Background: Pulmonary fibrosis is a common complication in patients with viral pneumonia, which causes restricted ventilation disorders and affects the prognosis of patients. However, the pulmonary function of patients with 2019 novel coronavirus (COVID-19)-induced pneumonia has not yet been reported.Methods: A retrospective analysis of 137 patients with COVID-19-induced pneumonia who were discharged from the Enze Hospital, Taizhou Enze Medical Center (Group), from January 31, 2020, to March 11, 2020. Follow-up occurred two weeks after hospital discharge, whereupon patients received a pulmonary function test. Results: Of the 137 patients who received a pulmonary function test two weeks after discharge, 51.8% were male, and the mean age was 47 years. Only 19.7% of the patients were identified as having severe novel coronavirus pneumonia. The pulmonary function test showed that for a small number of patients ((FEV1/FVC)/% <70%,) the mean ICV and FVC was 2.4±0.7 L, 3.2±0.8 L, respectively. In severe cases, 88.9% of patients had an IVC <80% of the predicted value and 55.6% of patients had an FVC <80% of the predicted value. The MEF25, MEF50, and MEF75 <70% values were 55.6%, 40.7%, and 25.9%, respectively. In the non-severe group, 79.1% of patients has an IVC <80% of the predicted value, and 16.4% of patients had an FVC <80% of the predicted value. The mean MEF25, MEF50, and MEF75 <70% values were 57.3%, 30%, and 13.6%, respectively.Conclusions: In this study, the results suggest that the pulmonary function of patients with 2019 novel coronavirus (COVID-19)-induced pneumonia manifested as restrictive ventilation disorder and small airway obstruction. The incidence was increased among critically ill patients.Trial registration number: ChiCTR2000029866.

Background Sepsis is defined as a systemic inflammatory response to microbial infections with multiple organ dysfunction. This study analysed untargeted metabolomics combined with proteomics of serum from patients with sepsis to reveal the underlying pathological mechanisms involved in sepsis. Methods A total of 63 patients with sepsis and 43 normal controls were enrolled from a prospective multicentre cohort. The biological functions of the metabolome were assessed by coexpression network analysis. A molecular network based on metabolomics and proteomics data was constructed to investigate the key molecules. Results Untargeted metabolomics analysis revealed widespread dysregulation of amino acid metabolism, which regulates inflammation and immunity, in patients with sepsis. Seventy-three differentially expressed metabolites (|log2 fold change| > 1.5, adjusted P value < 0.05 and variable importance in the projection (VIP) > 1.5) that could predict sepsis were identified. External validation of the hub metabolites was consistent with the derivation results (area under the receiver operating characteristic curve (AUROC): 0.81–0.96/0.62–1.00). The pentose phosphate pathway was found to be related to sepsis-associated encephalopathy. Phenylalanine metabolism was associated with sepsis-associated acute kidney injury. The key molecular alterations of the multiomics network in sepsis compared to normal controls implicate acute inflammatory response, platelet degranulation, myeloid cell activation involved in immune response and phenylalanine, tyrosine and tryptophan biosynthesis, and arginine biosynthesis. Conclusions Integrated analysis of untargeted metabolomics and proteomics revealed characteristic metabolite and protein alterations in sepsis, which were mainly involved in inflammation-related pathways and amino acid metabolism. This study depicted the pathological characteristics and pathways involved in sepsis and potential therapeutic targets.

Sepsis is defined as an organ dysfunction syndrome and it has high mortality worldwide. This study analysed the proteome of serum from patients with sepsis to characterize the pathological mechanism and pathways involved in sepsis. A total of 59 patients with sepsis were enrolled for quantitative proteomic analysis. Weighted gene co-expression network analysis (WGCNA) was performed to construct a co-expression network specific to sepsis. Key regulatory modules that were detected were highly correlated with sepsis patients and related to multiple functional groups, including plasma lipoprotein particle remodeling, inflammatory response, and wound healing. Complement activation was significantly associated with sepsis-associated encephalopathy. Triglyceride/cholesterol homeostasis was found to be related to sepsis-associated acute kidney injury. Twelve hub proteins were identified, which might be predictive biomarkers of sepsis. External validation of the hub proteins showed their significantly differential expression in sepsis patients. This study identified that plasma lipoprotein processes played a crucial role in sepsis patients, that complement activation contributed to sepsis-associated encephalopathy, and that triglyceride/cholesterol homeostasis was associated with sepsis-associated acute kidney injury.

