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Abstract Background Prolonged weaning is a major issue in intensive care patients and tracheostomy is one of the last resort options. Optimized patient-ventilator interaction is essential to weaning. The purpose of this study was to compare patient-ventilator synchrony between pressure support ventilation (PSV) and neurally adjusted ventilatory assist (NAVA) in a selected population of tracheostomised patients. Methods We performed a prospective, sequential, non-randomized and single-centre study. Two recording periods of 60 min of airway pressure, flow, and electrical activity of the diaphragm during PSV and NAVA were recorded in a random assignment and eight periods of 1 min were analysed for each mode. We searched for macro-asynchronies (ineffective, double, and auto-triggering) and micro-asynchronies (inspiratory trigger delay, premature, and late cycling). The number and type of asynchrony events per minute and asynchrony index (AI) were determined. The two respiratory phases were compared using the non-parametric Wilcoxon test after testing the equality of the two variances (F-Test). Results Among the 61 patients analysed, the total AI was lower in NAVA than in PSV mode: 2.1% vs 14% (p

IntroductionLow cardiac output syndrome (LCOS) is a common complication in cardiac surgery, and we evaluated the incidence of its early occurrence after mitral and tricuspid combined cardiac surgery and its associated risk factors.Material and methodRetrospective, single institution study. We included 88 consecutive adult patients with severe mitral insufficiency scheduled for elective mitral and tricuspid valve replacement surgery between January 2015 and November 2018. The primary endpoint was the occurrence of LCOS, defined as the need for inotropic support or circulatory assistance after surgery. The secondary endpoint was mortality at 30 days.ResultsLCOS occurred in 26 patients (29.5%) of the studied patients and its associated risk factors that appeared in the multivariate analysis were chronic kidney failure [adjusted odds ratio (OR) 3.1; 95% confidence interval (CI) 1.0–9.9, p = 0.05], pre-operative left ventricular heart failure (OR 5.3; 95% CI 1.3–10.9, p = 0.002), pre-operative right ventricular heart failure (OR 3.6; 95% CI 1.1–11.5, p = 0.02), and mitral valve replacement (OR 3.9; 95% CI 1.2–12.6, p = 0.03). LCOS affected the survival of patients (HR = 5.5; 95% CI 1.1–27.7 p = 0.04).ConclusionLCOS is a frequent complication after mitral and tricuspid combined surgery and is associated with poor prognosis.

Abstract Background Renal artery Doppler sonography with resistive index (RI) determination is a noninvasive, fast, and reliable diagnostic tool increasingly used in the intensive care unit (ICU) to predict and assess the reversibility of acute kidney injury (AKI). However, interpreting the RI can be challenging due to numerous influencing factors. While some studies have explored various confounding factors, arterial blood gases have received limited attention. Therefore, our study aims to evaluate the impact of arterial blood gases on the RI in the ICU setting. Methods This prospective observational study enrolled ICU patients who required blood gas analysis and had not experienced significant hemodynamic changes recently. The RI was measured using standardized Doppler ultrasound within an hour of the arterial blood gases sampling and analysis. Results A total of sixty-four patients were included in the analysis. Univariate analysis revealed a correlation between the RI and several variables, including PaCO2 (R = 0.270, p = 0.03), age (R = 0.574, p 58 years and PaCO2 were significant factors influencing the RI, with respective odds ratios of 18.67 (p = 0.0003) and 1.132 (p = 0.0267). Conclusion The interpretation of renal arterial RI should take into account thresholds for PaCO2, age, and diastolic arterial pressure. Further studies are needed to develop a comprehensive scoring system that incorporates all these cofactors for a reliable analysis of RI levels. Trial registration This observational study, registered under number 70–0914, received approval from local Ethical Committee of Toulouse University Hospital.

Background Out-of-hospital cardiac arrest (OHCA) represents a major burden for society and health care, with an average incidence in adults of 67 to 170 cases per 100,000 person-years in Europe and in-hospital survival rates of less than 10%. Patients and practitioners would benefit from a prognostication tool for long-term good neurological outcomes. Objective We aim to develop a machine learning (ML) pipeline on a local database to classify patients according to their neurological outcomes and identify prognostic features. Methods We collected clinical and biological data consecutively from 595 patients who presented OHCA and were routed to a single regional cardiac arrest centre in the south of France. We applied recursive feature elimination and ML analyses to identify the main features associated with a good neurological outcome, defined as a Cerebral Performance Category score less than or equal to 2 at six months post-OHCA. Results We identified 12 variables 24 h after admission, capable of predicting a six-month good neurological outcome. The best model (extreme gradient boosting) achieved an AUC of 0.96 and an accuracy of 0.92 in the test cohort. Conclusion We demonstrated that it is possible to build accurate, locally optimised prediction and prognostication scores using datasets of limited size and breadth. We proposed and shared a generic machine-learning pipeline which allows external teams to replicate the approach locally.

