Annals of Intensive Care最新文献

Introduction: Ventilator-associated pneumonia (VAP) and ventilated hospital-acquired pneumonia (vHAP) are major causes of morbidity and mortality in intensive care unit (ICU) patients. The role of viral co-infections in these conditions is an emerging area of interest; however, their impact on clinical outcomes remains poorly understood. This study aimed to assess the effect of viral detection on mortality and other clinical outcomes in patients with bacterial vHAP/VAP.

Materials and methods: We conducted a retrospective analysis of patients diagnosed with bacterial vHAP or VAP in a tertiary ICU between 2020 and 2024. All patients underwent distal respiratory sampling with quantitative culture and multiplex PCR (mPCR) testing for respiratory viruses (Biofire FilmArray Pneumonia Panel). Patients with SARS-CoV-2 infection were excluded. Those with bacterial and viral co-infections were matched 1:1 with patients having bacterial-only vHAP/VAP based on age, sex, SAPS II score, ICU admission cause, and causative bacteria. We compared clinical outcomes, including ICU mortality, 3-month mortality, ICU length of stay, and duration of mechanical ventilation between the two groups.

Results: Eighty patients were included, 40 with bacterial and viral detection and 40 with bacterial-only vHAP/VAP. The median age was 63 years, and 92% of the cohort were male. Common comorbidities included diabetes (25%), heart failure (20%), chronic renal failure (20%), and chronic lung disease (32%). Nineteen percent of patients were immunocompromised. The viral pathogens identified in the co-infection group were rhinovirus/enterovirus 33% (13/40), endemic coronaviruses 30% (12/40), influenza viruses 10% (4/40), parainfluenza viruses 8% (3/10), adenovirus 8% (3/10), metapneumovirus 5% (2/40), and respiratory syncytial virus 5% (2/40). Respiratory viruses were detected in a nasopharyngeal swab in 30% (12/30). The 3-month mortality rate was 36%, ICU mortality was 32%, the median duration of mechanical ventilation was 21 days [IQR 12-31.5], and the median ICU length of stay was 24 days [IQR 13-39.5]. There were no significant differences in these outcomes between the bacterial and viral group and the bacterial-only group.

Conclusions: In this cohort of patients with bacterial vHAP/VAP, the detection of respiratory viruses did not significantly impact ICU mortality, 3-month mortality, or ICU length of stay. These findings may suggest that bacterial infections are the primary determinants of clinical outcomes in vHAP/VAP.

Background: Critical illness myopathy (CIM) increases mortality and causes long-term disabilities. CIM is characterized by reduced muscle excitability, muscle atrophy, weakness, and impaired glucose metabolism. Functional circadian rhythms are important for skeletal muscle homeostasis. Circadian rhythms are often disrupted during critical illness in the Intensive Care Unit (ICU). This analysis investigates whether diurnal temperature rhythms differ in critically ill CIM compared to no-CIM patients.

Methods: This is a secondary analysis of two prospective trials including critically ill patients with CIM (n = 32) or no-CIM (n = 30) based on electrophysiological tests. Diurnal body temperature rhythms were compared between CIM and no-CIM groups in reference to n = 16 participants included in a bed rest study. Cosinor analysis was performed to determine the rhythm parameters and classify into rhythm classes. Aggregated and longitudinal data were compared between groups using non-parametric tests. Rhythm parameters were correlated with muscle atrophy, weakness and insulin sensitivity.

Results: CIM and no-CIM patients had severe multiorgan failure (median SOFA score 12 in both groups, p = 0.39). The temperature rhythm nadir timepoint was shifted in CIM patients (10:43 [09:21, 12:22]) and no-CIM (11:12 [09:43, 13:30]) compared to the healthy bed rest group (5:03 [3:22, 6:36]) p < 0.001. CIM patients showed lower temperature rhythm mesors than no-CIM patients (p = 0.041). The temperature rhythm amplitude was lower in both CIM and no-CIM patients compared to the healthy bed rest group (CIM: 0.3 °C [0.2, 0.4]; no-CIM: 0.2 °C [0.2, 0.3]; healthy bed rest: 0.5 °C [0.2, 0.6]; p < 0.01). Compared to no-CIM patients, CIM patients had higher temperature rhythm amplitudes (p = 0.021) and showed a less pronounced reduction in temperature rhythm amplitudes during ICU stay (p = 0.017). A higher temperature rhythm amplitude correlated negatively with M. vastus lateralis myocyte cross-sectional area.

Conclusions: Heterogeneous phase shifts of diurnal temperature rhythms in CIM and no-CIM groups compared to healthy bed rest volunteers may indicate ICU-related circadian disruption. Suppression of temperature rhythm amplitude during ICU stay could represent an adaptive response to this disruption. Blunted amplitude suppression observed in CIM compared to no-CIM patients might reflect reduced adaptation, potentially contributing to muscle catabolism. This hypothesis-generating analysis underlines the need for mechanistic studies exploring circadian regulation in skeletal muscle during critical illness.

