Although that definition is simple to apply in the clinical setting, it has been challenged over the years in several studies since the assessment of the oxygenation defect does not require standardized ventilatory support. We were the first to propose new guidelines, based on a specific, standard method of evaluating oxygenation status, a proposal that was later advocated by others. To address the limitations of the AECC definition, a modified ARDS definition has been proposed by a task force panel of experts, referred to as the Berlin Defintion, using a terminology similar to that we previously proposed. However, that proposal has several methodological flaws.
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Metrics details. Fifteen recommendations and a therapeutic algorithm regarding the management of acute respiratory distress syndrome ARDS at the early phase in adults are proposed. Lastly, for three aspects of ARDS management driving pressure, early spontaneous ventilation, and extracorporeal carbon dioxide removal , the experts concluded that no sound recommendation was possible given current knowledge.
The recommendations and the therapeutic algorithm were approved by the experts with strong agreement. Acute respiratory distress syndrome ARDS is an inflammatory process in the lungs that induces non-hydrostatic protein-rich pulmonary oedema. The immediate consequences are profound hypoxemia, decreased lung compliance, and increased intrapulmonary shunt and dead space.
The clinicopathological aspects include severe inflammatory injury to the alveolar-capillary barrier, surfactant depletion, and loss of aerated lung tissue. This is the main reason why these formal guidelines are not limited to patients presenting with severe ARDS, but are intended for application to all mechanically ventilated intensive care patients.
Results from the LUNG SAFE study suggest that the ventilator settings used did not fully respect the principles of protective mechanical ventilation [ 2 ]. Lung stress corresponds to transpulmonary pressure alveolar pressure—pleural pressure , and lung strain refers to the change in lung volume indexed to functional residual capacity of the ARDS lung at zero PEEP.
So, volutrauma corresponds to generalized excess stress and strain on the injured lung [ 6 , 7 , 8 ]. High-quality CT scan studies and physiological studies have revealed that lung lesions are unequally distributed, the injury or atelectasis coexisting with aerated alveoli of close-to-normal structure [ 9 ].
ARDS is not a disease; it is a syndrome defined by a numerous clinical and physiological criteria. It is therefore not surprising that lung-protective ventilatory strategies that are based on underlying physiological principles have been shown to be effective in improving outcome.
Minimizing VILI thus generally aims reducing volutrauma reduction in global stress and strain. Lowering airway pressures has the theoretical dual benefit of minimizing overdistension of the aerated areas and mitigating negative hemodynamic consequences.
The main aim with these formal guidelines was voluntarily to limit the topics to the best studied fields, so as to provide practitioners with solid guidelines with a high level of agreement between experts. Certain very important aspects of ARDS management were deliberately not addressed because there is insufficient assessment of their effects on prognosis respiratory rate, mechanical power, target oxygenation, pH, PaCO 2 ….
We also limited these guidelines to adult patients, to early phase of ARDS first few days , and to invasive mechanical ventilation. These guidelines have been formulated by an expert working group selected by the SRLF. The organizing committee first defined the questions to be addressed and then designated the experts in charge of each question. A level of proof was defined for each bibliographic reference cited as a function of the type of study and its methodological quality.
An overall level of proof was determined for each endpoint. When the literature was inexistent or insufficient, the question could be the subject of a recommendation in the form of an expert opinion the experts suggest…. The proposed recommendations were presented and discussed at a second meeting of the expert group. Each expert then reviewed and rated each recommendation using a scale of 1 complete disagreement to 9 complete agreement.
In the absence of strong agreement, the recommendations were reformulated and rated again, with a view to reaching a consensus Table 2. Evaluation of the efficacy and safety of mechanical ventilation settings and treatments is a cornerstone of the early phase of the management of ARDS patients.
As shown in these formal guidelines, the settings of ventilation parameters, such as PEEP, are based on their efficacy and tolerance. Moreover, the indication for some treatments depends on the severity of ARDS and these treatments will only be implemented when there is insufficient response to first-line treatments.
The safety of drug therapies and procedures must also be regularly evaluated. These guidelines also address the main safety problems of the treatments. Literature support for such practices is lacking, and they are guided by good clinical sense.
In this study, evaluation of the passive mechanics of the lung and thoracic cage, of the response to PEEP, and of alveolar recruitment prompted changes in ventilation parameters in most patients 41 of 61 analyzed.
