The research team, led by Annika Meyer of University Hospital Cologne together with colleagues from several German institutions, conducted the review in accordance with PRISMA 2020 guidelines and registered the protocol prospectively before data collection began. In January and February 2026, the investigators searched PubMed, Web of Science, Dimensions AI, The Lens, and the Cochrane Library, supplemented by screening of Google Scholar records and, notably, by artificial intelligence-assisted literature discovery tools including ChatGPT 5.2, OpenEvidence, and SciSpace, which were used in a supplementary role to catch studies that conventional database queries might have missed. The search yielded 778 records, from which ten studies encompassing 177 neurocritical care patients in Europe and China ultimately met the inclusion criteria. Eight of those studies, covering 120 patients, provided extractable data for the meta-analysis of the primary outcome: the change in intracranial pressure from a supine baseline to the prone position.

The pooled results showed a statistically significant but modest rise in intracranial pressure of 5.06 millimeters of mercury when patients were turned prone, with a 95 percent confidence interval spanning 2.05 to 8.06 millimeters of mercury. Between-study heterogeneity was substantial, with an I-squared statistic of 76.7 percent, reflecting the wide variety of protocols, patient populations, and positioning techniques across the included studies. In descriptive terms, pooled mean intracranial pressure increased from 11.10 millimeters of mercury at baseline to 16.13 millimeters of mercury during proning. Crucially, both values remained below the treatment thresholds commonly used to define intracranial hypertension, which typically begin around 20 to 22 millimeters of mercury. The increase, in other words, was real but generally did not push patients into the danger zone.

Perhaps the most clinically important finding concerned what happened after patients were turned back. In five studies with 45 patients, the pooled change in intracranial pressure between the supine baseline and the period after returning to supine was minus 0.41 millimeters of mercury, with a confidence interval of minus 2.34 to 1.51, meaning there was no meaningful difference from pre-proning values. The pressure elevation during proning was therefore transient and fully reversible, a position-dependent effect rather than a sustained deterioration of intracranial dynamics. Cerebral perfusion pressure, the gradient that actually drives blood flow to brain tissue, showed no significant change either during proning or afterward, with mean differences close to zero and wide confidence intervals. Only one included study reported vasopressor adjustments, and no changes in vasopressor requirements were observed during the prone phase.

Against this modest hemodynamic cost, the respiratory benefits were consistent and striking. Every one of the ten studies that reported systemic oxygenation parameters, whether the partial pressure of arterial oxygen alone or the PaO2-to-FiO2 ratio, documented improvement during prone positioning. Four studies went further and measured invasive brain tissue oxygenation directly, using parenchymal sensors, and found that brain tissue oxygen levels also rose while patients were prone. This detail carries particular weight because, in three of the four studies, baseline brain tissue oxygenation values fell within ranges previously associated with cerebral ischemia and unfavorable neurological outcomes. In one study, brain tissue oxygenation improved during proning even as cerebral perfusion pressure declined slightly, suggesting that better oxygenation of arterial blood can translate into better oxygen delivery to tissue even when perfusion pressure shifts modestly.

The physiological mechanism behind the transient pressure rise is well understood from decades of neurosurgical anesthesia practice. Prone positioning increases intrathoracic and intraabdominal pressures, which can impede cerebral venous outflow, and suboptimal head and neck alignment can compromise jugular venous drainage. Because the skull is a rigid compartment governed by the Monro-Kellie doctrine, any increase in venous blood volume must be offset by displacement of cerebrospinal fluid or arterial blood, and patients with limited intracranial compliance have less reserve to absorb the change. Consistent with this framework, several included studies found that tolerance of proning was usually apparent within the first hour and was associated with lower baseline intracranial pressure. One study observed larger pressure increases in patients without external ventricular drainage, underscoring the role of cerebrospinal fluid diversion in preserving intracranial reserve.

The clinical relevance of a five-millimeter-of-mercury rise is therefore highly patient dependent. In individuals with preserved compensatory reserve, the transient elevation can be buffered by normal autoregulatory displacement of fluid compartments. In patients already hovering near the threshold of intracranial hypertension, however, the same increase may exhaust the remaining reserve and trigger an exponential rise in pressure. This helps explain why, across six studies that reported it, roughly 8.89 percent of patients had prone positioning prematurely discontinued because of intracranial pressure elevation, with a confidence interval of 4.21 to 17.78 percent. The authors suggest a pragmatic interpretation: rather than treating proning as a binary yes-or-no decision, clinicians should implement it as a monitored therapeutic trial with an explicit early reassessment point, typically within the first hour, when vulnerability is most likely to declare itself.

The evidence base behind these conclusions comes with important caveats that the authors address candidly. Only two of the ten studies were randomized trials, and one of those was judged to have a high risk of bias due to problems with the randomization process and missing outcome data, while the other raised some concerns. The eight nonrandomized studies carried an overall moderate risk of bias, driven primarily by serious confounding and selective reporting. Using the GRADE framework, the overall certainty of evidence was rated very low. Notably, patients with intracranial pressure monitoring have been excluded from roughly 75 percent of prior trials evaluating prone positioning for acute respiratory distress syndrome, which is precisely why this population has remained so poorly characterized. Additional limitations include inconsistent control of arterial carbon dioxide levels, a major determinant of cerebral blood flow, and the fact that brain tissue oxygenation reflects only regional rather than global oxygen delivery.

The heterogeneity across studies also extended to technique, and the authors argue that positioning details are far from trivial technicalities. Whether patients were placed fully prone or semi-prone, whether the head was elevated or horizontal, and whether the head was kept neutral or rotated are likely to be major determinants of intracranial tolerance. Turning maneuvers themselves can provoke coughing, ventilator desynchrony, and sympathetic activation, all of which acutely raise intracranial pressure, while concomitant spinal injuries, which are relatively common in traumatic brain injury, can complicate mobilization. Excessive sedation stabilizes physiology but delays neurological assessment, a tradeoff that cannot be eliminated but can be managed through protocolized practice.