IntroductionThe COVID-19 pandemic prompted our team to develop new solutions for performing cardiac surgery without intravenous anesthetics due to a shortage of these drugs. We utilized an anesthetic conserving device (Sedaconda-ACD) to administer total inhaled anesthesia because specific vaporizers were unavailable for administering inhaled agents during cardiopulmonary bypass (CPB) in our center. We documented our experience and postoperative cardiovascular outcomes. The primary outcome was the peak level of troponin, with secondary outcomes encompassing other cardiovascular complications.Material and methodsA single-center retrospective study was conducted. We performed a multivariate analysis with a propensity score. This investigation took place at a large university referral center.ParticipantsAdult patients (age ≥ 18) who underwent elective cardiac surgery with CPB between June 2020 to March 2021.InterventionDuring the inclusion period, two anesthesia protocols for the maintenance of anesthesia coexisted—total inhaled anesthesia with Sedaconda-ACD and our classic protocol with intravenous drugs during and after CPB.Primary endpointTroponin peak level recorded after surgery (highest level recorded within 48 h following the surgery).ResultsOut of the 654 included patients, 454 were analyzed after matching (intravenous group = 297 and inhaled group = 157). No significant difference was found between the groups in postoperative troponin peak levels (723 ng/l vs. 993 ng/l–p = 0.2). Total inhaled anesthesia was associated with a decreased requirement for inotropic medications (OR = 0.53, 95% CI 0.29–0.99, p = 0.04).ConclusionIn our cohort, the Sedaconda-ACD device enabled us to achieve anesthesia without intravenous agents, and we did not observe any increase in postoperative complications. Total inhaled anesthesia with sevoflurane was not associated with a lower incidence of myocardial injury assessed by the postoperative troponin peak level. However, in our cohort, the use of inotropic drugs was lower.

Abstract Background Prevalence, risk factors and medical management of persistent pain symptoms after critical care illness have not been thoroughly investigated. Methods We performed a prospective multicentric study in patients with an intensive care unit (ICU) length of stay ≥ 48 h. The primary outcome was the prevalence of significant persistent pain, defined as a numeric rating scale (NRS) ≥ 3, 3 months after admission. Secondary outcomes were the prevalence of symptoms compatible with neuropathic pain (ID-pain score > 3) and the risk factors of persistent pain. Results Eight hundred fourteen patients were included over a 10-month period in 26 centers. Patients had a mean age of 57 (± 17) years with a SAPS 2 score of 32 (± 16) (mean ± SD). The median ICU length of stay was 6 [4–12] days (median [interquartile]). At 3 months, the median intensity of pain symptoms was 2 [1–5] in the entire population, and 388 (47.7%) patients had significant pain. In this group, 34 (8.7%) patients had symptoms compatible with neuropathic pain. Female (Odds Ratio 1.5 95% CI [1.1–2.1]), prior use of anti-depressive agents (OR 2.2 95% CI [1.3–4]), prone positioning (OR 3 95% CI [1.4–6.4]) and the presence of pain symptoms on ICU discharge (NRS ≥ 3) (OR 2.4 95% CI [1.7–3.4]) were risk factors of persistent pain. Compared with sepsis, patients admitted for trauma (non neuro) (OR 3.5 95% CI [2.1–6]) were particularly at risk of persistent pain. Only 35 (11.3%) patients had specialist pain management by 3 months. Conclusions Persistent pain symptoms were frequent in critical illness survivors and specialized management remained infrequent. Innovative approaches must be developed in the ICU to minimize the consequences of pain. Trial registration. NCT04817696. Registered March 26, 2021.

