Background:Myeloid-derived suppressor cells (MDSCs) are immature myeloid cells with immunosuppressive functions. While early expansion of MDSCs may be protective in various pathological states, their accumulation and role might differ in sepsis. This study aimed to compare the differences in circulating myeloid cells with MDSC phenotypes and their subsets between septic and non-septic patients in the early stage. Methods:This was a prospective, single-center, observational cohort study. Critically ill patients were enrolled and divided into sepsis and non-sepsis groups. Flow cytometry was used to determine the percentages of peripheral blood CD11b+CD33+HLA-DR-/low cells (herein referred to as MDSC-like cells) and their subsets (M-MDSC-like and PMN-MDSC-like cells). Levels of arginase-1 (ARG-1) and inducible nitric oxide synthase (iNOS) were measured. Clinical data were collected. All patients were followed for 28 days to record mortality. Results:Sixty patients were enrolled (sepsis group: n=38; non-sepsis group: n=22). No significant differences were found in gender, age, APACHE II score, ICU length of stay, or 28-day mortality between the two groups. However, the Charlson Comorbidity Index (CCI) was higher in the sepsis group (P = 0.005). Compared to the non-sepsis group, septic patients had significantly lower percentages of total MDSC-like cells and M-MDSC-like cells (P = 0.006; P = 0.003), while PMN-MDSC-like cells showed no difference. ARG-1 levels were higher in the sepsis group (P = 0.030). Furthermore, the sepsis group exhibited significantly elevated levels of IL-6, CRP, PCT, and SOFA scores (P<0.05), lower lymphocyte counts (P = 0.017), and more pronounced coagulation abnormalities, hypoalbuminemia, and increased cardiac/renal markers. Within the sepsis group, non-survivors had a significantly higher percentage of PMN-MDSC-like cells than survivors (P = 0.012). Conclusion:In the early stage, septic patients exhibit a distinct response profile of myeloid cells with MDSC phenotypes compared to non-septic patients, characterized by attenuated expansion of total MDSC-like cells and M-MDSC-like cells but enhanced ARG-1 expression, alongside more severe inflammation, organ dysfunction, and lymphopenia. An elevated percentage of PMN-MDSC-like cells is associated with poor prognosis in sepsis.

Background:Acute respiratory distress syndrome (ARDS) is a severe form of organ dysfunction and a common postoperative complication. This study aims to develop a predictive model for ARDS in postoperative patients with gastrointestinal perforation to facilitate early detection and effective prevention. Methods:In this single-center retrospective study, clinical data were collected from postoperative patients with gastrointestinal perforation admitted to the ICU in Hebei Provincial People's Hospital from October 2017 to May 2024. Univariate analysis and multifactorial logistic regression analysis were used to determine the independent risk factors for developing ARDS. Nomograms were developed to show predictive models, and the discrimination, calibration, and clinical usefulness of the models were assessed using the C-index, calibration plots, and decision curve analysis (DCA). Results:Two hundred patients were ultimately included for analysis. In the development cohort, 38 (27.1%) of 140 patients developed ARDS, and in the internal validation cohort, 13 (21.7%) of 60 patients developed ARDS. The multivariate logistic regression analysis revealed the site of perforation (OR = 0.164, P = 0.006), the duration of surgery (OR = 0.986, P = 0.008), BMI (OR = 1.197, P = 0.015), SOFA (OR = 1.443, P = 0.001), lactate (OR = 1.500, P = 0.017), and albumin (OR = 0.889, P = 0.007) as the independent risk factors for ARDS development. The area under the curve (AUC) was 0.921 (95% CI: 0.869, 0.973) for the development cohort and 0.894 (95% CI: 0.809, 0.978) for the validation cohort. The calibration curve and decision curve analysis (DCA) demonstrate that the nomogram possesses good predictive value and clinical practicability. Conclusion:Our research introduced a nomogram that integrates six independent risk factors, facilitating the precise prediction of ARDS risk in postoperative patients following gastrointestinal perforation.

