2018 Update: Acute Respiratory Distress Syndrome Advances in Diagnosis and Treatment

Importance  Acute respiratory distress syndrome (ARDS) is a life-threatening form of respiratory failure that affects approximately 200 000 patients each year in the United States, resulting in nearly 75 000 deaths annually. Globally, ARDS accounts for 10% of intensive care unit admissions, representing more than 3 million patients with ARDS annually.

Objective  To review advances in diagnosis and treatment of ARDS over the last 5 years.

Evidence Review  We searched MEDLINE, EMBASE, and the Cochrane Database of Systematic Reviews from 2012 to 2017 focusing on randomized clinical trials, meta-analyses, systematic reviews, and clinical practice guidelines. Articles were identified for full text review with manual review of bibliographies generating additional references.

Findings  After screening 1662 citations, 31 articles detailing major advances in the diagnosis or treatment of ARDS were selected. The Berlin definition proposed 3 categories of ARDS based on the severity of hypoxemia: mild (200 mm Hg<Pao₂/Fio₂≤300 mm Hg), moderate (100 mm Hg<Pao₂/Fio₂≤200 mm Hg), and severe (Pao₂/Fio₂ ≤100 mm Hg), along with explicit criteria related to timing of the syndrome’s onset, origin of edema, and the chest radiograph findings. The Berlin definition has significantly greater predictive validity for mortality than the prior American-European Consensus Conference definition. Clinician interpretation of the origin of edema and chest radiograph criteria may be less reliable in making a diagnosis of ARDS. The cornerstone of management remains mechanical ventilation, with a goal to minimize ventilator-induced lung injury (VILI). Aspirin was not effective in preventing ARDS in patients at high-risk for the syndrome. Adjunctive interventions to further minimize VILI, such as prone positioning in patients with a Pao₂/Fio₂ ratio less than 150 mm Hg, were associated with a significant mortality benefit whereas others (eg, extracorporeal carbon dioxide removal) remain experimental. Pharmacologic therapies such as β₂ agonists, statins, and keratinocyte growth factor, which targeted pathophysiologic alterations in ARDS, were not beneficial and demonstrated possible harm. Recent guidelines on mechanical ventilation in ARDS provide evidence-based recommendations related to 6 interventions, including low tidal volume and inspiratory pressure ventilation, prone positioning, high-frequency oscillatory ventilation, higher vs lower positive end-expiratory pressure, lung recruitment maneuvers, and extracorporeal membrane oxygenation.

Conclusions and Relevance  The Berlin definition of acute respiratory distress syndrome addressed limitations of the American-European Consensus Conference definition, but poor reliability of some criteria may contribute to underrecognition by clinicians. No pharmacologic treatments aimed at the underlying pathology have been shown to be effective, and management remains supportive with lung-protective mechanical ventilation. Guidelines on mechanical ventilation in patients with acute respiratory distress syndrome can assist clinicians in delivering evidence-based interventions that may lead to improved outcomes.

Full text

Impact of obstructive sleep apnea on chronic obstructive pulmonary disease: prospective, consecutive study

What is not known yet, about the topic
Coexistent chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA) are insufficiently studied in terms of prevalence, frequency and spectrum of complications, health risks and impact on quality of life.

Research hypothesis
Certain clinical and demographic parameters or data obtained from nocturnal polysomnography can have significant predictive value for overlap syndrome, induced by coexistent obstructive sleep apnea and chronic obstructive pulmonary
disease.
Article’s added novelty on this scientific topic
It was established that increased body mass index and high Epworth sleepiness score have significant predictive value for coexistent OSA and COPD.

Full text

Dual LABA/LAMA bronchodilators in COPD: why? when? and how?

Dual LABA/LAMA bronchodilators in COPD: why? when? and how?

Still many questions in our real everyday practice!

Read Editorial in Expert Review of Respiratory Medicine by great Italian team conducted by professor Mario Cazzola. 

http://www.tandfonline.com/doi/abs/10.1080/17476348.2018.1442216

LABA/LAMA combinations induce bronchorelaxant synergistic interaction when the drugs mixture is well-balanced and administered at low isoeffective concentrations.
The overall approach of Drug Companies has been to combine in a FDC a LABA and a LAMA at the same doses for which the monocomponents were previously approved. Indeed, this practice does not permit to optimize the synergy in the final
LABA/LAMA FDCs. Conversely, dose-finding studies are required to identify the correct dose-ratio and establish the minimal doses for each monocomponent in the FDC leading to the greater synergism with regard to the improvement in lung
function, symptoms, and exacerbations.
Furthermore, although LABA/LAMA FDCs are characterized by an acceptable safety profile, the cardiovascular toxicity of LABAs and LAMAs may overlap. Thus, postmarketing surveillance and observational studies are needed to assess the real risk of rare, but potentially serious, cardiovascular adverse events associated with the dual bronchodilation therapy in COPD patients.

Full text:

http://www.tandfonline.com/doi/abs/10.1080/17476348.2018.1442216

COPD in 2018: syndrome or disease - first steps to new classification

New article from ERJ Open Research by Celli and Agusti is dedicated to hot topic in COPD: new classification with absolutely fresh approach!

Due to well-conducted epidemiological studies and advances in genetics, molecular biology, translational research, the advent of computed tomography of the lungs and bioinformatics, the diagnosis of chronic obstructive pulmonary disease (COPD) as a single entity caused by susceptibility to cigarette smoke is no longer tenable. Furthermore, the once-accepted concept that COPD results from a rapid and progressive loss of lung function over time is not true for a sizeable proportion of adults with the disease. Now we know that some genetic predisposition and/or different environmental interactions (nutritional, infectious, pollution and immunological) may negatively modulate post-natal lung development and lead to poorly reversible airflow limitation later in life, consistent with COPD.

 

We believe it is time to rethink the taxonomy of this disease based on the evidence at hand. To do so, we have followed the principles outlined in the 1980s by J.D. Scadding who proposed that diseases can be defined by four key characteristics: 1) clinical description (syndrome), 2) disorder of structure (morbid anatomy), 3) disorder of function (pathophysiology) and 4) causation (aetiology). 

Here, we propose a pragmatic approach to the taxonomy of COPD based on different processes that result in a similar syndromic presentation. It can accommodate changes over time, as the pathobiology that may lead to COPD expands. We hope that stakeholders in the field may find it useful to better define the patients now boxed into one single entity, so that specific studies can be designed and conducted for each type of COPDs.

Free full text:

http://openres.ersjournals.com/content/4/1/00132-2017