The understanding of the response to stress in critical illness has significantly improved in recent years. These adaptations unfold across acute, subacute, and chronic phases, with an early adaptive catabolic state, marked anabolic resistance, and a later transition toward recovery. The aim of this updated review is to summarize recent advancements focusing on pathophysiological changes in endocrine, immune, gut, and mitochondrial functions and their effects on the metabolic shift in energy production, using glycolysis and the utilization of lactate and ketones as alternative pathways to meet cellular energy demands. Advances in understanding key elements such as energy expenditure and autophagy have expanded our knowledge. Furthermore, there is increased interest in the consequences of an intense and prolonged stress response, which can lead to ICU-acquired weakness (ICU AW) and post-intensive care syndrome. Recent evidence indicates that higher protein strategies generally do not improve survival or functional recovery and may signal harm in patients with renal dysfunction, supporting cautious, phase-appropriate protein dosing rather than routine high targets. New concepts, such as chronic critical illness (CCI) and persistent inflammation, immunosuppression, and catabolism syndrome (PICS), have also emerged to characterize prolonged stress responses. For glycaemic management, intensive control offers no outcome benefit and increases hypoglycaemia risk; moderate targets are preferred. Parallel advancements in monitoring techniques, such as indirect calorimetry and body composition analysis, have improved the assessment of the consequences of the metabolic changes. Metabolomics has offered deeper characterisation of the metabolic response to stress and nutrition, highlighting key metabolic pathways and potential therapeutic targets. Integrating biomarkers and metabolomics to define clinical endotypes may help time the transition from catabolic to anabolic strategies and personalize nutrition and pharmacologic support at the bedside. New therapeutic avenues have emerged or are under investigation, including glycaemic control, nutritional strategies, and some specific interventions targeting key components of the metabolic response. In this context, we present a narrative review of the literature with a focus on the clinical consequences of the pathophysiological and metabolic response to stress, alongside therapeutic implications and future perspectives.

Background: Sepsis is characterized by a dysregulated immune response to infection, with a balance between hyperinflammation and immunosuppression, which determines the patient's immune status. Real-time monitoring of the immune status in sepsis is crucial for guiding immunotherapy. However, reliable biomarkers are lacking. This study aims to identify a panel of biomarkers for rapid bedside assessment of immune status in sepsis to guide immunotherapy decisions.

Results: TBX21, GNLY, PRF1, and IL2RB represent the immune status in sepsis. These genes demonstrated discriminatory power in the external validation, with area under the curve values ranging from 0.891 to 0.909 across several machine learning models. 99 double-blind randomized patients with sepsis were clustered into two endotypes on the basis of the expression of the four-gene panel. Higher 90-day mortality was observed in patients with sepsis treated with hydrocortisone (Odds ratio 12.46, 95% confidence intervals 3.11 to 65.72) or thymosin (Odds ratio 4.17, 95% confidence intervals 1.13 to 16.51) within the high-expression 4-gene panel endotype, but not in another endotype.

Conclusions: The results support the potential utility of a four-gene panel to assess immune status and guide immunotherapy; further prospective validation and translational studies are warranted. Trial registration National Medical Research Registration and Filing Information of China, 2022ZDSYLL196-P01. Registered 26 May 2023, https://www.medicalresearch.org.cn/login.

Background: Patients with septic shock who survive the early resuscitation phase are prone to ICU-acquired infections. Although hyperglycemia harbors potent immunomodulatory properties, the impact of preexisting diabetes and the control of acute stress-induced hyperglycemia on the risk of further infections remains unclear.

Materials and methods: We conducted a retrospective (2008-2023) single-center study in patients with septic shock who remained alive in the ICU after 72 h. Glycemic control was assessed during the first 72 h. Mild and severe hyperglycemia were defined by blood glucose levels > 8 mmol/L and > 10 mmol/L, respectively. Poor glycemic control was defined when blood glucose levels were above 8 mmol/L for more than 20% of time. The primary outcome was ICU-acquired infections.

Results: The study involved 901 patients, with preexisting diabetes present in 22% of them. Most patients (71%) experienced hyperglycemic episodes > 8 mmol/L, prompting fast-acting insulin treatment. ICU-acquired infections developed in 243 patients (26.9%), with median time from ICU admission to diagnosis of 9 days, interquartile range [6-13]. There was no association between preexisting diabetes and ICU-acquired infections. Patients with further ICU-acquired infections displayed poorer control of stress-induced hyperglycemia, with longer exposure to hyperglycemia (78% with mild or severe hyperglycemia for more than 20% of time compared to 68% of patients without subsequent infections (p = 0.005)). Poor glycemic control was independently associated with the development of ICU-acquired infections.

Conclusion: 72-hour poor glycemic control, but not preexisting diabetes, was independently associated with an increased risk of ICU-acquired infections in septic shock patients and may therefore contribute to the post-aggressive immunosuppressive response. This argues for effective glycemic management to improve outcomes in this setting.

Objective: To understand the impact of obesity on outcomes of weaning from invasive mechanical ventilation (MV).

Methods: The study population consisted of patients enrolled in the WEAN SAFE study. We defined 4 groups based on body mass index (BMI), namely: Normal weight (BMI 18.5-24.9 kg/m²), Overweight (BMI 25-29.9 kg/m²), Obesity Class I (BMI 30-34.9 kg/m²), and obesity classes II and III (BMI ≥ 35 kg/m²). The primary outcome was the rate of successful extubation in patients in each BMI group. Secondary outcomes included the ICU and hospital survival, and PEEP levels at time of weaning eligibility in patients in each BMI group.

Results: In the study population, 1728 (38.2%) were of normal weight, 1395 (30.8%) were overweight, 590 (13.1%) were class I Obesity, and 431 (9.5%) were obesity classes II and III. Patients with obesity were more likely to be female, to be a medical admission, and to have comorbidities. Patients with grade II-III obesity had lower levels of sedation, later timing of the first separation attempt, longer time to weaning success, they received more noninvasive ventilation post extubation, and they had a longer ICU stay. In contrast, weaning success, and ICU and hospital mortality rates were not different in obese patients. There was no independent relationship between obesity and weaning delay, weaning success, or with overall survival outcomes. Higher PEEP at weaning eligibility was associated with weaning failure in normal and overweight patients but not in patients with obesity.

Conclusions: Patients with obesity had a more complex and longer weaning process, but obesity per se was not independently associated with adverse weaning outcomes.