Background:Myeloid-derived suppressor cells (MDSCs), comprising polymorphonuclear (PMN-MDSCs) and monocytic subsets (M-MDSCs), are immunosuppressive immature myeloid cells implicated in disease progression and prognosis across multiple pathologies. Purpose:To investigate the clinical significance of early MDSCs subset expansion in critical illness and identify novel prognostic biomarkers for risk stratification. Patients and Methods:This prospective study enrolled 85 critically ill adults (APACHE II ≥15), stratified into survivors (n=47) and non-survivors (n=38). MDSCs subsets were quantified via flow cytometry. Concurrent measurements included lactate, IL-6, CRP, lymphocyte subsets, and Tregs. Primary outcomes were 28-day all-cause mortality and secondary infection rates. Results:Survivors exhibited significantly higher M-MDSCs% (median [IQR]: 4.824 [1.863-9.776] vs 2.503 [1.480-5.224], P<0.05) and elevated M-MDSCs/PMN-MDSCs ratios (122.166 [34.220-307.500] vs 28.324 [5.042-88.128], P<0.01). Patients with M-MDSCs/PMN-MDSCs ratios ≥85.765 demonstrated markedly lower mortality (23.08% vs 59.19%; hazard ratio [HR] = 3.530, 95% confidence interval [CI]: 1.668-7.467, P<0.001), with the low-ratio group exhibiting a 2.56-fold higher mortality risk. A combined stratification model (M-MDSCs/PMN-MDSCs + APACHE II score) revealed a 7.48-fold increase in mortality in the low-ratio/high-APACHE II subgroup compared to the high-ratio/low-APACHE II subgroup (86.36% vs 11.54%, P<0.001). Conclusion:Elevated levels of M-MDSCs in the early stages of critical illness may exert protective effects. The ratio of M-MDSCs/PMN-MDSCs demonstrates predictive value for 28-day mortality, positioning it as a potential biomarker for prognostic assessment, but further multicenter studies are still needed to validate it.

BackgroundThis study aims to systematically assess the risk factors, the overall strength of association, and evidence quality related to sepsis-associated encephalopathy.MethodsA systematic search was conducted in the Cochrane Library, PubMed, Web of Science, and Embase for cohort or case-control studies published up to August 2023 on risk factors associated with sepsis-related encephalopathy. The selected studies were screened, data were extracted, and the quality was evaluated using the Newcastle–Ottawa Scale. Meta-analysis was performed using RevMan 5.3 software. The certainty of the evidence was assessed using the GRADE criteria.ResultsA total of 13 studies involving 1,906 participants were included in the analysis. Among these studies, 12 were of high quality, and one was of moderate quality. Our meta-analysis identified six risk factors significantly associated with Serious Adverse Events (SAE). These included APACHE II, SOFA, age, tau protein, and IL-6, which were found to be risk factors with significant effects (standard mean difference SMD: 1.24–2.30), and albumin, which was a risk factor with moderate effects (SMD: −0.55). However, the certainty of evidence for the risk factors identified in this meta-analysis ranged from low to medium.ConclusionThis systematic review and meta-analysis identified several risk factors with moderate to significant effects. APACHE II, SOFA, age, tau protein, IL-6, and albumin were associated with sepsis-related encephalopathy and were supported by medium- to high-quality evidence. These findings provide healthcare professionals with an evidence-based foundation for managing and treating hospitalized adult patients with sepsis-related encephalopathy.

