Do we need ARDS?

Vincent, Jean‐Louis; Santacruz, C.

doi:10.1007/s00134-015-4120-7

Cited by 12 publications

(9 citation statements)

References 8 publications

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“…Compared to patients who survived at the hospital discharge, those who died were more likely to have an aMDA-5 autoantibody ( n = 16/24, 67% vs. n = 3/23, 13%; p = 0.001), had a higher rate of ground-glass attenuation ( n = 22/24, 92% vs. 15/23, 65%; p = 0.04) and a lower rate of alveolar condensation ( n = 14/24, 58% vs. 21/23, 91%; p = 0.02) on chest CT scan, and were given 3 [ 2 , 3 ] versus 2 [ 1 , 2 ] different immunosuppressive regimens during the ICU stay ( p = 0.002) (Table 4 ). After adjustment on syndrome (anti-synthetase or aMDA-5 dermato-pulmonary syndrome), the presence of ground-glass attenuations on chest CT scan was no longer associated with in-hospital mortality ( p = 0.24).…”

Section: Resultsmentioning

confidence: 99%

“…Identifying the cause of acute respiratory distress syndrome (ARDS) is a crucial step for initiating a targeted treatment and improving prognosis [ 1 , 2 ]. However, two recent studies [ 3 , 4 ] showed that 8% of patients with ARDS according to the Berlin criteria [ 5 ] lacked exposure to “common” risk factors (e.g., pneumonia, acute pancreatitis, aspiration of gastric content or extra-pulmonary sepsis) with no etiology eventually retrieved in 80% of them [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

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Clinical features and outcome of patients with acute respiratory failure revealing anti-synthetase or anti-MDA-5 dermato-pulmonary syndrome: a French multicenter retrospective study

Vuillard

Chambrun

Prost

et al. 2018

Ann. Intensive Care

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BackgroundAnti-synthetase (AS) and dermato-pulmonary associated with anti-MDA-5 antibodies (aMDA-5) syndromes are near one of the other autoimmune inflammatory myopathies potentially responsible for severe acute interstitial lung disease. We undertook a 13-year retrospective multicenter study in 35 French ICUs in order to describe the clinical presentation and the outcome of patients admitted to the ICU for acute respiratory failure (ARF) revealing AS or aMDA-5 syndromes.ResultsFrom 2005 to 2017, 47 patients (23 males; median age 60 [1st–3rd quartiles 52–69] years, no comorbidity 85%) were admitted to the ICU for ARF revealing AS (n = 28, 60%) or aMDA-5 (n = 19, 40%) syndromes. Muscular, articular and cutaneous manifestations occurred in 11 patients (23%), 14 (30%) and 20 (43%) patients, respectively. Seventeen of them (36%) had no extra-pulmonary manifestations. C-reactive protein was increased (139 [40–208] mg/L), whereas procalcitonine was not (0.30 [0.12–0.56] ng/mL). Proportion of patients with creatine kinase ≥ 2N was 20% (n = 9/47). Forty-two patients (89%) had ARDS, which was severe in 86%, with a rate of 17% (n = 8/47) of extra-corporeal membrane oxygenation requirement. Proportion of patients who received corticosteroids, cyclophosphamide, rituximab, intravenous immunoglobulins and plasma exchange were 100%, 72%, 15%, 21% and 17%, respectively. ICU and hospital mortality rates were 45% (n = 21/47) and 51% (n = 24/47), respectively. Patients with aMDA-5 dermato-pulmonary syndrome had a higher hospital mortality than those with AS syndrome (n = 16/19, 84% vs. n = 8/28, 29%; p = 0.001).ConclusionsIntensivists should consider inflammatory myopathies as a cause of ARF of unknown origin. Extra-pulmonary manifestations are commonly lacking. Mortality is high, especially in aMDA-5 dermato-pulmonary syndrome.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Clinical features and outcome of patients with acute respiratory failure revealing anti-synthetase or anti-MDA-5 dermato-pulmonary syndrome: a French multicenter retrospective study

Vuillard

Chambrun

Prost

et al. 2018

Ann. Intensive Care

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“…Thus, future definitions may specify biologically distinct ARDS subphenotypes, identified via shared underlying precipitating factor(s), common respiratory physiology, or biomarker panels of alveolar epithelial and pulmonary vascular endothelial injury and inflammation [11–13]. The tension between generalizability and performance of future definitions will remain but may ease as diagnostics become more affordable and accessible over time.…”

