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We investigated serum soluble CD163 (sCD163) levels for use in the diagnosis, severity assessment, and prognosis of sepsis in the critical ill patients and compared sCD163 with other infection-related variables. During july 2010 and April 2011, serum was obtained from 102 sepsis patients (days 1, 3, 5, 7, and 10 after admission to an ICU) and 30 systemic inflammatory response syndrome (SIRS) patients with no sepsis diagnosed. Serum levels of sCD163, procalcitonon (PCT), and C reactive protein (CRP) were determined respectively. Sequential organ failure assessment (SOFA) scores for sepsis patients were also recorded. Then evaluated their roles in sepsis. The sCD163 levels were 0.88(0.78-1.00) ug/mL for SIRS patients, 1.50(0.92-2.00) ug/mL for moderate sepsis patients, and 2.95(2.18-5.57) ug/mL for severe sepsis patients on day 1. The areas under the ROC curves for sCD163, CRP, and PCT for the diagnosis of sepsis were, respectively, 0.856(95%CI: 0.791-0.921), 0.696(95%CI: 0.595-0.797), and 0.629(95%CI: 0.495-0.763), At the recommended cut-off 1.49 ug/mL for sCD163, the sensitivity is 74.0% with 93.3% specificity. Based on 28-day survivals, sCD163 levels in the surviving group stay constant, while they tended to gradually increase in the non-surviving group.The area under the ROC curve for sCD163 for sepsis prognosis was 0.706(95%CI 0.558-0.804). Levels of sCD163 with cut-off point >2.84 ug/mL have sensitivity of 55.8.0%, specificity 80.4%. Common risk factors for death and sCD163 were included in multivariate logistic regression analysis; the odds ratios (OR) for sCD163 and SOFA scores for sepsis prognosis were 1.173 and 1.396, respectively (P<0.05). Spearman rank correlation analysis showed that sCD163 was weakly, but positively correlated with CRP, PCT, and SOFA scores (0.2< r <0.4, P<0.0001), but not with leukocyte counts (r <0.2, P = 0.450). Serum sCD163 is superior to PCT and CRP for the diagnosis of sepsis and differentiate the severity of sepsis. sCD163 levels were more sensitive for dynamic evaluations of sepsis prognosis. Serum sCD163 and SOFA scores are prognostic factors for sepsis. www.chictr.orgChiCTR-ONC-10000812.

Background It is very important to assess the effectiveness of prone positioning (PP) in patients with severe acute respiratory distress syndrome (ARDS). However, it is difficult to identify patients who may benefit from PP. The purpose of this study was to investigate whether prone positioning potential (PPP) can be predicted by lung ultrasound in patients with ARDS. Methods In this prospective study, 45 patients with ARDS were included for the assessment of PPP. A PP lung ultrasound examination (PLUE) protocol was performed in the dorsal regions of the lung in 16 areas at H0, H3, and H6 (0, 3, and 6 h after PP). The ultrasonography videos were blindly evaluated by two expert clinicians to classify the lung regions as normal pattern (N), moderate loss of lung aeration (B1), severe loss of lung aeration (B2), and consolidation (C). The aeration scores were collected at H0, H3, and H6. According to the ratio of partial pressure of arterial oxygen to fraction of inspired oxygen (P/F ratio) at 7 days, patients were classified into PPP-positive (P/F ratio >300) and PPP-negative groups; also, the patients were classified into survival and nonsurvival groups according to 28-day mortality. Results Aeration scores was compared at H0, H3, and H6. The scores were significantly reduced between H3 and H0, but there was no difference between H3 and H6. The aeration score variation (ASV) of the PPP-positive group between H3 and H0 was significantly higher than that in the PPP-negative group, and the sensitivity and specificity of ASV ≥5.5 for the PPP-positive group were 73.9% and 86.4%, respectively. The area under the receiver operating characteristic curve (AUROC) was 0.852 for the ASV. The ASV between H3 and H0 in the survival group was significantly higher than in the nonsurvival group. The sensitivity and specificity of ASV ≥7 for survival were 51.5% and 75%, respectively. The AUROC was 0.702 for the ASV. Conclusions The PLUE protocol can be used to predict PPP and assess prognosis in patients with ARDS.

