptual framework for ARDS, 2 ) facilitate rapid ARDS diagnosis for clinical care and research, 3 ) be applicable in resource-limited settings, 4 ) be useful for testing specific therapies, and 5 ) be practical for communication to patients and caregivers. Results: The committee made four main recommendations: 1 ) include high-flow nasal oxygen with a minimum flow rate of ⩾30 L/min; 2 ) use Pa O 2 :Fi O 2  ⩽ 300 mm Hg or oxygen saturation as measured by pulse oximetry Sp O 2 :Fi O 2  ⩽ 315 (if oxygen saturation as measured by pulse oximetry is ⩽97%) to identify hypoxemia; 3 ) retain bilateral opacities for imaging criteria but add ultrasound as an imaging modality, especially in resource-limited areas; and 4 ) in resource-limited settings, do not require positive end-expiratory pressure, oxygen flow rate, or specific respiratory support devices. Conclusions: We propose a new global definition of ARDS that builds on the Berlin definition. The recommendations also identify areas for future research, including the need for prospective assessments of the feasibility, reliability, and prognostic validity of the proposed global definition.

Background: While the results of clinical research are clearly valuable in the care of critically ill patients, the limitations of such information and the role of other forms of medical knowledge for clinical decision making have not been carefully examined., Methods: The leadership of three large professional societies representing critical care practitioners convened a diverse group representing a wide variety of views regarding the role of clinical research results in clinical practice to develop a document to serve as a basis for agreement and a framework for ongoing discussion., Results: Consensus was reached on several issues. While the results of rigorous clinical research are important in arriving at the best course of action for an individual critically ill patient, other forms of medical knowledge, including clinical experience and pathophysiologic reasoning, remain essential. No single source of knowledge is sufficient to guide clinical decisions, nor does one kind of knowledge always take precedence over others. Clinicians will find clinical research compelling for a variety of reasons that go beyond study design. While clinical practice guidelines and protocols based upon clinical research may improve care and decrease variability in practice, clinicians must be able to understand and articulate the rationale as to why a particular protocol or guideline is used or why an alternative approach is taken. Making this clinical reasoning explicit is necessary to understand practice variability., Conclusions: Understanding the strengths and weaknesses of different kinds of medical knowledge for clinical decision making and factors beyond study design that make clinical research compelling to clinicians can provide a framework for understanding the role of clinical research in practice.

We conducted a prospective multi-institutional clinical study involving community hospitals and academic medical centers to more carefully define the value of computerized tomography (CT) of the chest with transbronchial needle aspiration (TBNA) in the staging of bronchogenic carcinoma (CA), and to assess the predictors of a positive aspirate. Of 360 individuals determined to have bronchogenic carcinoma, 50 of 81 (62%) with small cell carcinoma (SCC) and 135 of 279 (48%) with non-small cell carcinoma (NSCC) had positive aspirates (p = 0.034). TBNA precluded additional thoracic surgery in a total of 104 of 360 (29%) patients and was exclusively diagnostic of carcinoma in 65 of 360 (18%) cases. Right-sided tumors were more likely to have a positive mediastinal TBNA (p = 0.002 to 0. 01) as were histologic (67 of 118 [57%]) rather than cytology aspirates (228 of 532 [41%]) (p < 0.001). Sensitivity was > 57% in lymph nodes (LN) >/= 10 mm, and among LN of equivalent size, right paratracheal and subcarinal sites were most likely to establish malignancy. Preoperative CT is a valuable adjunct in the staging of CA by TBNA. Increasing LN size, right-sided tumors, right paratracheal and subcarinal locations, use of a histology needle, and the presence of SCC are the best predictors of a positive aspirate.

The hereditary thrombophilias are a group of inherited conditions that predispose to thrombosis. Heritable deficiencies of the endogenous anticoagulants protein C, protein S, and antithrombin have been recognized for some years, but their prevalence, even among patients with familial thrombosis, is low. The recent discoveries of two relatively common thrombophilias, resistance to activated protein C associated with an abnormal factor V gene (factor V Leiden), and prothrombin gene variant 20210A, have substantially increased the likelihood of identifying a heritable predisposing factor in patients with thromboembolism. Modestly elevated levels of plasma homocysteine, which are in part genetically determined, have also recently been associated with an increased risk for venous thromboembolism. A predisposition to thrombosis can now be identified in a substantial minority of patients with venous thromboembolism, and in the majority of patients with familial thrombosis, and there is accumulating evidence that multiple coexisting defects are present in persons with the most marked tendency to thrombosis. The most common causes of hereditary thrombophilia are reviewed with an emphasis on resistance to activated protein C, prothrombin variant 20210A, and hyperhomocystinemia, and the current status of laboratory testing for thrombophilia is discussed.

Primary pulmonary hypertension (PPH) is a rare and fatal disease of unknown etiology. Inflammatory oxidant mechanisms and deficiency in nitric oxide (NO) have been implicated in the pathogenesis of pulmonary hypertension. In order to investigate abnormalities in oxidants and antioxidants in PPH, we studied intrapulmonary NO levels, biochemical reaction products of NO, and antioxidants (glutathione [GSH], glutathione peroxidase [GPx], and superoxide dismutase [SOD]) in patients with PPH (n = 8) and healthy controls (n = 8). Intrapulmonary gases and fluids were sampled at bronchoscopy. Pulmonary hypertension was determined by right-heart catheterization. NO and biochemical reaction products of NO in the lung were decreased in PPH patients in comparison with healthy controls (NO [ppb] in airway gases: control, 8 +/- 1; PPH, 2.8 +/- 0. 9; p = 0.016; and NO products [microM] in bronchoalveolar lavage fluid [BALF]: control, 3.3 +/- 1.05; PPH, 0.69 +/- 0.21; p = 0.03). However, GSH in the lungs of PPH patients was higher than in those of controls (GSH [microM] in BALF: 0.55 +/- 0.04; PPH, 0.9 +/- 0.1; p = 0.015). SOD and GPx activities were similar in the two groups (p >/= 0.50). Biochemical reaction products of NO were inversely correlated with pulmonary artery pressures (R = -0.713; p = 0.047) and with years since diagnosis of PPH (R = -0.776; p = 0.023). NO reaction products are formed through interactions between oxidants and NO, with the end products of reaction dependent upon the relative levels of the two types of molecules. The findings of the study therefore show that NO and oxidant reactions in the lung are related to the increased pulmonary artery pressures in PPH.