The bottom line for clinicians is a cautious green light. The findings support considering prone positioning in selected neurocritical care patients with moderate-to-severe hypoxemic respiratory failure when invasive intracranial pressure monitoring is in place and timely de-escalation pathways are available, in line with European Society of Intensive Care Medicine consensus recommendations that already endorse proning when intracranial pressure is not elevated. Because hypoxemia is a major driver of secondary brain injury, and pulmonary complications affect an estimated 5 to 30 percent of acute brain injury patients while worsening outcomes and prolonging intensive care stays, the stakes of leaving respiratory failure untreated are considerable. The authors emphasize that current evidence supports a cautious approach but not definitive thresholds or protocols, and they call for larger prospective studies using standardized proning protocols, time-resolved intracranial pressure data, stratification by baseline intracranial reserve, and patient-centered neurological outcomes. Until such trials arrive, the message from this analysis is that the feared catastrophe of proning the injured brain is, in most monitored patients, a manageable and reversible bump rather than a cliff edge.

Subject of Research: Effects of prone positioning on intracranial pressure and oxygenation in neurocritical care patients with invasive intracranial pressure monitoring

Article Title: Prone Positioning in Neurocritical Care Patients with Invasive Intracranial Pressure Monitoring: A Systematic Review and Meta-analysis

Article References: Meyer, A., Overbeek, R., Mühlhausen, L., Küchler, J., Ditz, C., Foit, A., Hof, M., Goldbrunner, R., & Steinbicker, A. U. (2026). Prone Positioning in Neurocritical Care Patients with Invasive Intracranial Pressure Monitoring: A Systematic Review and Meta-analysis. Neurocritical Care. https://doi.org/10.1007/s12028-026-02667-0

Image Credits: AI Generated

DOI: 10.1007/s12028-026-02667-0

Keywords: prone positioning, intracranial pressure, neurocritical care, acute brain injury, ARDS, cerebral perfusion pressure, brain tissue oxygenation, systematic review, meta-analysis, traumatic brain injury, subarachnoid hemorrhage, intensive care medicine

The article, authored by Arzu Topeli of Hacettepe University, Melania Gizella Istrate of the European Society of Intensive Care Medicine and Pedro Póvoa of NOVA Medical School in Lisbon, sets out a competency-based educational continuum for patient- and family-centred practice. Its central claim is striking: humanisation in intensive care should be treated not as an aspirational ideal but as a set of observable, trainable behaviours that can be embedded into curricula, workplace assessment and everyday clinical routines.

The stakes are high. Critically ill patients frequently experience fear, vulnerability, pain, communication barriers and loss of autonomy, while their families confront uncertainty, emotional distress and complex decisions about treatment. Healthcare professionals, meanwhile, work under high cognitive load, ethical complexity and emotional burden. The authors argue that these realities demand an intentional educational response, because organisational culture and individual kindness cannot by themselves deliver consistent dignity and compassion at the bedside.

Competency-based education provides the framework. Beyond clinical expertise, the competencies identified include empathic communication, emotional awareness and regulation, ethical reasoning, reflective practice, shared decision-making, interprofessional collaboration and genuine engagement with patients and families. By aligning observable behaviours with learning objectives and assessment, such curricula give communication, teamwork, leadership and professionalism the same educational weight as technical skills. These principles underpin the CoBaTrICE competency framework for intensive care training in Europe. Evidence from the paediatric intensive care literature suggests targeted training can indeed strengthen key communication competencies, including eliciting family values, conducting family meetings, delivering difficult news and supporting families through end-of-life decisions.

Simulation-based education emerges as a cornerstone strategy. Traditionally focused on procedural skills and crisis management, simulation has evolved into a powerful platform for developing communication, teamwork, ethical reasoning and family-centred decision-making. High-fidelity scenarios can recreate family meetings, treatment limitation discussions, culturally sensitive conversations and end-of-life care within psychologically safe environments. Structured debriefing then reinforces learning through reflection and feedback, allowing clinicians to refine professional behaviours before transferring them into routine practice, where the cost of error is measured in human suffering rather than simulation scores.

Interprofessional education forms a second pillar. Learning with, from and about one another promotes mutual understanding of professional roles, strengthens communication and supports collaborative decision-making. Beyond improving teamwork, the approach reduces communication failures, enhances coordination and ensures that patients and families experience care as coherent and consistent across the critical care pathway, including transitions between the emergency department, hospital wards and the intensive care unit.

Digital technologies constitute the third strategy, and one with growing relevance. Virtual simulation, serious games, e-learning platforms and artificial intelligence-supported learning tools offer flexible access to high-quality education, personalised feedback and repeated practice throughout a clinician’s career. The authors note that these approaches also respond to contemporary pressures including workforce shortages, limited protected learning time, financial constraints and even the environmental footprint of continuing professional education. By improving access and scalability, digital strategies enable more professionals to develop and sustain human-centred competencies, particularly in resource-limited settings.

Training, however, is only effective if the desired competencies are consistently demonstrated in clinical practice. The commentary advocates programmatic assessment, a longitudinal approach combining workplace-based assessment, direct observation, multisource feedback, reflective portfolios, patient- and family-reported experience measures and simulation-based assessment. Assessment should not merely evaluate competence but actively drive learning and continuous improvement. Entrustable Professional Activities may further strengthen this integration by defining the level of supervision required, encouraging educators to judge whether clinicians can safely and independently deliver compassionate, patient- and family-centred care rather than simply demonstrating isolated skills.

The authors are equally clear that educational initiatives flourish only within supportive organisational cultures promoting psychological safety, family engagement, interprofessional collaboration and continuous learning. Humanising practices are more likely to endure when embedded within workflows, supported by shared interprofessional responsibility, leadership, role modelling and adaptation to local context. Notably, competency-based training should prepare professionals not only to deliver human-centred care but also to recognise organisational barriers and contribute to culture change. Clinician wellbeing features prominently too: burnout, moral distress and compassion fatigue erode the capacity for empathetic engagement, yet a human-centred approach may itself protect against burnout, since a persistent feeling of being unable to provide the quality of care clinicians believe patients deserve is a key driver of exhaustion. Positive communication may strengthen team cohesion and professional fulfilment, a hypothesis supported by a recent cluster-randomized trial of positive communication interventions among intensive care staff.

Ultimately, the commentary reframes the relationship between compassion and clinical excellence. Human-centred care is not an alternative to technical mastery but one of its defining dimensions, and competency-based education provides the continuum through which compassion, communication, collaboration and professionalism become sustainable clinical behaviours. The authors close with a demanding benchmark for medical education: the success of any course should be judged not by what healthcare professionals know when it ends, but by how effectively that learning supports the development, implementation and long-term sustainability of compassionate, humanised, patient- and family-centred care in everyday intensive care practice.