Acute respiratory distress syndrome (ARDS) is one of the most common severe diseases seen in the clinical setting. With the continuous exploration of ARDS in recent decades, the understanding of ARDS has improved. ARDS is not a simple lung disease but a clinical syndrome with various etiologies and pathophysiological changes. However, in the intensive care unit, ARDS often occurs a few days after primary lung injury or after a few days of treatment for other severe extrapulmonary diseases. Under such conditions, ARDS often progresses rapidly to severe ARDS and is difficult to treat. The occurrence and development of ARDS in these circumstances are thus not related to primary lung injury; the real cause of ARDS may be the \"second hit\" caused by inappropriate treatment. In view of the limited effective treatments for ARDS, the strategic focus has shifted to identifying potential or high-risk ARDS patients during the early stages of the disease and implementing treatment strategies aimed at reducing ARDS and related organ failure. Future research should focus on the prevention of ARDS.

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. The heart is one of the most important oxygen delivery organs, and dysfunction significantly increases the mortality of the body. Hence, the heart has been studied in sepsis for over half a century. However, the definition of sepsis-induced cardiomyopathy is not unified yet, and the conventional conception seems outdated: left ventricular systolic dysfunction (LVSD) along with enlargement of the left ventricle, recovering in 7 to 10 days. With the application of echocardiography in intensive care units, not only LVSD but also left ventricular diastolic dysfunction, right ventricular dysfunction, and even diffuse ventricular dysfunction have been seen. The recognition of sepsis-induced cardiomyopathy is gradually becoming complete, although our understanding of it is not deep, which has made the diagnosis and treatment stagnate. In this review, we summarize the research on sepsis-induced cardiomyopathy. Women and young people with septic cardiomyopathy are more likely to have LVSD, which may have the same mechanism as stress cardiomyopathy. Elderly people with ischemic cardiomyopathy and hypertension tend to have left ventricular diastolic dysfunction. Patients with mechanical ventilation, acute respiratory distress syndrome or other complications of increased right ventricular afterload mostly have right ventricular dysfunction. Diffuse cardiac dysfunction has also been shown in some studies; patients with mixed or co-existing cardiac dysfunction are more common, theoretically. Thus, understanding the pathophysiology of sepsis-induced cardiomyopathy from the perspective of critical care echocardiography is essential.

Background To investigate the epidemiology and in-hospital mortality of veno-venous (VV) and veno-arterial (VA) extracorporeal membrane oxygenation (ECMO) in Mainland China throughout 2018. Methods Patients supported by ECMO from 1700 tertiary hospitals in 31 provinces from January 1 to December 31, 2018, were selected from the National Clinical Improvement System database. Results The 1700 included hospitals had 2073 cases of ECMO in 2018, including 714 VV and 1359 VA ECMOs. The average patient age was 50 years (IQR 31–63), and 1346 were male. The average hospital stay was 17 days (IQR 7–30), and the average costs per case was $36,334 (IQR 22,547–56,714). The three provinces with the highest number of ECMO cases were Guangdong, Beijing, and Zhejiang; the southeast coastal areas and regions with higher GDP levels had more cases. Overall in-hospital mortality was 29.6%. Mortality was higher among patients who were male, over 70 years old, living in underdeveloped areas, and who were treated during the summer. Mortality in provinces with more ECMO cases was relatively low. The co-existence of congenital malformations, blood system abnormalities, or nervous system abnormalities increased in-hospital mortality. Conclusions Mortality and medical expenses of ECMO among patients in China were relatively low, but large regional and seasonal differences were present. Risk factors for higher in-hospital mortality were older age, male sex, in underdeveloped areas, and treatment during the summer. Additionally, congenital malformations and blood system and nervous system abnormalities were associated with in-hospital mortality.

