Objectives: We performed a national cross-sectional survey to determine the epidemiologic characteristics of patients with sepsis in ICU in China. Design: A cross-section survey study. Setting: Forty-four hospitals in mainland China from December 1, 2015, to January 31, 2016. Patients: All septic patients diagnosed according sepsis-1 criteria admitted to participating ICU. Interventions: None. Measurements and Main Results: We recorded demographic, physiologic, and microbiological data with follow-up for 90 days or death, if sooner. The frequency of sepsis and 90-day mortality rate were computed, and the relationship with gross domestic product determined. Multivariate logistic regression analysis was used to determine risk factors for 90-day mortality in patients with sepsis. Two-thousand three-hundred twenty-two patients with sepsis were included in the analysis, of whom 786 patients (33.9%) had hospital-acquired sepsis. The most common infection site was the lung (68.2%), followed by abdomen (26.6%) and bloodstream (7.8%). The frequency of sepsis in the ICU was 20.6 cases per 100 ICU admissions (95% CI, 15.8–25.4) with a 90-day mortality of 35.5%. The proportion of sepsis, severe sepsis, and septic shock were 3.10%, 43.6%, and 53.3% with a 90-day mortality of 2.78%, 17.69%, and 51.94%, respectively. Older age, low body weight, higher Sequential Organ Failure Assessment score, the number of systemic inflammatory response syndrome criteria, comorbid with heart failure, hematologic cancer, immunosuppression, higher level of lactate, infection site (pneumonia and bloodstream) were associated with 90-day mortality. Conclusions: Sepsis affects a fifth of patients admitted to ICUs in mainland China with a 90-day mortality rate of 35.5%. Our findings indicate that a large burden of sepsis, and we need to focus on sepsis as a quality improvement target in China given the high mortality. In addition, further studies are needed to delineate the epidemiology of sepsis outside the ICU.

BackgroundThe effect of corticosteroids on influenza A(H1N1)pdm09 viral pneumonia patients remains controversial, and the impact of dosage has never been studied.MethodsUsing data of hospitalized adolescent and adult patients with influenza A(H1N1)pdm09 viral pneumonia, prospectively collected from 407 hospitals in mainland China, the effects of low‐to‐moderate‐dose (25‐150 mg d−1) and high‐dose (>150 mg d−1) corticosteroids on 30‐day mortality, 60‐day mortality, and nosocomial infection were assessed with multivariate Cox regression and propensity score‐matched case–control analysis.ResultsIn total, 2141 patients (median age: 34 years; morality rate: 15.9%) were included. Among them, 1160 (54.2%) had PaO2/FiO2<300 mm Hg on admission, and 1055 (49.3%) received corticosteroids therapy. Corticosteroids, without consideration of dose, did not influence either 30‐day or 60‐day mortality. Further analysis revealed that, as compared with the no‐corticosteroid group, low‐to‐moderate‐dose corticosteroids were related to reduced 30‐day mortality (adjusted hazard ratio [aHR] 0.64 [95% CI 0.43‐0.96, P=.033]). In the subgroup analysis among patients with PaO2/FiO2<300 mm Hg, low‐to‐moderate‐dose corticosteroid treatment significantly reduced both 30‐day mortality (aHR 0.49 [95% CI 0.32‐0.77]) and 60‐day mortality (aHR 0.51 [95% CI 0.33‐0.78]), while high‐dose corticosteroid therapy yielded no difference. For patients with PaO2/FiO2 ≥300 mm Hg, corticosteroids (irrespective of dose) showed no benefit and even increased 60‐day mortality (aHR 3.02 [95% CI 1.06‐8.58]). Results were similar in the propensity model analysis.ConclusionsLow‐to‐moderate‐dose corticosteroids might reduce mortality of influenza A(H1N1)pdm09 viral pneumonia patients with PaO2/FiO2<300 mm Hg. Mild patients with PaO2/FiO2 ≥300 mm Hg could not benefit from corticosteroid therapy.