Subject of Research: Competency-based education for human-centred, patient- and family-centred care in intensive care units

Article Title: Training for humanization in intensive care: a competency-based educational continuum for patient- and family-centred practice

Article References: Topeli, A., Istrate, M. G., & Póvoa, P. (2026). Training for humanization in intensive care: a competency-based educational continuum for patient- and family-centred practice. Intensive Care Medicine. https://doi.org/10.1007/s00134-026-08625-w

Image Credits: AI Generated

DOI: 10.1007/s00134-026-08625-w

Keywords: intensive care medicine, competency-based education, humanization, patient- and family-centred care, simulation-based education, interprofessional education, Entrustable Professional Activities, clinician burnout, medical education, communication skills, digital learning, ICU culture

The core of the debate lies in a trade-off that every intensivist performs at the bedside, often several times a day. When lung-protective limits cap the tidal volume, the ventilator must increase the respiratory rate to sustain adequate minute ventilation, the total volume of air moved in and out of the lungs each minute. Minute ventilation is simply the product of tidal volume and respiratory rate, so mathematically the two settings can be traded against one another while the total remains constant. In theory, halving the tidal volume and doubling the rate should deliver the same gas exchange. In practice, the lungs and the body do not obey such neat arithmetic, and the consequences of shifting the balance in one direction or the other have remained surprisingly difficult to pin down.

The reason the trade-off is not neutral lies in the architecture of the respiratory system. Not all inhaled air reaches the alveoli, the tiny sacs where oxygen and carbon dioxide are actually exchanged. A substantial fraction of each breath fills the conducting airways, the trachea, bronchi and bronchioles, where no gas exchange takes place. This volume is known as anatomical dead space. When tidal volume is reduced, each breath carries a proportionally larger burden of dead space gas, air that is inhaled and exhaled without ever contributing to gas exchange. To compensate, the respiratory rate must rise even further than simple minute ventilation calculations would suggest, because the effective, alveolar ventilation falls faster than the total ventilation. Higher rates, in turn, shorten the time available for exhalation, raising the risk of air trapping and the build-up of intrinsic positive end-expiratory pressure, a phenomenon that can quietly strain the lungs and the right side of the heart.

Jung and her colleagues frame this problem through the lens of ventilatory efficiency, a concept that captures how much of the work of breathing actually translates into useful gas exchange. Ventilatory efficiency is commonly assessed by relating ventilation to carbon dioxide elimination, and it deteriorates when dead space fraction rises or when the matching between ventilation and perfusion within the lung worsens. The Hannover group contends that when clinicians and researchers trade tidal volume against respiratory rate, they typically track pressures, volumes and driving pressure, but rarely ask whether the resulting pattern of breathing is actually efficient. Two ventilator configurations that look equivalent on a monitor, delivering identical minute ventilation and similar airway pressures, can differ substantially in how much carbon dioxide they clear per liter of air moved, and that difference carries metabolic and mechanical consequences for the patient.

The correspondence appears alongside and responds to a study by Grieco and colleagues, also published in Intensive Care Medicine, which examined how respiratory mechanics modify the impact of ventilator settings on clinical outcomes in patients with acute brain injury. That work adds an important dimension to the debate, because patients with injured brains are exquisitely sensitive to changes in carbon dioxide levels, intrathoracic pressure and the hemodynamic effects of ventilation. In this population, the choice between a low tidal volume with a high rate and a slightly larger tidal volume with a lower rate is not merely a question of lung protection. It can influence cerebral blood flow, intracranial pressure and brain tissue oxygenation, making the trade-off a matter of neurological as well as pulmonary consequence.

To probe the physiological side of the question directly, the Hannover authors point to their own prospective physiological pilot study, published in Annals of Intensive Care, in which they systematically increased respiratory rate during low tidal volume ventilation and measured what happened to ventilatory efficiency and to the mechanical costs of breathing. The study, led by Jung with colleagues including Markou and Storch, was designed to isolate the effect of rate under controlled conditions, allowing the researchers to observe how the efficiency of carbon dioxide elimination and the energetic burden on the respiratory system changed as breaths became faster and smaller. Although pilot studies of this kind involve limited numbers of patients and are intended to generate hypotheses rather than definitive answers, they provide the kind of granular physiological data that large outcome trials often cannot capture.

The significance of this line of research extends beyond the physiology laboratory. Mechanical ventilation is one of the most common interventions in critical care, and the energy cost of breathing, whether performed by the patient’s own muscles or by a machine, is a real metabolic burden for patients whose reserves are already depleted. Inefficient ventilation means that the body, or the ventilator, must move more air to achieve the same gas exchange, and every liter of air moved imposes stress on the lung tissue, on the airways and on the circulation. If a high rate strategy systematically degrades ventilatory efficiency, then the apparent safety of very low tidal volumes may come with a hidden price that current protective ventilation protocols do not account for. Conversely, if efficiency is preserved across a wide range of rate settings, clinicians would gain welcome flexibility in tailoring ventilation to individual patients.

The Hannover authors also emphasize that respiratory mechanics, the elastic and resistive properties of the individual patient’s respiratory system, modify how these trade-offs play out. A stiff, poorly compliant lung in acute respiratory distress syndrome behaves very differently from a more compliant one, and the same ventilator settings can impose very different stresses depending on the underlying disease, the body size and the geometry of the airways. This is precisely the message reinforced by the Grieco study in brain-injured patients, where the impact of ventilator settings on outcomes depended on respiratory mechanics. The implication is uncomfortable but important: there may be no universal answer to the question of how to distribute ventilation between volume and rate, and the optimal balance may need to be determined for each patient rather than dictated by a single protocol.

What the correspondence ultimately calls for is a change in perspective rather than a change in practice. The authors do not dispute the value of low tidal volume ventilation, which remains one of the most robustly supported interventions in critical care. Instead, they argue that ventilatory efficiency deserves a place at the table when ventilator settings are chosen and when clinical trials are designed. Modern ventilators already measure many of the variables needed to estimate dead space and efficiency at the bedside, and incorporating these measurements into routine monitoring could allow clinicians to see not just how much air they are moving, but how effectively that air is working. As the field moves toward increasingly personalized ventilation strategies, the question posed by Jung, Gillmann and Stueber is likely to shape both research agendas and bedside decision-making in the years ahead.