ObjectivesThe purpose of this study was to evaluate the performance of urinary C-C motif chemokine ligand 14 (CCL14) and the renal resistive index (RI) in predicting persistent AKI in unselected critically ill patients.MethodsThis prospective observational study was conducted in a tertiary hospital's general intensive care unit (ICU). Consecutive adults who were admitted to the ICU were enrolled, with a primary endpoint of AKI lasting 48 h or longer. Urinary CCL14 was evaluated upon inclusion, and the renal RI was determined within 12 h of ICU admission. The individual discriminative ability of urinary CCL14 and the renal RI to predict persistent AKI was evaluated by the area under the receiver operating characteristic curve (AUC).ResultsOverall, 166 patients were included, of whom 56 had persistent AKI. Urinary CCL14 showed good ability to predict persistent AKI, with an AUC of 0.817. However, the overall performance of the renal RI was fair, with an AUC of 0.739. Forty-nine patients presented with mild AKI at inclusion, and the values of CCL14 were significantly lower than those of patients with moderate or severe AKI (0.205 [0.125-0.300] vs. 0.302 [0.157-0.501]; p = 0.034). In the subgroup analysis, although the diagnostic performance of CCL14 was excellent in patients with moderate or severe AKI, it was fair in patients with mild AKI [AUC = 0. 738; 95% confidence interval (CI) 0.593-0.853].ConclusionUrinary CCL14 was an excellent predictor of persistent AKI in patients with moderate or severe AKI, but its performance was not good in patients with mild AKI. The renal RI cannot discriminate between transient and persistent AKI.

目的 观察微小RNA-21(miR-21)对脓毒症小鼠急性肺损伤(ALI)的改善作用,并探讨其可能作用机制.方法 40只雄性昆明小鼠随机分为miR-21前体 + ALI组(Pre-miR-21 + ALI组)、miR-21前体 + 磷脂酰肌醇3 激酶(phosphatidylinositol 3 kinase,PI-3K)/丝氨酸-苏氨酸蛋白激酶(Akt)抑制剂LY294002 + ALI组(Pre-miR-21 + LY + ALI组)、PI3K/Akt抑制剂LY294002 + ALI组(LY + ALI组)、ALI组、假手术组,每组各8只.ALI组小鼠采用盲肠结扎穿孔术(CLP)造成脓毒症ALI;Pre-miR-21 + ALI组小鼠先尾静脉注射miR-21 前体腺病毒 0.2 mL(1×109pfu/mL),4天后采用CLP造成脓毒症ALI;Pre-miR-21 + LY + ALI组小鼠先尾静脉注射miR-21前体腺病毒0.2ml(1×109pfu/mL),4天后尾静脉注射LY(0.3 mg/g),注射30 min后进行CLP;LY + ALI组小鼠先尾静脉注射LY(0.3 mg/g),注射30 min后进行CLP;假手术组小鼠仅开腹探查盲肠.干预24 h时麻醉各组小鼠后取腹主动脉血,测算各组小鼠氧合指数(OI),采用ELISA法检测血清炎症因子TNF-α、IL-6和氧化应激指标ROS、SOD;处死各组小鼠后取右肺组织,HE染色观察肺组织病理学变化,测算肺组织肺湿重/干重比值(W/D);取各组小鼠左肺组织,采用qRT-PCR法检测miR-21,采用WESTERN Blotting法检测各组小鼠左肺组织磷脂酶和张力蛋白同源物(PTEN)、磷酸化Akt(p-Akt)蛋白.结果 与假手术组比较,ALI组小鼠OI下降,血清TNF-α、IL-6、ROS、SOD水平、肺组织W/D、miR-21表达升高(P均<0.05),光镜下可见肺泡结构破坏、肺泡出血,PTEN蛋白相对表达量下降,p-Akt蛋白相对表达量增加(P均<0.05);与ALI组比较,Pre-miR-21 + ALI组小鼠OI高,血清TNF-α、IL-6、ROS、SOD水平、肺组织W/D降低,miR-21相对表达量高(P均<0.05),光镜下可见肺泡结构破坏、肺泡出血减轻,PTEN蛋白相对表达量下降,p-Akt蛋白相对表达量增加(P均<0.05);与ALI组比较,Pre-miR-21 + LY + ALI组OI降低,血清TNF-α、IL-6、ROS、SOD水平、肺组织W/D、miR-21相对表达量升高(P均<0.05),光镜下可见肺泡结构破坏、肺泡出血加重,PTEN蛋白相对表达量下降,p-Akt蛋白相对表达量升高(P均<0.05);与ALI组比较,LY + ALI组OI降低,血清TNF-α、IL-6、ROS、SOD水平、肺组织W/D升高(P均<0.05),肺泡结构破坏、肺泡出血加重;与Pre-miR-21 + LY + ALI组比较,LY + ALI组OI降低,血清TNF-α、IL-6、ROS、SOD水平、肺组织W/D升高,miR-21相对表达量下降(P均<0.05),光镜下可见肺泡结构破坏、肺泡出血加重,PTEN蛋白相对表达量升高,p-Akt蛋白相对表达量下降(P均<0.05).结论 尾静脉预注射miR-21前体腺病毒的脓毒症小鼠急性肺损伤程度较轻,肺组织PTEN蛋白相对表达量低、p-Akt蛋白相对表达量高.miR-21可能通过抑制肺组织PTEN表达、促进p-Akt表达,减轻脓毒症小鼠肺组织炎症反应和氧化应激水平,从而减轻脓毒症小鼠ALI.