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BackgroundThe aim of the present study was to investigate the incidence of adverse events (AEs) during intra-hospital transport (IHT) of critically ill patients and evaluate the risk factors associated with these events.MethodsThis prospective multicenter observational study was performed in 34 intensive care units in China during 20 consecutive days from 5 November to 25 November 2012. All consecutive patients who required IHT for diagnostic testing or therapeutic procedures during the study period were included. All AEs that occurred during IHT were recorded. The incidence of AEs was defined as the rate of transports with at least one AE. The statistical analysis included a description of demographic and clinical characteristics of the cohort as well as identification of risk factors for AEs during IHT by univariate and multivariate logistic regression analyses.ResultsIn total, 441 IHTs of 369 critically ill patients were analyzed. The overall incidence of AEs was 79.8 % (352 IHTs). The proportion of equipment- and staff-related adverse events was 7.9 % (35 IHTs). The rate of patient-related adverse events (P-AEs) was 79.4 % (349 IHTs). The rates of vital sign–related P-AEs and arterial blood gas analysis–related P-AEs were 57.1 % (252 IHTs) and 46.9 % (207 IHTs), respectively. The incidence of critical P-AEs was 33.1 % (146 IHTs). The rates of vital sign–related critical P-AEs and arterial blood gas analysis–related critical P-AEs were 22.9 % (101 IHTs) and 15.0 % (66 IHTs), respectively. All data collected in our study were considered potential risk factors. In the multivariate analysis, predictive factors for P-AEs were pH, partial pressure of carbon dioxide in arterial blood, lactate level, glucose level, and heart rate before IHT. Furthermore, the Acute Physiology and Chronic Health Evaluation II score, partial pressure of oxygen in arterial blood, lactate level, glucose level, heart rate, respiratory rate, pulse oximetry, and sedation before transport were independent influential factors for critical P-AEs during IHT.ConclusionsThe incidence of P-AEs during IHT of critically ill patients was high. Risk factors for P-AEs during IHT were identified. Strategies are needed to reduce their frequency.Trial registrationChinese Clinical Trial Register identifier ChiCTR-OCS-12002661. Registered 5 November 2012.

The aim of this study was to determine the efficacy of immunonutrition vs standard nutrition in cancer patients treated with surgery. Cochrane Central Register of Controlled Trials, EMBASE, MEDLINE, EBSCOhost, and Web of Science were searched. Sixty‐one randomized controlled trials were included. Immunonutrition was associated with a significantly reduced risk of postoperative infectious complications (risk ratio [RR] 0.71 [95% CI, 0.64–0.79]), including a reduced risk of wound infection (RR 0.72 [95% CI, 0.60–0.87]), respiratory tract infection (RR 0.70 [95% CI, 0.59–0.84]), and urinary tract infection (RR 0.69 [95% CI, 0.51–0.94]) as well as a decreased risk of anastomotic leakage (RR 0.70 [95% CI, 0.53–0.91]) and a reduced hospital stay (MD −2.12 days [95% CI −2.72 to −1.52]). No differences were found between the 2 groups with regard to sepsis or all‐cause mortality. Subgroup analyses revealed that receiving arginine + nucleotides + ω‐3 fatty acids and receiving enteral immunonutrition reduced the rates of wound infection and respiratory tract infection. The application of immunonutrition at 25–30 kcal/kg/d for 5–7 days reduced the rate of respiratory tract infection. Perioperative immunonutrition reduced the rate of wound infection. For malnourished patients, immunonutrition shortened the hospitalization time. Therefore, immunonutrition reduces postoperative infection complications and shortens hospital stays but does not reduce all‐cause mortality. Patients who are malnourished before surgery who receive arginine + nucleotides + ω‐3 fatty acids (25–30 kcal/kg/d) via the gastrointestinal tract during the perioperative period (5–7 days) may show better clinical efficacy.

Glycolytic metabolism plays an important role in mediating sepsis-induced septic cardiomyopathy. The mechanisms may involve regulation of inflammatory response and apoptotic signaling.

Recent studies have shown that myocardial ischemia/reperfusion (I/R)-induced necrosis can be controlled by multiple genes. In this study, we observed that both strands (5p and 3p) of miR-223 were remarkably dysregulated in mouse hearts upon I/R. Precursor miR-223 (pre-miR-223) transgenic mouse hearts exhibited better recovery of contractile performance over reperfusion period and lesser degree of myocardial necrosis than wild type hearts upon ex vivo and in vivo myocardial ischemia. Conversely, pre-miR-223 knock-out (KO) mouse hearts displayed opposite effects. Furthermore, we found that the RIP1/RIP3/MLKL necroptotic pathway and inflammatory response were suppressed in transgenic hearts, whereas they were activated in pre-miR-223 KO hearts upon I/R compared with wild type controls. Accordingly, treatment of pre-miR-223 KO mice with necrostatin-1s, a potent necroptosis inhibitor, significantly decreased I/R-triggered cardiac necroptosis, infarction size, and dysfunction. Mechanistically, we identified two critical cell death receptors, TNFR1 and DR6, as direct targets of miR-223-5p, whereas miR-223-3p directly suppressed the expression of NLRP3 and IκB kinase α, two important mediators known to be involved in I/R-induced inflammation and cell necroptosis. Our findings indicate that miR-223-5p/-3p duplex works together and cooperatively inhibits I/R-induced cardiac necroptosis at multiple layers. Thus, pre-miR-223 may constitute a new therapeutic agent for the treatment of ischemic heart disease.

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