For now, the message for the intensive care community is one of measured caution and renewed curiosity. The trade between tidal volume and respiratory rate is not a zero-sum game played out on the ventilator display; it is a physiological negotiation with consequences for gas exchange, energy expenditure, hemodynamics and, in vulnerable populations such as patients with brain injury, the injured organ itself. By insisting that ventilatory efficiency be considered in that negotiation, the Hannover group has added a compelling voice to a growing conversation about what protective ventilation truly means. The answer to their title question, on the evidence they marshal, appears to be a qualified yes, and the next generation of studies will need to determine exactly how that consideration should change the numbers entered on the ventilator each morning.

Subject of Research: Ventilatory efficiency in the trade-off between tidal volume and respiratory rate during protective mechanical ventilation

Article Title: Should ventilatory efficiency be considered when trading tidal volume against respiratory rate?

Article References: Jung, C., Gillmann, H.-J., & Stueber, T. (2026). Should ventilatory efficiency be considered when trading tidal volume against respiratory rate?. Intensive Care Medicine. https://doi.org/10.1007/s00134-026-08627-8

Image Credits: AI Generated

DOI: 10.1007/s00134-026-08627-8

Keywords: mechanical ventilation, tidal volume, respiratory rate, ventilatory efficiency, dead space, acute respiratory distress syndrome, intensive care medicine, respiratory mechanics, carbon dioxide elimination, acute brain injury, lung protection, minute ventilation

A new review published online in the Journal of Intensive Medicine on July 6, 2026, led by a team including researchers at Mayo Clinic in Arizona, with collaborators at the University of Pennsylvania in the United States and Mansoura University in Egypt, assembles the current evidence on sepsis-associated atrial fibrillation, abbreviated SAAF. The review examines how often the arrhythmia occurs, which patients are most vulnerable, how it is detected and diagnosed, and how it is currently managed, before laying out the research agenda needed to close the remaining gaps. The corresponding author, Sameh Hozayen, MB, BCh, of the Division of Hospital Internal Medicine at Mayo Clinic in Arizona, describes the condition as sitting in a clinical blind spot: common, dangerous, and treated without a map. The stated aim of the review is to bring existing evidence together in one place and to define precisely what still needs to be learned so that these patients can receive standardized, evidence-based care rather than ad hoc, institution-by-institution improvisation.

The clinical stakes are considerable. Unlike primary atrial fibrillation, which arises without a clear acute trigger and is supported by decades of randomized trial data and established treatment guidelines, SAAF develops in response to the acute stress of critical illness. In many patients it resolves once the underlying infection is brought under control, which has historically encouraged the assumption that it is a transient and relatively benign companion to sepsis. The review makes clear that this assumption is untenable. Sepsis-associated atrial fibrillation is associated with a 4.6-fold increase in stroke risk and a 1.7-fold increase in in-hospital mortality compared with sepsis patients who never develop the arrhythmia. Recurrence is common, affecting up to half of patients within five years, and survivors carry elevated risks of heart failure, stroke, and death that persist long after they have been discharged from the hospital and the acute infection has been cured.

Part of what makes SAAF so difficult to manage is that its causes are fundamentally multifactorial. The review traces a convergence of mechanisms: systemic inflammation driven by the septic response, autonomic dysfunction that disrupts the neural regulation of heart rate, direct myocardial injury, hemodynamic stress from fluctuating blood pressure and fluid shifts, and electrolyte disturbances that destabilize the electrical properties of the atria. Each of these forces alone can promote arrhythmia; together, in a critically ill patient, they create an environment in which the heart’s upper chambers are pushed toward disorganized electrical activity. This mechanistic complexity also explains why the arrhythmia’s course tracks so closely with the trajectory of the underlying illness, waxing and waning as the infection, the inflammatory response, and the patient’s hemodynamic status evolve hour by hour.

That volatility would be challenging enough on its own, but the therapeutic landscape is complicated by a more fundamental problem: no randomized studies have compared management strategies specifically in this population. Clinicians are therefore forced to extrapolate from trials conducted in patients with primary atrial fibrillation, an imperfect fit for critically ill patients whose physiology can shift dramatically within hours and whose organ dysfunction alters drug metabolism, tolerance, and risk. The review is explicit that this extrapolation, while unavoidable in current practice, leaves every major treatment decision shadowed by uncertainty, and that acknowledging that uncertainty is the first step toward designing the studies that will eventually resolve it.

The uncertainties begin with the simplest question: how fast should the heart be allowed to beat? For rate control, beta-blockers appear superior to alternative agents in observational data, but no randomized trial has confirmed which approach is genuinely best in septic patients, who may tolerate beta-blockade poorly when blood pressure is fragile. For rhythm control, electrical cardioversion can restore normal sinus rhythm, yet it frequently fails to hold while the underlying illness persists, because the same inflammatory, autonomic, and metabolic forces that triggered the arrhythmia remain active and quickly reassert themselves. Choosing between accepting a rapid rhythm and repeatedly attempting to restore sinus rhythm is, at present, a matter of clinical judgment rather than evidence.

The thorniest question of all is anticoagulation, the use of blood-thinning medication to prevent the clots that cause stroke in atrial fibrillation. Critically ill patients with sepsis face simultaneous and opposing risks: dangerous clotting on one side and dangerous bleeding on the other. Standard stroke-risk prediction tools used to guide anticoagulation in primary atrial fibrillation have not been validated in the sepsis setting, so the usual calculus for deciding who should be treated does not reliably apply. In observational studies, anticoagulation has not clearly reduced stroke risk in these patients—and in one multicenter cohort it actually increased bleeding—leading many clinicians to defer it. The review stresses that deferral or initiation must be individualized to each patient’s phase of illness, weighing the evolving clotting and bleeding risks as sepsis progresses or resolves, rather than applying a fixed rule.

