Annals of Intensive Care最新文献

Severe polytrauma and hemorrhage is a common and life-threatening condition often leading to intensive care unit admission for those who survive their initial injury. The injury itself, hypoperfusion from hemorrhagic shock, and resuscitative efforts introduce a complex set of hemostatic derangements collectively referred to as trauma-induced coagulopathy (TIC). Although the trauma population is notoriously heterogenous, TIC can generally be divided into an "early" hypocoagulable phase and then a "late" hypercoagulable, prothrombotic phase. Existing literature on TIC focuses heavily on reversing and preventing hypocoagulation in the early, acute phase. However, intensivists commonly manage patients throughout the later post-acute resuscitation phase of TIC, during which thrombotic complications are common and may lead to major morbidity and mortality. Derangements in platelet activation, endothelial dysfunction, suppression of fibrinolysis, and crosstalk between the innate immune and coagulation systems all contribute to the prothrombotic late TIC phenotype. Deep venous thrombosis and other macrovascular thrombotic complications also commonly occur after trauma. Thrombosis prophylaxis and treatment present a challenge for patients still at high risk for bleeding. An in-depth understanding of risk factors specific to trauma patients, including iatrogenic contributions from resuscitation and hemostatic efforts in the pre-intensive care phase, can help stratify thromboembolic risk and optimize prophylaxis and surveillance efforts. We stress the importance of an individualized approach to assessment of hemorrhagic and thrombotic risks for each patient. Here, we summarize the underlying contributors to the prothrombotic phenotype in late TIC, including a description of emerging roles for HMGB1, extracellular vesicles, and endogenous inhibitors. Additionally, a general approach to thromboprophylaxis, monitoring, and anticoagulation in this patient population are discussed. Finally, we summarize relevant risk stratification systems and guidelines for clinical management of thromboembolic risk among trauma patients, and highlight limitations in these systems and guidelines as areas for future research.

Background: Carbapenem-resistant Acinetobacter baumannii (CRAB) poses a significant global threat due to limited therapeutic options and high rates of associated mortality. CRAB-related bloodstream infections (BSIs) in intensive care units (ICUs) represent a major clinical challenge. This study aimed to investigate the clinical outcomes of CRAB-BSIs in ICU settings and evaluate the prognostic effect of different antimicrobial regimens.

Methods: This multicenter, retrospective observational study was conducted at five medical centers in Taiwan and included 393 critically ill patients with CRAB-BSIs between January 2015 and December 2019. Clinical and microbiological outcomes were analyzed. Multivariable regression analysis was used to identify independent prognostic factors for day-28 mortality.

Results: The most common causes of CRAB-BSIs were pneumonia (42.5%) and catheter-related infections (38.7%). The day-28 mortality rate following BSI onset was 56.5%. A higher sequential organ failure assessment (SOFA) score independently predicted increased day-28 mortality. Colistin-based therapy was associated with improved survival outcomes in the original (adjusted hazard ratio [aHR], 0.56; 95% confidence intervals (CI), 0.35-0.88) and time-window bias-adjusted (aHR, 0.59; 95% CI, 0.37-0.94) cohorts. Among patients with pneumonia-related CRAB-BSIs, colistin-based therapy did not significantly improve day-28 survival, whereas sulbactam-based therapy showed survival benefit (aHR, 0.37; 95% CI, 0.15-0.91). Neither carbapenem-based nor tigecycline-based therapies demonstrated a mortality benefit on day 28.

Conclusion: CRAB-BSIs are associated with high mortality in critically ill patients. In settings where novel antibiotics are not available, colistin-based therapy was associated with improved clinical outcomes. Among patients with pneumonia-related CRAB-BSIs, sulbactam-based therapy was associated with lower mortality.

Background: Patients with comorbidities who are liberated from invasive mechanical ventilation could be at risk of extubation failure in the intensive care unit (ICU). Incidence and associated outcomes of reintubation in patients with cirrhosis have been poorly studied. We aimed to evaluate the incidence, causes and mortality of reintubation in patients with cirrhosis.

Methods: We conducted a post hoc analysis of the French prospective multicenter observational trial (FREE-REA) evaluating the incidence and risk factors of extubation failure in 26 ICUs. The primary outcome was the incidence of extubation failure defined as the need for reintubation within 7 days after extubation. Secondary outcomes were the incidence of reintubation at 48 h, the causes and risk factors of extubation failure, ICU length of stay and in-hospital mortality. We compared patients with cirrhosis and patients without cirrhosis.

Results: Of the 1,443 analyzed patients, 165 (11%) had cirrhosis. The incidence of reintubation within 7 days was 21% (34/165) in patients with cirrhosis and 13% (167/1278) in patients without cirrhosis (p < 0.01). Reintubation at 48 h was not significantly different between patients with cirrhosis and patients without cirrhosis (9% versus 10%, p = 0.55). Admission for shock was identified as the only independent risk factor for extubation failure in multivariate analysis [OR 3.24, 95% CI (1.24-8.44), p = 0.02]. In patients with extubation failure, ICU length of stay was significantly longer in patients with cirrhosis compared to those without (28 ± 25 versus 18 ± 12 days, p < 0.01); In-hospital mortality was higher in extubation failure patients with cirrhosis in comparison to patients without cirrhosis without reaching significance (16/34 (47%) versus 51/167 (31%), p = 0.06).