Sepsis is a deadly infection that causes injury to tissues and organs. Infection and anti-infective treatment are the eternal themes of sepsis. The successful control of infection is a key factor of resuscitation for sepsis and septic shock. This review examines evidence for the treatment of sepsis. This evidence is combined with clinical experiments to reveal the rules and a standard flowchart of anti-infection therapy for sepsis. We retrieved information from the PubMed database up to October 2018 using various search terms and their combinations, including sepsis, septic shock, infection, antibiotics, and anti-infection. We included data from peer-reviewed journals printed in English on the relationships between infections and antibiotics. By combining the literature review and clinical experience, we propose a 6Rs rule for sepsis and septic shock management: right patients, right time, right target, right antibiotics, right dose, and right source control. This rule encompasses rational decisions regarding the timing of treatment, the identification of the correct pathogen, the selection of appropriate antibiotics, the formulation of a scientifically based antibiotic dosage regimen, and the adequate control of infectious foci. This review highlights how to recognize and treat sepsis and septic shock and provides rules and a standard flowchart for anti-infection therapy for sepsis and septic shock for use in the clinical setting.This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0.

It has recently been recognized that serum vimentin is elevated in infectious diseases, and that vimentin plays a role in regulating neutrophils and macrophages associated inflammation. However, the mechanisms are unclear. This study was designed to explore the role of vimentin in regulating monocyte survival or apoptosis as well as inflammatory cytokine secretion in response to lipopolysaccharides (LPSs). A human monocytic leukemia cell line (THP-1) was transfected with vimentin-specific small interfering RNA (siRNA) or vimentin over-expressing plasmid. Apoptosis was assessed by TdT-mediated dUTP Nick-End Labeling (TUNEL) and DNA content assay. Immunoblotting was performed to detect apoptosis-associated proteins. Cytokines (interleukin [IL]-6, IL-10, and tumor necrosis factor α [TNF-α]) were measured by enzyme-linked immuno sorbent assay. Two-way analysis of variance followed by Student's t test was used to compare means between different groups. Suppression of vimentin in THP-1 cells resulted in increased apoptotic response in the presence of LPS, while over-expression of vimentin could prevent the cells from apoptosis in response to LPS. LPS alone or suppression of vimentin resulted in significant up-regulation of caspase-3 (1.42 ± 0.20 of LPS alone and 1.68 ± 0.10 of vimentin suppression vs. control, t = 5.21 and 10.28, respectively, P < 0.05). In addition, pro-inflammatory cytokines (IL-6 and TNF-α) was significantly increased (IL-6: 577.90 ± 159.90 pg/day/10 cells vs. 283.80 ± 124.60 pg/day/10 cells of control, t = 14.76, P < 0.05; TNF-α: 54.10 ± 5.80 vs. 17.10 ± 0.10 pg/day/10 cells of control, t = 6.71, P < 0.05), while anti-inflammatory cytokine (IL-10) was significantly up-regulated in the THP-1 cells that over-expressed vimentin (140.9 ± 17.2 pg/day/10 cells vs. undetectable in control cells). In summary, the vimentin may regulate innate immunity through modulating monocytes viability as well as inflammatory response in sepsis through shifting the balance of pro-inflammatory and anti-inflammatory cytokines.

Background Tissue oxygen saturation (StO 2 ) decrease could appear earlier than lactate alteration. However, the correlation between StO 2 and lactate clearance was unknown. Methods This was a prospective observational study. All consecutive patients with circulatory shock and lactate over 3 mmol/L were included. Based on the rule of nines, a BSA (body surface area) weighted StO 2 was calculated from four sites of StO 2 (masseter, deltoid, thenar and knee). The formulation was as follows: masseter StO 2  × 9% + (deltoid StO 2  + thenar StO 2 ) × (18% + 27%)/ 2 + knee StO 2  × 46%. Vital signs, blood lactate, arterial and central venous blood gas were measured simultaneously within 48 h of ICU admission. The predictive value of BSA-weighted StO 2 on 6-hour lactate clearance > 10% since StO 2 initially monitored was assessed. Results A total of 34 patients were included, of whom 19 (55.9%) had a lactate clearance higher than 10%. The mean SOFA score was lower in cLac ≥ 10% group compared with cLac < 10% group (11 ± 3 vs. 15 ± 4, p = 0.007). Other baseline characteristics were comparable between groups. Compared to non-clearance group, StO 2 in deltoid, thenar and knee were significantly higher in clearance group. The area under the receiver operating curves (AUROC) of BSA-weighted StO 2 for prediction of lactate clearance (0.92, 95% CI [Confidence Interval] 0.82-1.00) was significantly higher than StO 2 of masseter (0.65, 95% CI 0.45–0.84; p < 0.01), deltoid (0.77, 95% CI 0.60–0.94; p = 0.04), thenar (0.72, 95% CI 0.55–0.90; p = 0.01), and similar to knee (0.87, 0.73-1.00; p = 0.40), mean StO 2 (0.85, 0.73–0.98; p = 0.09). Additionally, BSA-weighted StO 2 model had continuous net reclassification improvement (NRI) over the knee StO 2 and mean StO 2 model (continuous NRI 48.1% and 90.2%, respectively). The AUROC of BSA-weighted StO 2 was 0.91(95% CI 0.75-1.0) adjusted by mean arterial pressure and norepinephrine dose. Conclusions Our results suggested that BSA-weighted StO 2 was a strong predictor of 6-hour lactate clearance in patients with shock.