Against this backdrop of uncertainty, the review distills the field’s needs into concrete research priorities. The authors call for a universally accepted definition of sepsis-associated atrial fibrillation, without which studies cannot be compared or pooled; validated prediction models to identify high-risk patients early in their illness; prospective randomized trials comparing rate control and rhythm control strategies; clearer, evidence-based anticoagulation strategies tailored to the phases of sepsis; and standardized rhythm monitoring after discharge to capture recurrence and long-term outcomes that are currently invisible to follow-up care. The authors also underscore the economic dimension of the problem: SAAF adds roughly 9,000 dollars in charges per patient, a substantial burden multiplied across the millions of sepsis admissions worldwide each year. Emerging technologies may help close the detection gap, and the review points to growing roles for artificial intelligence in predicting and detecting the arrhythmia in real time, potentially flagging high-risk patients before the rhythm deteriorates.

Until dedicated trials are completed and the research priorities are fulfilled, the authors conclude, the management of sepsis-associated atrial fibrillation will remain a matter of careful, individualized judgment. The central message for clinicians is to treat the whole critically ill patient rather than the arrhythmia in isolation: controlling the infection, correcting electrolyte disturbances, supporting hemodynamics, and reassessing rhythm and anticoagulation decisions continuously as the patient’s condition changes. For researchers, the message is equally direct. A condition that affects as many as one in five sepsis patients, multiplies stroke risk nearly fivefold, and drives measurable excess mortality and cost can no longer be managed on borrowed evidence from a different disease. The review’s roadmap—definition, prediction, randomized comparison of treatments, rational anticoagulation, and structured follow-up—offers the first coordinated plan for turning a clinical blind spot into standardized, evidence-based care.

Subject of Research: Sepsis-associated atrial fibrillation: incidence, risks, diagnosis, and management

Article Title: Atrial fibrillation during sepsis: what clinicians know—and what remains unclear

Article References: Atrial fibrillation during sepsis: what clinicians know—and what remains unclear. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: atrial fibrillation, sepsis, critical care, stroke risk, anticoagulation, rate control, rhythm control, intensive care medicine, arrhythmia, clinical review, artificial intelligence, research priorities

ARDS is a life-threatening form of acute lung injury in which the air sacs of the lungs become inflamed and filled with fluid, dramatically reducing the tissue available for gas exchange. The stiffness of the respiratory system, measured as elastance, reflects how much pressure is required to deliver a given volume of air. Crucially, this total elastance is the sum of two distinct components: the lung itself and the chest wall, which includes the rib cage, the diaphragm and the abdomen. Standard ventilator management in ARDS has historically treated the respiratory system as a single unit, adjusting tidal volumes and pressures according to predicted body weight and plateau pressure thresholds. This approach implicitly assumes that the contribution of the chest wall remains relatively uniform across patients, an assumption that severe obesity decisively violates.

In patients with severe obesity, the massive accumulation of adipose tissue around the thorax and abdomen, together with the upward displacement of the diaphragm by intra-abdominal fat, substantially increases chest wall elastance. The chest wall becomes stiffer and resists expansion more strongly, which means that a larger fraction of the pressure generated by the ventilator is consumed in deforming the chest wall rather than in aerating the lung. As a consequence, clinically measured pressures at the airway opening can appear alarmingly high even when the lung itself is only mildly injured, or conversely, the true stress borne by the lung parenchyma may be underestimated if the clinician assumes that all measured pressure reflects lung injury. This partitioning problem lies at the heart of the argument advanced by the Marseille team.

The physiological consequences of elevated chest wall elastance in obese patients with ARDS are far-reaching. Transpulmonary pressure, the pressure difference across the lung that actually determines lung stress and strain, cannot be directly measured at the airway. It must be inferred by subtracting an estimate of pleural pressure, typically obtained with an esophageal balloon catheter, from the airway pressure. When chest wall elastance is high, pleural pressure rises, and the airway pressure needed to achieve adequate oxygenation and alveolar recruitment increases accordingly. A ventilator strategy calibrated to airway pressures alone may therefore deliver insufficient tidal volumes and inadequate positive end-expiratory pressure to an obese patient whose lungs are, in fact, recruitable, leading to derecruitment, atelectasis and worsening hypoxemia.

The Marseille authors situate their commentary within an ongoing discussion prompted by a recent debate in the same journal on whether the esophageal balloon catheter should be deployed to personalize ventilation of ARDS. Esophageal manometry is not a new technique; it has been used in respiratory physiology for decades. Yet its adoption in routine intensive care remains limited, partly because of concerns about technical complexity, the expertise required for correct placement and interpretation, and the absence until recently of large randomized trials demonstrating outcome benefits. The correspondence by Barrau and colleagues underscores that in specific patient populations, severe obesity chief among them, the assumptions underlying conventional ventilator titration break down in ways that esophageal measurements can reveal.

Supporting evidence for the physiological argument comes from earlier work cited by the authors. A study by Behazin and colleagues published in the Journal of Applied Physiology demonstrated that morbid obesity is associated with respiratory restriction and elevated pleural and esophageal pressures, providing direct experimental confirmation that the chest wall, rather than the lung, accounts for much of the measured stiffness in this population. In parallel, a multicenter study by Coudroy and colleagues published in Anesthesiology investigated the prevalence of complete airway closure according to body mass index in patients with ARDS, documenting that higher body mass index is associated with a greater frequency of complete airway closure, a phenomenon that further complicates pressure interpretation and ventilator management at the bedside.

Complete airway closure deserves particular attention because it illustrates how obesity transforms the mechanical behavior of the respiratory system in ARDS. When the airways close completely at a certain lung volume, the pressure measured at the airway no longer communicates with the alveoli until the closing pressure is exceeded. In obese patients, the elevated pleural pressures generated by the heavy chest wall and abdomen can promote such closure, meaning that a substantial portion of each delivered breath may initially serve simply to reopen collapsed airway segments. Clinicians unaware of this mechanism may misinterpret high measured pressures as evidence of overdistension or severe lung injury and may inappropriately reduce ventilatory support, when in fact the underlying problem is the mechanical load imposed by the chest wall.

The clinical stakes of these considerations are considerable. Obesity is a rapidly growing condition worldwide, and patients with severe obesity constitute an increasing share of intensive care admissions, including admissions for ARDS triggered by pneumonia, sepsis and other causes. If ventilator protocols designed around average chest wall mechanics systematically misjudge the lung stress experienced by obese patients, then a large and expanding group of critically ill individuals may receive suboptimal care. Personalized ventilation guided by esophageal manometry offers a way to partition respiratory system elastance into its lung and chest wall components, allowing clinicians to titrate positive end-expiratory pressure and tidal volume according to transpulmonary pressures that reflect what the lung tissue itself is actually experiencing.