Conclusion: Extubation failure was significantly higher in patients with cirrhosis compared to patients without cirrhosis. A trend for higher in-hospital mortality was observed in reintubatedpatients with cirrhosis. Neurologic failure was the main cause for reintubation at 48 h in patients with cirrhosis.

Clinical trials: The study was registered on clinicaltrials.gov (identifier no. NCT02450669). Registered 01/12/2013.

Background: Despite the increasing use of venoarterial extracorporeal membrane oxygenation (VA-ECMO) in cardiogenic shock (CS), reliable predictors of successful weaning remain poorly defined. This study investigated the role of carbon dioxide elimination parameters in VA-ECMO weaning.

Methods and results: To assess the potential role of end-tidal carbon dioxide (EtCO₂) in predicting successful VA-ECMO weaning, we conducted a prospective observational study at Anzhen Hospital between January 2023 and December 2024. The primary endpoint was the predictive performance of EtCO₂ and VCO₂NL ratio for successful VA-ECMO weaning. Real-time EtCO₂ monitoring was performed using infrared capnography in mechanically ventilated patients, and the ratio of native lung carbon dioxide elimination (VCO₂NL) to total carbon dioxide elimination (VCO₂TOT) was calculated as the VCO₂NL ratio. Dynamic changes in these parameters were analysed in relation to weaning outcomes. Among 294 patients receiving VA-ECMO for refractory CS during the study period, 91 were included, yielding 562 data points. Both EtCO₂ (odds ratio [OR] = 1.26, 95% confidence interval [CI] 1.17-1.37, p < 0.0001) and the VCO₂NL ratio (1.14, 95% CI 1.09-1.21, p < 0.0001) showed significant correlations with successful weaning. A VCO₂NL ratio > 79% and EtCO₂ > 34 mmHg showed strong predictive value for successful weaning (area under the receiver operating characteristics (ROC) curve values of 0.85 [95% CI 0.80-0.89] and 0.84 [95% CI 0.79-0.89], p < 0.0001).

Conclusions: EtCO₂ and the VCO₂NL ratio may be valuable indicators for predicting successful VA-ECMO weaning. Higher EtCO₂ and VCO₂NL ratio values are associated with a greater likelihood of successful weaning.

Introduction: Socio-economic inequalities have been identified as a potential risk factor for adverse outcomes in patients with Covid-19. In the specific setting of critical care, data are currently more controversial. The aim of our study is to assess the impact of social inequalities on the outcome of patients admitted to intensive care unit (ICU) for Covid-19 through a national French observational study.

Methods: Based on the French administrative health care database, we identified all adults living in metropolitan France admitted in ICU for COVID-19 between March 1, 2020 and December 31, 2021. Two covariates were used to measure social vulnerability: an ecological deprivation index, the French deprivation index (Fdep), categorized in quintile (Q5 represented the most deprivated localization), and being a beneficiary of a complementary health coverage for the most deprived (CSS/AME beneficiary status). Primary outcome was in-hospital death. Secondary outcome was need for mechanical ventilation and post-acute care transfer in rehabilitation unit. Fine-Gray survival analysis or logistic regression were used according the competitive risk context. Three sensitivity analyses were performed: (1) restriction to patients admitted after January 1, 2021, adjusting for vaccination status; (2) multilevel logistic regression with a hospital-level random intercept; and (3) sex-stratified analyses.

Results: There were 120 191 patients admitted to ICU with Covid-19 across metropolitan France. Among them, 29 580 (24.6%) patients lived in the most disadvantage areas and 12 462 (10.4%) were CSS/AME beneficiaries. In multivariate analysis, Fdep and CSS/AME beneficiary status were both associated with higher likelihood of in-hospital death (aSHR = 1,21 ; 95%CI = 1,16 - 1,27 for Fdep-Q5 and aSHR = 1,06 ; 95%CI = 1,01-1,11 for being beneficiary of CSS/AME) and need for invasive mechanical ventilation (aSHR = 1,16 ; 95%CI = 1,12 - 1,20 for Fdep-Q5 and aSHR = 1,06 ; 95%CI = 1,02 - 1,09 for being beneficiary of CSS/AME). Among survivors, a post-acute care transfer was negatively associated Fdep-Q5 in patients above 60 years (OR = 0.88; 95%CI = 0.81-0.94), in CSS/AME beneficiaries under 60 years (OR = 0.87; 95%CI = 0.80-0.98) as well as above 60 years (aSHR = 0.81; 95%CI = 0.74-0.88). Results were consistent across all sensitivity analyses.

Conclusion: Social vulnerability was associated with higher hospital mortality, higher use of invasive mechanical ventilation and lower post-acute care transfer in rehabilitation unit in patients admitted to the ICU for COVID-19.