IntroductionIn November 2021, the SARS-CoV-2 Omicron variant of concern has emerged and is currently dominating the COVID-19 pandemic over the world. Omicron displays a number of mutations, particularly in the spike protein, leading to specific characteristics including a higher potential for transmission. Although Omicron has caused a significant number of deaths worldwide, it generally induces less severe clinical signs compared to earlier variants. As its impact on blood platelets remains unknown, we investigated platelet behavior in severe patients infected with Omicron in comparison to Delta.MethodsClinical and biological characteristics of severe COVID-19 patients infected with the Omicron (n=9) or Delta (n=11) variants were analyzed. Using complementary methods such as flow cytometry, confocal imaging and electron microscopy, we examined platelet activation, responsiveness and phenotype, presence of virus in platelets and induction of selective autophagy. We also explored the direct effect of spike proteins from the Omicron or Delta variants on healthy platelet signaling.ResultsSevere Omicron variant infection resulted in platelet activation and partial desensitization, presence of the virus in platelets and selective autophagy response. The intraplatelet processing of Omicron viral cargo was different from Delta as evidenced by the distribution of spike protein-positive structures near the plasma membrane and the colocalization of spike and Rab7. Moreover, spike proteins from the Omicron or Delta variants alone activated signaling pathways in healthy platelets including phosphorylation of AKT, p38MAPK, LIMK and SPL76 with different kinetics.DiscussionAlthough SARS-CoV-2 Omicron has different biological characteristics compared to prior variants, it leads to platelet activation and desensitization as previously observed with the Delta variant. Omicron is also found in platelets from severe patients where it induces selective autophagy, but the mechanisms of intraplatelet processing of Omicron cargo, as part of the innate response, differs from Delta, suggesting that mutations on spike protein modify virus to platelet interactions.

During severe sepsis, platelet activation may induce disseminate microvascular thrombosis, which play a key role in critical organ failure. Crucially, most of the studies in this field have explored platelet–leukocyte interactions in animal models, or explored platelets under the spectrum of thrombocytopenia or disseminated intravascular coagulation and have not taken into account the complex interplay that might exist between platelets and leukocytes during human septic shock nor the kinetics of platelet activation. Here, we assessed platelet activation parameters at the admission of patients with sepsis to the intensive care unit (ICU) and 48 hours later. Twenty-two patients were enrolled in the study, thirteen (59.1%) of whom were thrombocytopenic. The control group was composed of twelve infection-free patients admitted during the study period. The activation parameters studied included platelet-leukocyte interactions, assessed by flow cytometry in whole blood, as well as membrane surface and soluble platelet activation markers measured by flow cytometry and dedicated ELISA kits. We also investigated platelet aggregation and secretion responses of patients with sepsis following stimulation, compared to controls. At admission, the level of circulating monocyte-platelet and neutrophil-platelet heterotypic aggregates was significantly higher in sepsis patients compared to controls and returned to a level comparable to controls or even below 48 hours later. Basal levels of CD62P and CD63 platelet membrane exposure at admission and 48 hours later were low and similar to controls. In contrast, plasma level of soluble GPVI and soluble CD40 ligand was significantly increased in septic patients, at the two times of analysis, reflecting previous platelet activation. Platelet aggregation and secretion responses induced by specific agonists were significantly decreased in septic conditions, particularly 48 hours after admission. Hence, we have observed for the first time that critically ill septic patients compared to controls have both an early and durable platelet activation while their circulating platelets are less responsive to different agonists.

Abstract Background The long-term fate of severely injured patients in terms of their quality of life is not well known. Our aim was to assess the quality of life of patients who have suffered moderate to severe trauma and to identify primary factors of long-term quality of life impairment. Methods A prospective monocentric study conducted on a number of patients who were victims of moderate to severe injuries during the year 2012. Patients were selected based on an Injury Severity Score (ISS) more than or equal to 9. Quality of life was assessed by the MOS SF-36 and NHP scores as a primary evaluation criterion. The secondary evaluation criteria were the determination of the socio-economic impact on quality of life and the identification of factors associated with disability. Results Two hundred and eight patients were contacted by e-mail or telephone. Fifty-five patients participated in this study (with a participation level of 26.4%), including 78.2% men, with a median age of 46. Significant alterations in quality of life were observed with the NHP and MOS SF-36 scale, including physical and psychological components. This resulted in a major socio-economic impact as 26% of the patients could not resume their professional activities (n = 10), 20% required retraining in other lines of work, and 36.4% had a disability status. The study showed that scores ≤ 85 on the physical functioning variable of the MOS SF 36 scale was associated with disability. Conclusion More than five years after a moderate to severe injury, patients’ quality of life was significantly impacted, resulting in significant socio-economic consequences. Disability secondary to major trauma seems to be associated with a score ≤ 85 on the physical functioning dimension of the MOS SF-36 scale. This study raises the question of whether or not early rehabilitation programs should be implemented in order to limit the long-term impact of major trauma.