It is difficult to define how often to assess ventilation parameters and treatments in ARDS. It seems that a frequency at least similar to that proposed for the evaluation of criteria for weaning from the ventilator i. Nonetheless, more frequent assessment might be necessary and benefit in some cases.
Too high a rate, however, engenders a risk of dynamic hyperinflation and also increases each minute cumulative exposure to potentially risky insufflation. A reduction in instrumental dead space is also appropriate, and a heated humidifier should be used in first intention.
The tidal volume delivered will induce a pressure increase from the PEEP, thus necessitating monitoring of plateau pressure, which should be kept below 30 cmH 2 O. Clinicians need to be aware of the potential risks of low tidal volume, such as dyssynchrony and double triggering.
Guidelines on pressure and volume reduction issued in the late s were based on experimental and clinical data [ 13 , 14 , 15 , 16 ]. Several randomized clinical trials with rather few subjects in the s found no survival advantage of low tidal volume [ 17 , 18 ]. A lack of power may, of course, explain these negative results. Note also that these trials were not intended to achieve control of PaCO 2 , which may have contributed to the deleterious effects of hypercapnic acidosis in the study arms using reduced tidal volume.
Although the clinical evidence is not easy to demonstrate, hypercapnia has unquestionable side effects [ 19 ], like increased pulmonary vascular resistance, which can worsen prognosis. The use of PBW calculated as a function of sex and height was an important innovation in adapting tidal volume to the expected lung volume. In this study, increased respiratory rate leading to low-volume ventilation was associated with only a minimal increase in PaCO 2 , a result that may have contributed to the benefits of this treatment arm.
This study had an enormous impact on clinical practice. It was not the first to use low volumes successfully, that accolade falls to the two-center study by Amato et al. Other studies using the same approach as Amato et al. Meta-analyses of tidal volume reduction have often included rather heterogenous studies [ 23 ].
The most recent included seven randomized trials in patients [ 24 ] and concluded that lower mortality was associated with low-volume ventilation in primary analysis hazard ratio 0. However, when the studies that combined high PEEP and low volumes were excluded, the effect of reduced tidal volume was just a non-significant trend 0.
According to the authors, this suggests, but does not prove, that reduced tidal volumes significantly decrease mortality during ARDS.
In an observational study, 11, ventilation parameters were available for ARDS patients identified prospectively [ 25 ]. The authors compared the patients with volumes of 6. A secondary increase in tidal volume was also associated with an increase in mortality risk, but the mortality risk of too high a first tidal volume was higher than the effect of the following volumes [ 25 ]. There was no difference in survival in the patients whose tidal volume was equal to or greater than the median value of 7.
In addition, the use of lower tidal volumes in patients with severe ARDS may involve potentially confounding effects, which are difficult to analyze completely in purely observational data [ 26 ]. In all analyses, however, the pressures peak pressure, plateau pressure, driving pressure, and PEEP carried more significant weight than tidal volume in the prognosis [ 26 ]. Mechanical ventilation should limit VILI, thereby limiting mortality.
Even if VILI was initially observed on application of a high plateau pressure with a high tidal volume [ 16 ], there is less lung injury with the same high plateau pressure when the tidal volume is reduced by means of thoracic stiffness [ 13 ], a situation encountered in the very obese.
An ancillary study of LUNG SAFE has shown that plateau pressure, which can be modified by the intensivist, is strongly and positively correlated with mortality [ 26 ]. A high plateau pressure is an independent mortality risk factor, as it reflects either great severity associated with poor lung compliance or inadequate mechanical ventilation [ 27 ].
The only way to monitor plateau pressure routinely is to ventilate the patient with an end-inspiratory pause, which should not be too long, so as to facilitate any increase in respiratory rate, or too short, so that the respirator can measure the pressure. A pause of 0. In a given patient, plateau pressure is an imperfect reflection of lung distension [ 28 ].
This is particularly so in patients with abnormal compliance of the chest wall, and in some obese patients. Five controlled and randomized studies compared a strategy of low tidal volume and limited plateau pressure with a strategy using higher tidal volume and plateau pressure [ 17 , 18 , 20 , 21 , 30 ]. A significant decrease in mortality in the group with limited volume and pressure was observed only in the 2 studies [ 20 , 21 ] where difference in plateau pressure was particularly large between the 2 strategies tested.