Background: Cardiac surgery is associated with a substantial risk of major adverse events. Although carbon dioxide (CO2)-derived variables such as venous-to-arterial CO2 difference (ΔPCO2), and PCO2 gap to arterial–venous O2 content difference ratio (ΔPCO2/C(a−cv)O2) have been successfully used to predict the prognosis of non-cardiac surgery, their prognostic value after cardiopulmonary bypass (CPB) remains controversial. This hospital-based study explored the relationship between ΔPCO2, ΔPCO2/C(a−cv)O2 and organ dysfunction after CPB.Methods: We prospectively enrolled 114 intensive care unit patients after elective cardiac surgery with CPB. Patients were divided into the organ dysfunction group (OI) and non-organ dysfunction group (n-OI) depending on whether organ dysfunction occurred or not at 48 h after CPB. ΔPCO2 was defined as the difference between central venous and arterial CO2 partial pressure.Results: The OI group has 37 (32.5%) patients, 27 of which (23.7%) had one organ dysfunction and 10 (8.8%) had two or more organ dysfunctions. No statistical significance was found (P = 0.84) for ΔPCO2 in the n-OI group at intensive care unit (ICU) admission (9.0, 7.0–11.0 mmHg), and at 4 (9.0, 7.0–11.0 mmHg), 8 (9.0, 7.0–11.0 mmHg), and 12 h post admission (9.0, 7.0–11.0 mmHg). In the OI group, ΔPCO2 also showed the same trend [ICU admission (9.0, 8.0–12.8 mmHg) and 4 (10.0, 7.0–11.0 mmHg), 8 (10.0, 8.5–12.5 mmHg), and 12 h post admission (9.0, 7.3–11.0 mmHg), P = 0.37]. No statistical difference was found for ΔPCO2/C(a−cv)O2 in the n-OI group (P = 0.46) and OI group (P = 0.39). No difference was detected in ΔPCO2, ΔPCO2/C(a−cv)O2 between groups during the first 12 h after admission (P &gt; 0.05). Subgroup analysis of the patients with two or more failing organs compared to the n-OI group showed that the predictive performance of lactate and Base excess (BE) improved, but not of ΔPCO2 and ΔPCO2/C(a−cv)O2. Regression analysis showed that the BE at 8 h after admission (odds ratio = 1.37, 95%CI: 1.08–1.74, P = 0.009) was a risk factor for organ dysfunction 48 h after CBP.Conclusion : ΔPCO2 and ΔPCO2/C(a−cv)O2 cannot be used as reliable indicators to predict the occurrence of organ dysfunction at 48 h after CBP due to the pathophysiological process that occurs after CBP.