Abstract Background To compare patients hospitalised in the intensive care unit (ICU) after surgery for community-acquired intra-abdominal infection (CA-IAI) and hospital-acquired intra-abdominal infection (HA-IAI) in terms of mortality, severity and complications. Methods Retrospective study including all patients admitted to 2 ICUs within 48 h of undergoing surgery for peritonitis. Results Two hundred twenty-six patients were enrolled during the study period. Patients with CA-IAI had an increased 28-day mortality rate compared to those with HA-IAI (30% vs 15%, respectively (p = 0.009)). At 90 days, the mortality rates were 36.7 and 37.5% in the CA-IAI group and HA-IAI group, respectively, with a similar APACHE II score on admission (median: 21 [15–25] vs. 21 [15–24] respectively, p = 0.63). The patients with HA-IAI had prolonged ICU and hospital stays (median: 17 [7–36] vs. 6[3–12] days, p

BackgroundThe effects of SARS-CoV-2 (COVID-19) on the myocardium and their role in the clinical course of infected patients are still unknown. The severity of SARS-CoV-2 is driven by hyperinflammation, and the effects of SARS-CoV-2 on the myocardium may be significant. This study proposes to use bedside observations and biomarkers to characterize the association of COVID-19 with myocardial injury. ObjectiveThe aim of the study is to describe the myocardial function and its evolution over time in patients infected with SARS-CoV-2 and to investigate the link between inflammation and cardiac injury. MethodsThis prospective, monocentric, observational study enrolled 150 patients with suspected or confirmed SARS-CoV-2 infection at Toulouse University Hospital, Toulouse, France. Patients admitted to the intensive care unit (ICU), regular cardiologic ward, and geriatric ward of our tertiary university hospital were included during the pandemic period. Blood sampling, electrocardiography, echocardiography, and morphometric and demographic data were prospectively collected. ResultsA total of 100 patients were included. The final enrolment day was March 31, 2020, with first report of results at the end of the first quarter of 2021. The first echocardiographic results at admission of 31 patients of the COCARDE-ICU substudy population show that biological myocardial injury in COVID-19 has low functional impact on left ventricular systolic function. ConclusionsA better understanding of the effects of COVID-19 on myocardial function and its link with inflammation would improve patient follow-up and care. Trial RegistrationClinicaltrials.gov NCT04358952; https://clinicaltrials.gov/ct2/show/NCT04358952 International Registered Report Identifier (IRRID)DERR1-10.2196/24931

Abstract In the intensive care unit, patients are subject to discomforts and pain. Their management is essentially based on pharmacologic approaches. Immersive virtual reality could represent an adjunctive non-invasive and non-pharmacological pain control technique. It is based on real-time interaction with an artificial 360° immersive world using interfaces that enable physical and emotional perceptions to make the user feel better trying to reduce pain perception and to limit anxiety. Evaluation of virtual reality in intensive care unit is lacking and further studies are necessary before to introduce this alternative method for critical patients.

Considering virus-related and drug-induced immunocompromised status of critically ill COVID-19 patients, we hypothesize that these patients would more frequently develop ventilator-associated pneumonia (VAP) than patients with ARDS from other viral causes. We conducted a retrospective observational study in two intensive care units (ICUs) from France, between 2017 and 2020. We compared bacterial co-infection at ICU admission and throughout the disease course of two retrospective longitudinally sampled groups of critically ill patients, who were admitted to ICU for either H1N1 or SARS-CoV-2 respiratory infection and depicted moderate-to-severe ARDS criteria upon admission. Sixty patients in the H1N1 group and 65 in the COVID-19 group were included in the study. Bacterial co-infection at the endotracheal intubation time was diagnosed in 33% of H1N1 and 16% COVID-19 patients (p = 0.08). The VAP incidence per 100 days of mechanical ventilation was 3.4 (2.2–5.2) in the H1N1 group and 7.2 (5.3–9.6) in the COVID-19 group (p < 0.004). The HR to develop VAP was of 2.33 (1.34–4.04) higher in the COVID-19 group (p = 0.002). Ten percent of H1N1 patients and 30% of the COVID-19 patients had a second episode of VAP (p = 0.013). COVID-19 patients have fewer bacterial co-infections upon admission, but the incidence of secondary infections increased faster in this group compared to H1N1 patients.