The correspondence does not claim that esophageal manometry is a panacea. Interpreting esophageal pressure requires attention to the position of the catheter, the effects of patient positioning and the influence of abdominal pressure, and measurements obtained in the supine, sedated and paralyzed patient differ from those in upright spontaneous breathing. Nevertheless, the authors’ central message is that ignoring chest wall elastance in severe obesity risks systematic error, whereas measuring it offers the possibility of tailoring ventilator settings to the individual patient’s physiology. In their view, the question is no longer whether chest wall mechanics matter in obese patients with ARDS, but whether the tools to measure them should be deployed more widely to translate that understanding into practice.

As the debate over personalized ventilation continues, the contribution from the Marseille intensive care team adds a clear physiological anchor. Severe obesity elevates chest wall elastance, redistributes the pressure generated by the ventilator away from the lung and toward the chest wall, and thereby distorts the conventional interpretation of airway pressures in ARDS. Whether esophageal balloon catheters become a routine part of ARDS management will depend on ongoing research, training and the accumulation of clinical evidence, but for patients with severe obesity the case for looking beyond the airway pressure gauge has rarely been more compelling.

Subject of Research: The effect of severe obesity on chest wall elastance and personalized mechanical ventilation in ARDS

Article Title: Severe obesity and chest wall elastance in ARDS

Article References: Barrau, D., Hraiech, S., & Guervilly, C. (2026). Severe obesity and chest wall elastance in ARDS. Intensive Care Medicine. https://doi.org/10.1007/s00134-026-08624-x

Image Credits: AI Generated

DOI: 10.1007/s00134-026-08624-x

Keywords: ARDS, severe obesity, chest wall elastance, mechanical ventilation, esophageal manometry, transpulmonary pressure, pleural pressure, airway closure, critical care, respiratory mechanics, positive end-expiratory pressure, intensive care medicine

Sodium dominates the chemistry of the body’s extracellular fluid, accounting for roughly ninety percent of its osmolality. The plasma sodium concentration therefore serves as a sensitive barometer of the balance between sodium and water intake and excretion. Hypernatremia, defined as a plasma sodium concentration exceeding 145 millimoles per liter, arises whenever there is a net gain of sodium, a deficit of free water, or a combination of both, and it is invariably accompanied by hyperosmolality. The review also highlights a subtlety that laboratory reports obscure: because only about ninety-three percent of plasma volume is actually water, the physiologically active sodium concentration is slightly higher than the measured value. In hyperglycemic patients, osmotic water shifts from inside cells to the extracellular space can dilute the measured sodium and mask the true severity of the disturbance.

Under normal circumstances, the body defends its osmolality with remarkable precision. Osmoreceptors in the hypothalamus detect even small rises in plasma osmolality and trigger two compensatory responses: the release of antidiuretic hormone from the posterior pituitary, which increases water reabsorption in the collecting tubules of the kidney, and the activation of thirst. Antidiuretic hormone secretion begins when plasma osmolality exceeds approximately 275 to 285 milliosmoles per kilogram, while thirst is triggered at a slightly higher threshold. Hypovolemia independently stimulates hormone release, and expanded blood volume mildly suppresses it. Crucially, even when the kidney achieves maximal urinary concentration, it cannot offset insensible water losses without additional intake, making an intact thirst response indispensable. Intensive care dismantles this defense: sedation, intubation, and impaired consciousness silence thirst, creating a dysregulated regulatory loop in which patients cannot signal their own dehydration.

The scale of the problem is substantial. ICU-acquired hypernatremia affects between six and forty-seven percent of patients depending on the definition, timing of diagnosis, and clinical setting, and multiple cohorts have linked it independently with increased mortality. The elderly are particularly vulnerable because aging raises the osmotic threshold for thirst and reduces baroreceptor sensitivity. The causes divide into two broad categories: free water deficits caused by reduced intake or excessive losses, and positive sodium balance caused by sodium administration or impaired sodium excretion. Non-renal water losses include vomiting, diarrhea, insensible losses, and drainage from surgical sites, while renal losses can follow osmotic diuresis driven by non-reabsorbed solutes such as glucose, mannitol, or urea, or impaired urinary concentrating ability in diabetes insipidus, tubular dysfunction, or recovering acute kidney injury.

Among the underappreciated culprits, the authors single out urea-mediated osmotic diuresis. Increased urea generation associated with burn injury, sepsis, polytrauma, high-protein feeding, or recovery from acute kidney injury elevates urine osmolality and can quietly increase electrolyte-free water losses. Exogenous glucocorticoids, widely used in septic shock, may compound the problem by enhancing urea-mediated osmotic diuresis and possibly suppressing antidiuretic hormone secretion. On the sodium side of the ledger, inappropriate renal retention can result from mineralocorticoid excess, including glucocorticoid therapy, while in shock states the expected suppression of the renin-angiotensin-aldosterone system may be blunted by hemodynamic instability and sympathoadrenergic activation, perpetuating sodium retention. Notably, studies in polytrauma patients have observed reduced urinary sodium and chloride excretion before hypernatremia developed, suggesting that impaired natriuresis is not merely a consequence but may be an early warning sign.

Iatrogenic sodium loading deserves equal scrutiny. Every sodium-containing intravenous fluid contributes to the daily sodium load regardless of its tonicity, and therapeutic hypertonic saline can raise serum sodium rapidly. Less obvious contributors include certain antibiotics such as fosfomycin, trisodium-citrate anticoagulation during continuous renal replacement therapy, sodium bicarbonate, enteral and parenteral nutrition, and drug-dilution fluids prepared in 0.9 percent saline, which contains 154 millimoles of sodium per liter. Even potassium administration, particularly during correction of major potassium deficits, can raise serum sodium by causing intracellular water shifts. These insights reframe hypernatremia prevention as a matter of auditing the total daily sodium burden rather than simply reacting to a laboratory number.

The physiological consequences extend well beyond the laboratory values. Hypernatremia impairs insulin-mediated glucose uptake and glucagon-dependent glucose release, contributing to hyperglycemia. In the central nervous system, osmotic fluid shifts can shrink brain cells and damage cerebral vessels, potentially producing neurological deficits or delirium. Experimental data further suggest that hyperosmolality may impair myocardial contractility through the induction of proinflammatory cytokines, hinting that elevated osmolality could compound the cardiovascular dysfunction already present in critically ill patients. These systemic effects help explain the consistent association between hypernatremia and death across observational cohorts, though the authors are careful to note that association does not prove causation.