Background: Sepsis, as a clinical emergency, usually causes multiorgan dysfunction and can lead to high mortality. Establishment of specific and sensitive biomarkers for early diagnosis is critical to identify patients who would benefit from targeted therapy. In this study, we investigated this syndrome by analyzing the transcriptome of peripheral blood mononuclear cells (PBMCs) from patients with sepsis and identified sepsis-specific biomarkers. Methods: In this study, a total of 87 patients with sepsis and 40 healthy controls from a prospective multicenter cohort were enrolled. Samples from 44 subjects (24 patients with sepsis and 20 healthy controls) were sequenced and the remaining patients were included in the validation group. Using high-throughput sequencing, a gene expression profile of PBMCs from patients with sepsis was generated to elucidate the pathophysiology of sepsis and identify sepsis-specific biomarkers. Results: Principal component analysis (PCA) and unsupervised hierarchical cluster analysis showed that patients with sepsis separated from healthy controls. A total of 1639 differentially expressed genes (DEGs) were identified (|log2 fold change|>2, adjusted P value <0.05) between these two groups, with 1278 (78.0%) upregulated and 361 (22.0%) downregulated in patients with sepsis. Gene Ontology (GO) analysis of the upregulated DEGs identified 194 GO terms that were clustered into 27 groups, and analysis of the downregulated DEGs identified 20 GO terms that were clustered into 4 groups. Four unique genes were identified that could be predictive of patients with sepsis. External validation of the four genes using quantitative real-time polymerase chain reaction (qRT-PCR) was consistent with the results of mRNA sequencing, revealing their potential in sepsis diagnosis. Conclusions: The transcriptome characteristics of PBMCs, which were significantly altered in sepsis patients, provide new insights into sepsis pathogenesis. The four identified gene expression changes differentiated patients with sepsis from healthy subjects, which could serve as a convenient tool contributing to sepsis diagnosis.

A 55-year-old man who suffered from acute myocardial infarction complicated with cardiogenic shock was administered veno-arterial extracorporeal membrane oxygenation. Ultra-high pre-membrane lung oxygen saturation of 93% was observed. Transthoracic echocardiography revealed the presence of patent foramen ovale. The four-chamber view showed that the tip of the cannula was located in the patent foramen ovale, which resulted in a left-to-right shunt. Without adjusting the position of the drainage cannula, the patient was weaned from extracorporeal membrane oxygenation at 136 hours after initiation and survived to hospital discharge.

Background: The time of enteral nutrition (EN) administration on patients with sepsis is controversial.The study was to explore the effect of early enteral nutrition (EEN) on the prognosis of patients with sepsis.Methods: We performed a secondary analysis of the acute gastrointestinal injury grade study. The patients were divided into two groups from the time of EN administration: EEN group (n=85): EN within 24 hours; Control group (N=78): EN after 24 hours. The key observation was the length of ICU stay, and length of hospital stay, and 28-and 60-day mortality.Results: Of 676 patients, 163 were included. There are no significant between-group differences in the characteristics at baseline. The overall mortality rate at 28 days in the EEN group was 28.2% vs. 43.6% in the control group (P=0.041). The mortality rate at 60 days in the EEN group was 36.5% vs. 52.6% in the control group (P=0.039). In a subgroup analysis of patients who whether used vasoactive drugs: the EEN group was found to be significantly associated with 60-day mortality (P=0.039). The ICU stay length in the EEN group was longer than in the control group {11 [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] vs. 10 [6-16]; P=0.022}. Also, the length of the hospital stay was longer than in the Control group {23 [14-53] vs. 18 [10-39]; P=0.023}. Univariate Cox regression analysis showed that EEN, using vasoactive drugs, Acute kidney injury (AKI), Acute Physiology and Chronic Health Evaluation II (APACHE II) score, and the global acute gastrointestinal injury (AGI) grade were significantly (P<0.05) associated with 60-day mortality. In a multivariate analysis including these

The incidence of heart disease in pregnancy ranges from 0.5% to 3.0% and is regarded as one of the top three causes of maternal death. The mortality rate of patients with pulmonary hypertension and Eisenmenger syndrome is as high as 16.7%–50%. Changes in haemodynamics during pregnancy and childbirth increase the burden on the heart, and induced pulmonary hypertension crisis is one of the main causes of maternal death. Extracorporeal Membrane Oxygenation (ECMO) is the last-resort treatment strategy to treat patients with pulmonary hypertension crisis. We report a ventricular septal defect in a pregnant woman with pulmonary hypertension and Eisenmenger’s syndrome, which is a postpartum pulmonary hypertension crisis that leads to respiratory and circulatory disorders. The patient was successfully treated with venous-venous extracorporeal membrane oxygenation.