Background: Several studies suggest an increased incidence of thrombosis in COVID-19 patients. However, evidence on how to prevent and even treat it is scarce. The aim of this study was to compare the cumulative incidence of venous thromboembolism (VTE) of two different methods for lower extremity deep vein thrombosis (LE-DVT) diagnosis: systematic vs. clinically guided complete compression venous ultrasonography (CCUS). We conducted a monocentric, prospective, open-label, non-randomized study. All consecutive patients admitted in three intensive care units (ICUs) of University Hospital of Toulouse for COVID-19 pneumonia were included: one performed systematic screening for LE-DVT, the others did not. The primary outcome was the 21-day cumulative incidence of VTE. The secondary end points were the 21-day cumulative incidences of major bleeding and death.Results: Among the 78 patients included, 27 (34.6%) underwent systematic screening for DVT 7 ± 2 days after ICU admission. Thirty-two patients (41.0%) were diagnosed with VTE, with a 21-day cumulative incidence of 42.3% (95% CI, 31.4–55.2), without difference between screened and non-screened patients (hazard ratio 1.45, 95% CI, 0.72–2.93). In the screened group, the frequency of isolated DVT was higher (25.9 vs. 5.9%, p-value = 0.027), but the frequency of pulmonary embolism was not reduced (25.9 vs. 29.4%, p-value = 0.745). The 21-day cumulative incidences of major bleeding and death were 9.6% (95% CI, 4.7–19.2) and 10.3% (95% CI, 5.0–20.8), respectively, without difference between the two groups.Conclusions: A systematic screening for DVT in patients hospitalized in ICU was not associated with a higher diagnosis of VTE or a reduced diagnosis of PE.

IntroductionThrombocytopenia is well recognized as a poor prognosis sign associated with increased mortality and prolonged Intensive Care Unit (ICU) stay, particularly in septic patients. Mean platelet volume (MPV) could represent a relevant predictive marker of mortality. Here we investigated whether MPV kinetics during the first 15 days after hospital admission has a potential prognostic value for clinical outcome in septic shock.MethodsWe performed a retrospectively analysis of a cohort of 301 septic patients admitted in ICU. Three-month mortality was the primary endpoint. The prognostic value of the covariates of interest was ascertained by multidimensional analysis. We proposed a classification and regression trees analysis to predict survival probability.ResultsMPV kinetics was significantly different between 90-day survivors and non-survivors when followed during 15 days (except on day 3). 10-day MPV >11.6fL was an independent predictive factor of 90-day mortality (Hazard Ratio (HR) 3.796, 95% Confidence Interval (CI) [1.96-7.35], p = 0.0001) in multivariate analysis. Base excess on day 4 ConclusionMPV increase during the first 15 days after ICU admission in non-survivors was observed during septic shock and 10-day MPV >11.6fL was an independent predictive factor of 90-day mortality. This could be explained by the emergent response to acute platelet loss during septic shock, leading to megakaryocyte rupture to produce new but potentially immature platelets in the circulation. Therefore, continuous monitoring of MPV may be a useful parameter to stratify mortality risk in septic shock.

Abstract Background In sepsis, the endothelial barrier becomes incompetent, with the leaking of plasma into interstitial tissues. VE-cadherin, an adherens junction protein, is the gatekeeper of endothelial cohesion. Kinins, released during sepsis, induce vascular leakage and vasodilation. They act via two G-protein coupled receptors: B1 (B1R) and B2 (B2R). B1R is inducible in the presence of pro-inflammatory cytokines, endotoxins or after tissue injury. It acts at a later stage of sepsis and elicits a sustained inflammatory response. The aim of our study was to investigate the relationships between B1R and VE-cadherin destabilization in vivo in a later phase of sepsis. Methods Experimental, prospective study in a university research laboratory. We used a polymicrobial model of septic shock by cecal ligation and puncture in C57BL6 male mice or C57BL6 male mice that received a specific B1R antagonist (R-954). We studied the influence of B1R on sepsis-induced vascular permeability 30 h after surgery for several organs, and VE-cadherin expression in the lung and kidneys by injecting R-954 just before surgery. The 96-h survival was determined in mice without treatment or in animals receiving R-954 as a “prophylactic” regimen (a subcutaneous injection of 200 µg/kg, prior to CLP and 24 h after CLP), or as a “curative” regimen (injection of 100 µg/kg at H6, H24 and H48 post-surgery). Results B1R inactivation helps to maintain MAP above 65 mmHg but induces different permeability profiles depending on whether or not organ perfusion is autoregulated. In our model, VE-cadherin was destabilized in vivo during septic shock. At a late stage of sepsis, the B1R blockade reduced the VE-cadherin disruption by limiting eNOS activation. The survival rate for mice that received R-954 after sepsis induction was higher than in animals that received an antagonist as a prophylactic treatment. Conclusions B1R antagonizing reduced mortality in our model of murine septic shock by limiting the vascular permeability induced by VE-cadherin destabilization through maintenance of the macrohemodynamics, consequently limiting organ dysfunctions.