Diagnostically, the review prescribes a structured approach anchored in assessment of volume status and urine production. Calculation of the free water deficit and free water clearance helps determine the appropriate volume and rate of fluid replacement, with the free water deficit computed from total body water and the difference between the current sodium concentration and a target of 140 millimoles per liter. In critically ill patients, the authors argue that electrolyte-free water clearance, which incorporates urinary sodium and potassium concentrations, may more accurately reflect ongoing water losses than conventional free water clearance, particularly when urea- or glucose-driven osmotic diuresis is suspected. This distinction matters because a patient losing electrolyte-free water through an osmotic diuresis needs a very different fluid strategy than one retaining sodium.

Treatment, the review emphasizes, must target the underlying cause rather than applying a one-size-fits-all water infusion. In hypovolemic patients, resuscitation with isotonic fluids takes priority, with free water added only once hemodynamic stability is achieved. In euvolemic or hypervolemic patients with adequate urine output, the focus shifts to quantifying and reducing the daily sodium load. Replacing 0.9 percent saline drug solvents with glucose-based solutions, adopting low-sodium maintenance fluid strategies, and limiting fluid creep have all been shown to lower the incidence of hypernatremia, although drug compatibility and stability constraints must be considered when changing diluents. Perhaps most provocatively, the long-standing teaching that serum sodium should be corrected at a rate below 0.5 millimoles per liter per hour has been challenged by a large analysis suggesting that faster correction may be safe and associated with shorter hospitalization and decreased mortality, a finding likely to spark debate among nephrologists and intensivists.

Pharmacological options remain limited but evolving. Hydrochlorothiazide was tested as an adjunct for ICU-acquired hypernatremia in a single small randomized controlled trial that showed no significant effect. A separate trial of forty fluid-overloaded ICU patients found that adding indapamide to furosemide produced larger natriuresis, 210 versus 119 millimoles of sodium, with similar urine volumes, and the furosemide-only group, unlike the combination group, experienced a rise in serum sodium after twenty-four hours. Mineralocorticoid receptor antagonists can induce natriuresis and represent a potential therapy, though clinical data are lacking. Animal work has shown that free water improves sodium mobilization in furosemide-treated pigs after a hyperosmotic sodium load, supporting combined strategies, while renal replacement therapy remains an option when free water administration risks fluid overload. For diabetes insipidus, management depends on etiology: nephrogenic cases call for correcting electrolyte disturbances and reversible causes, whereas central diabetes insipidus typically responds to desmopressin. The authors conclude that hypernatremia in the critically ill demands a thorough evaluation of fluid status, electrolytes, and urine chemistry, grounded in a clear understanding of the underlying physiology, if outcomes are to improve.

Subject of Research: ICU-acquired hypernatremia and its mechanisms, diagnosis, and management in critically ill patients

Article Title: Hypernatremia in the critically Ill: beyond free water replacement

Article References: Paraskevas, T., Ostermann, M., & Joannidis, M. (2026). Hypernatremia in the critically Ill: beyond free water replacement. Intensive Care Medicine. https://doi.org/10.1007/s00134-026-08566-4

Image Credits: AI Generated

DOI: 10.1007/s00134-026-08566-4

Keywords: hypernatremia, ICU-acquired hypernatremia, sodium regulation, antidiuretic hormone, osmoreceptors, free water deficit, osmotic diuresis, electrolyte-free water clearance, fluid management, critical care, diabetes insipidus, intensive care medicine

The review’s central reframing is subtle but consequential. Historically, adjuvant therapies were held back as rescue strategies, deployed only when refractory hypoxemia left clinicians with no other options. Current guidelines, by contrast, recommend applying them earlier in the disease course, reflecting the importance of minimizing stress and strain on the injured lung and potentially modulating the immune dysregulation that drives the syndrome. The authors organize commonly used adjuvants not by fashion or habit, but by the relative certainty of their utility and the frequency of their use—a taxonomy that reveals an uncomfortable truth: how often a therapy is used does not always match how well the evidence supports it.

At the top of the evidence hierarchy sits prone positioning, one of the most effective non-pharmacologic strategies for reducing mortality in moderate-to-severe ARDS. Its benefits extend well beyond improved oxygenation. Turning a patient face-down redistributes transpulmonary pressures more homogeneously across the lung, reduces overdistension of dorsal regions, recruits collapsed dependent lung tissue, and mitigates ventilator-induced lung injury. The PROSEVA trial demonstrated a substantial mortality reduction when prone positioning was applied early and for prolonged sessions in severe ARDS, and subsequent meta-analyses confirmed the benefit was greatest when it was combined with low-tidal-volume ventilation and sustained for more than sixteen hours per session. Despite this strong evidence and guideline endorsement, real-world adoption remains inconsistent, hampered by logistical demands and variability in clinician familiarity—a gap the authors describe as both common and serious.

Continuous neuromuscular blockade occupies a more contested middle ground. The physiological rationale is compelling: paralytic agents halt patient–ventilator dyssynchrony, eliminate excessively forceful spontaneous breathing efforts that can themselves injure the lung, control transpulmonary pressures, and reduce oxygen consumption. The ACURASYS trial showed improved survival and less barotrauma with a 48-hour course of early neuromuscular blockade in patients with moderate-to-severe but persistent ARDS. But the later ROSE trial, which applied the drugs slightly earlier in the disease course, found no mortality benefit. The discrepancy may reflect evolving practice—ROSE was conducted amid lighter sedation and higher PEEP, which may have blunted the incremental value of paralysis—or the fact that ACURASYS enrolled patients slightly later, enriching the study population for persistent, harder-to-treat disease. Current guidance favors short-course, targeted use, balanced against the risks of diaphragmatic inactivity and ICU-acquired weakness.

Conservative fluid management tells a different kind of story: modest evidence, near-universal adoption. Pulmonary edema worsens hypoxemia, decreases lung compliance, and amplifies ventilator-induced injury, so draining excess fluid with diuretics—or occasionally renal replacement therapy—directly supports the goals of lung-protective ventilation. The FACTT trial found that a conservative fluid strategy improved oxygenation, shortened the duration of mechanical ventilation, and reduced ICU length of stay, though it produced no mortality benefit. Even without a survival signal, the approach has become standard supportive care, fitting neatly into a broader philosophy of de-resuscitation: meticulous fluid stewardship for critically ill patients who have already received aggressive resuscitation, regardless of whether they carry an ARDS diagnosis.