OBJECTIVE To observe the expression of deleted in malignant brain tumor protein 1 (DMBT1) in rat acute respiratory distress syndrome (ARDS) model induced by sepsis and its relationship with ARDS related biomarkers. METHODS Forty-eight healthy male rats were randomly divided into sham operation group (Sham group) and ARDS model group, and the rats in each group were further divided into three subgroups at 6, 12 and 24 hours after operation, with 8 rats in each subgroup. The rats in the Sham group were exposed to the cecum only, and sepsis induced ARDS model was reproduced by cecal ligation and puncture (CLP) in the ARDS model group. The general performance was observed at 6, 12, 24 hours after operation. Abdominal aortic blood of rats was collected, and the levels of DMBT1, surfactant-associated protein D (SP-D), vascular endothelial growth factor (VEGF), interleukins (IL-6, IL-10) in serum were determined by enzyme-linked immunosorbent assay (ELISA). The lung tissues were collected, and the lung wet/dry weight (W/D) ratio was determined. The lung tissue pathological changes were observed under light microscope after hematoxylin-eosin (HE) staining, and the lung tissue injury score was evaluated. The expression of DMBT1 protein in lung tissue was determined by Western blotting. The relationship between the serum DMBT1 and SP-D, VEGF, IL-6, IL-10, lung tissue injury score were analyzed by Pearson correlation analysis. RESULTS Rats in the ARDS model group showed obvious pathological manifestations after operation. The alveolar structure destruction, inflammatory cell infiltration, and alveolar hemorrhage were observed under microscope. Compared with the Sham group, the lung tissue injury score and the lung W/D ratio at 12 hours after operation in the ARDS model group were significantly increased (lung tissue injury score: 3.35±0.13 vs. 1.16±0.07, lung W/D ratio: 5.36±0.44 vs. 4.38±0.35, both P < 0.05), and pulmonary edema was present, which suggested that the ARDS model caused by CLP was successfully reproduced. The results of ELISA and Western blotting showed that the levels of serum DMBT1, SP-D, VEGF and IL-6 in the ARDS model group increased gradually with time, while the level of IL-10 increased first and then decreased. Compared with the Sham group, the levels of DMBT1 in serum and the expressions of DMBT1 protein in lung tissue in the ARDS model group were significantly increased from 6 hours after operation [serum (ng/L) : 231.96±19.17 vs. 187.44±10.19, lung tissue (DMBT1/β-actin): 2.05±0.19 vs. 0.93±0.25, both P < 0.05], and the levels of SP-D, VEGF, IL-6 and IL-10 in serum were significantly increased from 12 hours after operation [SP-D (ng/L): 73.35±8.05 vs. 43.28±5.77, VEGF (ng/L): 89.85±8.47 vs. 43.19±5.11, IL-6 (ng/L): 36.01±2.48 vs. 17.49±1.77, IL-10 (ng/L): 84.55±8.41 vs. 39.83±5.02, all P < 0.05]. Pearson correlation analysis showed that serum DMBT1 was positively correlated with serum SP-D, VEGF, IL-6, IL-10 and lung injury score at 12 hours and 24 hours in the ARDS model group (12 hours: r values were 0.946, 0.942, 0.931, 0.936, 0.748, respectively; 24 hours: r values were 0.892, 0.945, 0.951, 0.918, 0.973, respectively; all P < 0.05). CONCLUSIONS DMBT1 is a novel early biomarker of ARDS by affecting alveolar epithelial cell, alveolar capillary permeability and inflammatory response.