Section: Redefining Ards Againmentioning

confidence: 99%

Personalized medicine for ARDS: the 2035 research agenda

et al. 2016

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Survival from ARDS has increased substantially in the last twenty years as a result of key advances in lung-protective ventilation and resuscitation. Similarly, clinical practice improvements have contributed to an impressive decline in nosocomial ARDS incidence. Personalizing mechanical ventilation for further lung protection is a top research priority for the years ahead. However, the ARDS research agenda must be broader in scope. The clinical syndrome of ARDS includes a heterogeneous assemblage of pathophysiological processes leading to lung injury. Further understanding of these varied, complex biological underpinnings of ARDS pathogenesis is needed to inform therapeutic discovery and tailor management strategy to the individual patient. While some therapies may be applicable broadly to all ARDS patients, others may benefit only certain biologically distinct subsets. The twenty-year ARDSne(x)t research agenda calls for bringing personalized medicine to ARDS, asking simultaneously both whether a treatment affords clinically meaningful benefit and for whom. This expanded scope necessitates acquisition of highly granular biological, physiological, and clinical data as the new standard across studies. Tremendous investment in research infrastructure and global collaboration will be vital to fulfilling this agenda.

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“…Cumulative data have suggested that ARDS is a heterogeneous syndrome with diverse radiographic lung morphology, respiratory mechanics and biomarker pro les [8,9]. The heterogeneity of ARDS may explain the negative results observed in many clinical trials [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Etiology-associated heterogeneity in acute respiratory distress syndrome

Ruan

Huang

Chien

et al. 2020

Preprint

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Background: Heterogeneity in acute respiratory distress syndrome (ARDS) has led to many statistically negative clinical trials. Etiology is considered an important source of pathogenesis heterogeneity in ARDS but previous studies have usually adopted a dichotomous classification, such as pulmonary versus extrapulmonary ARDS, to evaluate it. Etiology-associated heterogeneity in ARDS remains poorly described.Methods: In this retrospective cohort study, we described etiology-associated heterogeneity in gas exchange abnormality (PaO2/FiO2 [P/F] and ventilatory ratios), hemodynamic instability, non-pulmonary organ dysfunction as measured by the Sequential Organ Failure Assessment (SOFA) score, biomarkers of inflammation and coagulation, and 30-day mortality. Linear regression was used to model the trajectory of P/F ratios over time. Wilcoxon rank-sum tests, Kruskal-Wallis rank tests and Chi-squared tests were used to compare between-etiology differences. Results: From 1725 mechanically ventilated patients in the ICU, we identified 258 (15%) with ARDS. Pneumonia (48.4%) and non-pulmonary sepsis (11.6%) were the two leading causes of ARDS. Compared with pneumonia associated ARDS, extra-pulmonary sepsis associated ARDS had a greater P/F ratio recovery rate (difference = 13 mmHg/day, p = 0.01), more shock (48% versus 73%, p = 0.01), higher non-pulmonary SOFA scores (6 versus 9 points, p < 0.001), higher d-dimer levels (4.2 versus 9.7 mg/L, p = 0.02) and higher mortality (43% versus 67%, p = 0.02). In pneumonia associated ARDS, there was significant difference in proportion of shock (p = 0.005) between bacterial and non-bacterial pneumonia.Conclusion: This study showed that there was remarkable etiology-associated heterogeneity in ARDS. Heterogeneity was also observed within pneumonia associated ARDS when bacterial pneumonia was compared with other non-bacterial pneumonia. Future studies on ARDS should consider reporting etiology-specific data and exploring possible effect modification associated with etiology.

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Do we need ARDS?

Cited by 12 publications

References 8 publications

Clinical features and outcome of patients with acute respiratory failure revealing anti-synthetase or anti-MDA-5 dermato-pulmonary syndrome: a French multicenter retrospective study

Clinical features and outcome of patients with acute respiratory failure revealing anti-synthetase or anti-MDA-5 dermato-pulmonary syndrome: a French multicenter retrospective study

Personalized medicine for ARDS: the 2035 research agenda

Etiology-associated heterogeneity in acute respiratory distress syndrome

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