Corticosteroids, meanwhile, have ridden decades of enthusiasm and disappointment. By attenuating the inflammatory cascade underlying ARDS, steroids promise reduced alveolar inflammation and less fibroproliferation. Recent trials and meta-analyses suggest early corticosteroids may shorten mechanical ventilation and ICU stays, particularly when initiated early in moderate-to-severe disease, and the COVID-19 pandemic cemented dexamethasone as standard care for severe hypoxemic viral pneumonia. Yet uncertainty persists over optimal dosing, duration, and applicability across etiologies. In late-phase ARDS, the evidence is mixed at best: an early trial of prolonged methylprednisolone in unresolving disease was followed by a larger study that failed to replicate a mortality benefit and raised a late mortality signal when treatment began more than fourteen days after ARDS onset. The authors conclude that steroids are best considered a phenotype-dependent therapy rather than a universally effective one, with trial heterogeneity likely reflecting biological differences among patients rather than absent efficacy.

Then there are the therapies that persist despite thin evidence. Inhaled pulmonary vasodilators—nitric oxide and epoprostenol—offer an elegant physiological fix for severe hypoxemia, selectively directing blood flow toward better-ventilated alveoli and reducing pulmonary vascular resistance. Studies consistently show transient oxygenation improvements, but none has demonstrated a mortality benefit, and harms such as renal dysfunction are documented. Guidelines do not recommend routine use. Nevertheless, inhaled vasodilators remain widely employed as short-term bridges to prone positioning, transfer, or escalation to extracorporeal support, and they may ease right ventricular afterload in acute cor pulmonale, though that indication has never been tested in randomized trials. Their persistence, the authors note, embodies the recurring tension between immediate physiological rescue and outcome-based evidence.

The deeper message of the review is that the right question is no longer whether an adjuvant works, but which therapy should be applied, in which patient, at what stage of disease, and to achieve which physiological objective. Timing matters as much as selection: prone positioning early and for long sessions in severe disease, neuromuscular blockade selectively when dyssynchrony and injurious breathing efforts dominate, fluids tightened once resuscitation is complete, steroids matched to inflammatory phenotype and etiology. The authors propose a framework mapping each adjuvant onto the evolving phases of ARDS, treating the syndrome as a moving target rather than a static diagnosis. Static classification at the bedside, they suggest, may ultimately matter less than dynamic reassessment throughout the illness.

Looking forward, the future of adjuvant therapy may be defined less by discovering new drugs than by deploying existing ones better. Advances in phenotyping—biological, physiological, and imaging-based—could identify which patients benefit from which interventions. The hyperinflammatory and hypoinflammatory subphenotypes described by Calfee and colleagues have already shown differential responses to several therapies, suggesting treatment effect varies with host biology rather than the syndrome label alone. Physiological phenotyping—respiratory mechanics, recruitability, respiratory drive, right ventricular function—may sharpen selection further. Equally important, the authors argue, is a willingness to de-adopt therapies lacking a strong evidence base. Adjuvants, they conclude, should not be regarded as rescue therapies of last resort but as targeted tools applied thoughtfully within a broader lung-protective strategy. The goal is deceptively simple to state and hard to achieve: the right adjuvant, for the right patient, at the right time.

Subject of Research: Adjuvant therapies for acute respiratory distress syndrome across the course of the disease

Article Title: Beyond the ventilator: deploying adjuvant therapies across the course of ARDS

Article References: Beyond the ventilator: deploying adjuvant therapies across the course of ARDS. (n.d.). https://doi.org/10.1007/s00134-026-08594-0

Image Credits: AI Generated

DOI: 10.1007/s00134-026-08594-0

Keywords: ARDS, mechanical ventilation, prone positioning, neuromuscular blockade, corticosteroids, conservative fluid management, inhaled pulmonary vasodilators, lung-protective ventilation, phenotyping, critical care, ventilator-induced lung injury, intensive care medicine

In practical terms, an Impact Factor offers more than prestige. It functions as a signal to authors, clinicians, and research teams that the work circulating in a journal is being engaged by the wider scientific and medical community—particularly important in time-sensitive domains like intensive care medicine, where findings can influence protocols and bedside decision-making.

Hayley Gershengorn, MD, FCCP, Editor in Chief of CHEST Critical Care, emphasized that the achievement is rooted in the ecosystem around the journal. Authors contribute original and reproducible studies; reviewers help refine rigor and clarity; editorial leadership maintains standards; and readers ensure the research travels beyond publication.

The journal was designed to accelerate dissemination of high-quality critical care research while keeping access frictionless. Because CHEST Critical Care is fully open access, its content can be read by practitioners, investigators, and policymakers worldwide without subscription barriers—an element that can broaden citation pathways and facilitate adoption of evidence-based practices.

Beyond original studies, the journal publishes a range of formats, including reviews and case reports, as well as “How I Do It” clinical education articles. This blend supports both scientific discovery and translational learning, which can be critical for managing complex syndromes such as sepsis, respiratory failure, and septic shock.

For biomedical audiences, open-access visibility plus peer-reviewed credibility creates a compelling combination: findings are discoverable, accessible, and citable. That coupling helps explain why emerging journals can gain momentum quickly when their content resonates with urgent clinical needs.

To follow updates across the CHEST journal ecosystem, readers can visit the CHEST website and track news via the journal’s social channels. The organization frames the Impact Factor as a validation of community effort—and as motivation to keep publishing research that improves outcomes in critical care.

Subject of Research: Critical care medicine; scholarly publishing metrics
Article Title: CHEST Critical Care Achieves First Journal Impact Factor of 2.7
News Publication Date: Not provided
Web References: https://www.chestnet.org/guidelines-and-topic-collections/publications ; https://www.twitter.com/journal_chest
References: Clarivate Journal Citation Reports (Journal Impact Factor methodology)
Image Credits: Not provided
Keywords: CHEST Critical Care, Journal Impact Factor, Clarivate, open access publishing, critical care medicine, citations, peer review, intensive care research