Abstract Background The objective of this study was to determine the main risk factors of Pseudomonas aeruginosa mutation as well as the mechanisms of acquired resistance. Methods We conducted a 2-year prospective study in patients who were carriers of a Pseudomonas aeruginosa strain and who had been admitted to a medical/surgical ICU. Results Of the 153 patients who were included, 34 had a mutation in their strain. In a multivariate analysis, a duration of ventilation > 24 days was a risk factor for mutation (risk ratio 4.29; CI 95% 1.94–9.49) while initial resistance was a protective factor (RR 0.36; CI 95% 0.18–0.71). In a univariate analysis, exposure of P. aeruginosa to ceftazidime was associated with an over-production of AmpC cephalosporinase and exposure to meropenem was associated with impermeability. A segmentation method based on the duration of ventilation (> 24 days), initial resistance, and exposure of strains to ceftazidime made it possible to predict at 83% the occurrence of mutation. Conclusion The duration of ventilation and the presence of resistance as soon as P. aeruginosa is identified are predictive factors of mutation in ICU patients.

Platelets are mainly known for their key role in hemostasis and thrombosis. However, studies over the last two decades have shown their strong implication in mechanisms associated with inflammation, thrombosis, and the immune system in various neoplastic, inflammatory, autoimmune, and infectious diseases. During sepsis, platelets amplify the recruitment and activation of innate immune cells at the site of infection and contribute to the elimination of pathogens. In certain conditions, these mechanisms can lead to thromboinflammation resulting in severe organ dysfunction. Here, we discuss the interactions of platelets with leukocytes, neutrophil extracellular traps (NETs), and endothelial cells during sepsis. The intrinsic properties of platelets that generate an inflammatory signal through the NOD-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome are discussed. As an example of immunothrombosis, the implication of platelets in vaccine-induced immune thrombotic thrombocytopenia is documented. Finally, we discuss the role of megakaryocytes (MKs) in thromboinflammation and their adaptive responses.

Posteromedial cortex (PMC) is a highly segregated and dynamic core, which appears to play a critical role in internally/externally directed cognitive processes, including conscious awareness. Nevertheless, neuroimaging studies on acquired disorders of consciousness, have traditionally explored PMC as a homogenous and indivisible structure. We suggest that a fine-grained description of intrinsic PMC topology during coma, could expand our understanding about how this cortical hub contributes to consciousness generation and maintain, and could permit the identification of specific markers related to brain injury mechanism and useful for neurological prognostication.To explore this, we used a recently developed voxel-based unbiased approach, named functional connectivity density (CD). We compared 27 comatose patients (15 traumatic and 12 anoxic), to 14 age-matched healthy controls. The patients' outcome was assessed 3months later using Coma Recovery Scale-Revised (CRS-R).A complex pattern of decreased and increased connections was observed, suggesting a network imbalance between internal/external processing systems, within PMC during coma. The number of PMC voxels with hypo-CD positive correlation showed a significant negative association with the CRS-R score, notwithstanding aetiology. Traumatic injury specifically appeared to be associated with a greater prevalence of hyper-connected (negative correlation) voxels, which was inversely associated with patient neurological outcome. A logistic regression model using the number of hypo-CD positive and hyper-CD negative correlations, accurately permitted patient's outcome prediction (AUC=0.906, 95%IC=0.795–1). These points might reflect adaptive plasticity mechanism and pave the way for innovative prognosis and therapeutics methods. Keywords: Acute brain injury, Coma, Connection density, Prognosis, Resting state