目的 观察脓毒症急性肺损伤(ALI)小鼠肺组织中微小RNA-21(miR-21)的表达情况,以及干预miR-21表达对肺水肿、血清炎症因子及氧化应激的影响,探讨该作用机制与PTEN的关系.方法 取96只健康雄性昆明小鼠,采用随机数字表法分为6组:假手术组(n=32)、模型组(n=32)、miR-21前体组(MP组,n=8)、miR-21抑制剂组(MI组,n=8)、miR-21前体+PTEN抑制剂组(MP+Anti-PTEN组,n=8)、miR-21抑制剂+PTEN抑制剂组(MI+Anti-PTEN组,n=8).假手术组仅进行开腹探查盲肠;模型组采用盲肠结扎穿孔术制作ALI模型;MP组、MI组分别在尾静脉注射miR-21前体腺病毒、miR-21抑制剂腺病毒4 d后再造模;MP+Anti-PTEN组、MI+Anti-PTEN组分别在转染miR-21前体、miR-21抑制剂后,造模前30 min给予尾静脉注射PTEN抑制剂.造模后24 h,取小鼠腹主动脉取血进行血气分析,计算氧合指数(OI).取小鼠左肺组织,称取肺湿重和肺干重,计算肺湿重/干重比值(W/D).取小鼠腹主动脉血,采用ELISA法检测血清炎症因子肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)和氧化应激指标活性氧(ROS)、超氧化物歧化酶(SOD)水平.分别于造模后6、12、24、48 h采用qRT-PCR法检测假手术组、模型组肺组织miR-21的相对表达量.于造模后24 h对假手术组、模型组、MP组、MI组采用qRT-PCR法检测肺组织miR-21表达,Western blotting法检测肺组织PTEN蛋白表达.结果 造模后24 h,与假手术组比较,模型组OI下降,W/D、TNF-α、IL-6、ROS、SOD水平升高(P均<0.05);与模型组比较,MP组、MP+Anti-PTEN组、MI+Anti-PTEN组OI升高,W/D、TNF-α、IL-6、ROS、SOD水平下降(P均<0.05),MI组OI下降,W/D、TNF-α、IL-6、ROS、SOD水平升高(P均<0.05);与MP+Anti-PTEN组比较,MI+Anti-PTEN组OI、W/D、TNF-α、IL-6、ROS、SOD水平无明显变化(P均>0.05).与假手术组比较,模型组造模后6、12、24、48 h肺组织miR-21表达均升高(P均<0.05),并于造模后24 h达峰.造模后24 h,与假手术组比较,模型组和MP组miR-21表达均升高、PTEN蛋白表达均下降,MI组miR-21表达下降、PTEN蛋白表达升高(P均<0.05);与模型组比较,MP组miR-21表达升高、PTEN蛋白表达下降,MI组miR-21表达下降、PTEN蛋白表达升高(P均<0.05).结论 脓毒症小鼠肺组织中miR-21表达增加,miR-21过表达可减轻脓毒症炎症反应及氧化应激,从而减轻肺损伤,其机制可能与抑制PTEN有关.