Survey on the demand for a Chinese critical care database From March to May 2020, supervised by the Critical Care Medicine Branch of the China Health Information and Health Care Big Data Association, a survey was conducted among critical care physicians in 20 tertiary hospitals across China. [...]these results represent the characteristics of China's current critical care medicine database management and demand. Data collection at this rate may fail to produce the number of cases that sufficient for carrying out scientific research in a short period of time [Supplemental Figure 1B, http://links.lww.com/CM9/A455]. Low data source access rate and low data security reliability Regarding data storage methods, >85% of hospitals use intra-hospital network storage models.

Increased extravascular lung water (EVLW) in shock is common in the critically ill patients. This study aimed to explore the effect of cardiac output (CO) on EVLW and its relevant influence on prognosis. The hemodynamic data of 428 patients with pulse-indicated continuous CO catheterization from Department of Critical Care Medicine, Peking Union Medical College Hospital were retrospectively collected and analyzed. The patients were assigned to acute respiratory distress syndrome group, cardiogenic shock group, septic shock group, and combined shock (cardiogenic and septic) group according to their symptoms. Information on 28-day mortality and renal function was also collected. The CO and EVLW index (EVLWI) in the cardiogenic and combined shock groups were lower than those in the other groups (acute respiratory distress syndrome group vs. cardiogenic shock group vs. septic shock group vs. combined shock group: CO, 5.1 [4.0, 6.2] vs. 4.7 [4.0, 5.7] vs. 5.5 [4.3, 6.7] vs. 4.6 [3.5, 5.7] at 0 to 24 h, P = 0.009; 4.6 [3.8, 5.6] vs. 4.8 [4.1, 5.7] vs. 5.3 [4.4, 6.5] vs. 4.5 [3.8, 5.3] at 24 to 48 h, P = 0.048; 4.5 [4.1, 5.4] vs. 4.8 [3.8, 5.5] vs. 5.3 [4.0, 6.4] vs. 4.0 [3.2, 5.4] at 48 to 72 h, P = 0.006; EVLWI, 11.4 [8.7, 19.1] vs. 7.9 [6.6, 10.0] vs. 8.8 [7.4, 11.0] vs. 8.2 [6.7, 11.3] at 0 to 24 h, P < 0.001; 11.8 [7.7, 17.2] vs. 7.8 [6.3, 10.2] vs. 8.7 [6.6, 12.2] vs. 8.0 [6.6, 11.1] at 24 to 48 h, P < 0.001; and 11.3 [7.7, 18.7] vs. 7.5 [6.3, 10.0] vs. 8.8 [6.3, 12.2] vs. 8.4 [6.4, 11.2] at 48 to 72 h, P < 0.001. The trend of the EVLWI in the septic shock group was higher than that in the cardiogenic shock group (P < 0.05). Moreover, there existed some difference in the pulmonary vascular permeability index among the cardiogenic shock group, the septic shock group, and the combined shock group, without statistical significance (P > 0.05). In addition, there was no significant difference in tissue perfusion or renal function among the four groups during the observation period (P > 0.05). However, the cardiogenic shock group had a higher 28-day survival rate than the other three groups [log rank (Mantel-Cox) = 31.169, P < 0.001]. Tissue-aimed lower CO could reduce the EVLWI and achieve a better prognosis.