When these 5 studies are pooled, there is a strong relation between plateau pressure and mortality [ 31 ]. In a recent study in patients, a threshold plateau pressure of 29 cmH 2 O was identified beyond which hospital mortality increased [ 32 ]. These results were validated in the same study in a different cohort of patients [ 32 ]. This limitation can be envisaged as a complement to limitation of plateau pressure in some special instances. One study retrospectively evaluated the influence of driving pressure on prognosis by means of a complex statistical analysis of nine randomized controlled studies of ventilation strategy comparison of different values of tidal volume and PEEP, during ARDS [ 33 ].
The authors concluded that driving pressure was the best predictor of mortality in these studies. Nonetheless, as the authors themselves acknowledge, this was a retrospective study of studies whose main aim was not to examine the usefulness of driving pressure. No randomized study has since corroborated the value of limiting driving pressure.
In contrast, the results of the observational study LUNG SAFE [ 2 , 26 ] showed no obvious superiority of driving pressure over plateau pressure as a predictor of the risk of mortality. The same was true when the data of two studies showing improved survival during ARDS by neuromuscular block and by prone positioning were combined [ 34 ]. Prudence regarding the role of driving pressure is advised, and other studies have even yielded some concerns regarding the validity of this physiological concept.
Unlike plateau pressure, which translates dynamic and static lung distension, driving pressure translates dynamic distension. Indeed, plateau pressure was lower in the group with lower mortality, whereas driving pressure was lower in the group with higher mortality [ 35 ]. This would therefore amount to comparing two levels of PEEP during ventilation with limited plateau pressure.
In practical terms, it would be best first to measure and limit plateau pressure, an approach which the LUNG SAFE study [ 2 ] has clearly shown is insufficiently used. In this case, it can be useful to reduce driving pressure by further limiting tidal volume, while increasing PEEP, if this maneuver is well tolerated hemodynamically.
PEEP settings should be individualized. PEEP is an integral part of the protective ventilation strategy. The expected beneficial effect of high PEEP is optimized alveolar recruitment, which, on the one hand, decreases the intrapulmonary shunt, thus improving arterial oxygenation, and, on the other hand, decreases the amount of lung tissue exposed to alveolar opening-closing, thus reducing the risk of VILI [ 38 , 39 ].
Conversely, the deleterious effects of high PEEP are increased end-inspiratory lung volume, hence increased risk of volutrauma [ 13 ], hemodynamic worsening linked to a decrease in preload, and above all to an increase in right ventricular afterload [ 40 , 41 ]. The extent of the beneficial and deleterious effects of high PEEP varies greatly from one patient to another and cannot be predicted from the simple clinical data available at the bedside.
Individually, the effect of high PEEP in terms of recruitment cannot be assessed from changes in respiratory system compliance [ 45 , 47 ]. No blood gas or respiratory mechanics parameter easily available at the bedside allows quantification of the risk of volutrauma induced by the use of high PEEP.
High-frequency oscillation ventilation HFOV is an unconventional mode of ventilation proposed to improve gas exchange while protecting against VILI using a tidal volume below or equal to the anatomical dead space [ 52 ]. The gas flow and the inflation of a balloon valve allow adjustment of cP aw , which determines oxygenation proportionally. Tidal volume increases with the amplitude of the membrane movements and decreases when the frequency increases, which explains why CO 2 removal is inversely proportional to the frequency used.
Thanks to exchange mechanisms distinct from simple exchange by convection [ 53 ], HFOV enables a greater reduction in tidal volume and decreases the amplitude of cyclic variations in transpulmonary pressure, thus allowing the use of a high cP aw so as to optimize lung recruitment.
By increasing the proportion of parenchyma ventilated, the recruitment induced in HFOV may reduce lung stress and strain, reduce the sheer stress associated with the cyclic opening and closing of unstable alveoli, and limit VILI.
Acute Respiratory Distress Syndrome: The Berlin Definition
We'd like to understand how you use our websites in order to improve them. Register your interest. Treatment of acute respiratory distress syndrome ARDS has been subject to many researches, sometimes leading to intense controversy. New findings in this field are varied. Effects on prognosis of commonly used treatments for ARDS have recently been investigated. Consistently, prone position, previously known to improve oxygenation without effect on mortality, has been shown to improve survival of the most severely hypoxemic patients. Administration of neuromuscular blocking agents in the acute phase of ARDS has been also shown to be beneficial on survival.
Nouveautés thérapeutiques sur le SDRA
Formal guidelines: management of acute respiratory distress syndrome
Acute Respiratory Distress Syndrome Definitions