Background: Sepsis is associated with dynamic metabolic alterations influencing energy expenditure and substrate utilization. This study aimed to evaluate time-course changes in energy metabolism in critically ill patients with sepsis and identify clinical and nutritional predictors of resting energy expenditure (REE) and respiratory quotient (RQ).

Methods: In this prospective observational study, 30 mechanically ventilated adult patients with sepsis were assessed using indirect calorimetry on days 1, 2, 3, 5, and 7 following diagnosis. Nutritional treatment, biochemical markers, and clinical variables were recorded. Linear mixed-effects models were applied to evaluate temporal changes and identify predictors of REE and RQ.

Results: REE increased by Day 5 versus Day 1 (+ 163.7 kcal/day; p = 0.049), with a concurrent rise in RQ (p = 0.013). Higher body temperature, higher arterial pH, a greater protein-to-non-protein calorie ratio, and higher protein intake were associated with higher REE, whereas higher lactate concentrations and use of CRRT were associated with lower REE. RQ was positively associated with energy intake, REE coverage, and blood glucose. Clinical-severity scores and inflammatory markers showed no significant associations with REE or RQ.

Conclusions: Energy metabolism in sepsis evolves dynamically, with significant changes in REE and substrate utilization over time. Temperature, acid-base balance, CRRT, and nutritional strategies were associated with variability in energy expenditure. These findings support the need for individualised metabolic assessment and targeted nutritional strategies in critically ill patients with sepsis.

Background: Liberal administration of crystalloid fluid is often required to maintain adequate tissue perfusion when treating life-threatening conditions. Current knowledge indicates that either overhydration or underhydration can promote complications. This review describes how fluid distributes between body compartments, with the aim of finding insights into pathophysiological mechanisms that can explain why fluid overload may cause complications and even be fatal.

Main text: The skin, intestinal wall, and lungs are known primary locations of excess amounts of crystalloid fluid in humans. Microscopic studies in animals show that infusion of > 100 mL/kg of crystalloid fluid also causes interstitial dilatation and swelling of the heart, tissue breakup, and cardiac hypoxia. Volume kinetic analysis has identified several factors that promote peripheral edema during general anesthesia. Volume kinetics also shows that increasing volumes of crystalloid fluid sequentially expands three body fluid compartments: the plasma, a fast-exchange interstitial volume, and a more remote slow-exchange interstitial volume (in scientific jargon called "the third fluid space"). In settings of overhydration, the slow-exchange space operates as an overflow reservoir and quickly begins to accumulate fluid when the fast-exchange compartment has increased by 600-800 mL, which corresponds to infusing approximately 1.3-1.5 L of crystalloid fluid into the plasma over 30 min. Apart from overhydration, accumulation of fluid in the slow-exchange space occurs in inflammatory conditions, whereby cytokines and vasoactive molecules create a suction pressure that withdraws fluid from the fast-exchange space. This suction decreases lymphatic flow, causing hypovolemia and hypoalbuminemia in addition to peripheral edema. Preeclampsia and sepsis are examples of this complex kinetic situation. Albumin (20%), a hyper-oncotic colloid, might be used to modify peripheral edema by recruiting interstitial (lymphatic) fluid and stimulating diuresis.

Conclusion: Excess amounts of crystalloid fluid accumulate in body regions, such as the skin and intestinal walls, that have a high compliance for volume expansion. The heart is potentially a key trouble spot in severe overhydration. Accumulation of fluid in an interstitial fluid space that equilibrates slowly with the plasma volume occurs in settings of overhydration and inflammation. Pathophysiological mechanisms that explain the complications and fatal outcomes of overhydration are insufficiently known in humans.

Severe malaria, caused by Plasmodium falciparum, poses a critical public health challenge, with cerebral malaria (CM) representing its most severe and life-threatening neurological manifestation. Defined by impaired consciousness (Glasgow Coma Score < 11) after the exclusion of other causes of encephalopathy, CM remains a critical condition with a mortality rate of 15-25% and long-term neurological sequelae in survivors. CM pathogenesis involves parasitized erythrocyte sequestration in cerebral microvasculature, immune hyperactivation, blood-brain barrier disruption, and cerebral edema, potentially leading to elevated intracranial pressure (ICP) and cerebral ischemia. These processes culminate in severe neurological injury, emphasizing the importance of ICP management in minimizing secondary brain damage. Neuromonitoring (NM) strategies, including invasive and non-invasive techniques, are critical yet underutilized in adults with CM due to limited evidence and logistical challenges. Treatment relies on antimalarial therapy, with intravenous artesunate as the first-line drug, supported by targeted interventions to manage seizures and systemic complications. Adjunctive therapies remain experimental, with no proven benefit in routine care. Emerging evidence from pediatric studies offers valuable insights, though significant gaps in adult-focused research persist. This review, which examines severe CM pathophysiology, clinical manifestations, and management, focusing on adult populations, underscores the need for tailored NM approaches, protocolized management strategies, and further investigation to improve outcomes in adults with CM, advocating for a multidisciplinary approach within the intensive care setting.