Introduction:Pneumocystis jirovecii pneumonia (PJP) occurs in immunocompromised hosts. It is classified as PJP with human immunodeficiency virus (HIV) infection (HIV-PJP) and PJP without HIV infection (non-HIV PJP). Compared with HIV-PJP, non-HIV PJP is more likely to develop rapidly into respiratory failure, with difficult diagnosis and high mortality.Patient concerns:A 46-year-old male with membranous nephropathy was treated with oral corticosteroids and tacrolimus. He was admitted to our hospital for fever and dyspnea which developed 4 days ago. Laboratory data revealed that leukocytes were 10.99 x 109/L, neutrophils 87.7%, lymphocytes 9.6%, C-reactive protein 252.92 mg/L, New coronavirus nucleic acid detection negative. CT scan of chest revealed ground-glass opacity in both lungs. He was admitted to the respiratory department of our hospital, and then transferred to ICU because of his critical condition.Diagnosis:High throughput gene detection of pathogenic microorganisms in alveolar lavage fluid showed that the detection sequence of Pneumocystis yersiniae increased significantly. The serum HIV-antibody was negative. Therefore, the patient was diagnosed as non-HIV PJP.Interventions:After admission, the patient was assisted by noninvasive ventilator and treated with compound trimethoprim-sulfamethoxazole (SMX-TMP) and caspofungin. The patient's condition continued to deteriorate, and then underwent endotracheal intubation and veno-venous extracorporeal membrane oxygenation (VV-ECMO) combined with prone position ventilation until the lung lesion improved.Outcomes:VV-ECMO was stopped on day 12, tracheal intubation was removed after 2 days. The patient was transferred to the respiratory department on day 15, discharged after 12 days without complications. Two months later, the follow-up showed that the patient was in good condition.Conclusion:VV-ECMO combined with prone position ventilation could be a useful choice for respiratory assistance in non-HIV PJP patients.

Introduction: Sepsis can cause acute lung injury (ALI), one of the leading causes of death in critically ill patients. The underlying mechanisms of sepsis-induced acute lung injury include excessive inflammation, oxidative stress, cell apoptosis, pulmonary edema, and lung tissue dysfunction. Recent studies have shown that miRNA-21 (miR-21) plays a vital role in sepsis-induced acute kidney injury. Relatively few studies have focused on the protective effects of ALI. This study aimed to determine the potential role of miR-21 in sepsis-induced ALI. Methods: We performed quantitative real-time polymerase chain reaction in a septic mouse model induced by cecal ligation and puncture (CLP) and found that miR-21 expression was upregulated. We then transfected the miR-21 precursor to upregulate miR-21 expression and miR-21 inhibitor to downregulate miR-21 expression. The sham group was exposed only to the cecum. ALI was induced by CLP, and the pre-miR-21+ALI and anti-miR-21+ALI groups were treated with miR-21 precursor or miR-21 inhibitor in the caudal vein before CLP. Pre-miR-21+ALI+PTEN inhibition (Pre-miR-21+ALI+PI) and anti-miR-21+ALI+PTEN inhibition (Anti-miR-21+ALI+PI) groups were treated with PTEN inhibition into the caudal vein after miR-21 transfection. Inflammatory cytokines, oxidative stress indicators, lung tissue cell apoptosis, oxygenation index (OI), lung wet/dry weight ratio, and lung pathological changes in the lung were observed in each group. Results: Compared with ALI mice, inflammatory response, oxidative stress indicators, lung tissue cell apoptosis, and the degree of lung injury were remarkably alleviated in Pre-miR-21+ALI mice and aggravated in Anti-miR-21+ALI mice. Western blot analysis showed that phosphatase and tensin homolog (PTEN) protein expression was decreased in CLP-treated mics. PTEN protein expression was decreased in the Pre-miR-21+ALI group but increased in the Anti-miR-21+ALI group. Moreover, the effect of miR-21 on anti-inflammatory, anti-oxidative stress, and anti-apoptosis enhanced after PTEN inhibition. Conclusion: This study revealed that miR-21 has a protective effect in sepsis-induced ALI by regulating PTEN in mice.

Background Early recognition of persistent acute kidney injury (AKI) could optimize management and prevent deterioration of kidney function. The Doppler-based renal resistive index (RI) has shown promising results for predicting persistent AKI in preliminary studies. Here, we aimed to evaluate the performance of renal RI, clinical indicators, and their combinations to predict short-term kidney prognosis in septic shock patients.Method We performed a retrospective study based on data from a prospective study in a single-center general ICU between November 2017 and October 2018. Patients with septic shock were included. Clinical indicators were evaluated immediately at inclusion, and renal RI was measured within the first 12 h of ICU admission after hemodynamic stabilization. Persistent AKI was defined as AKI without recovery within 72 h. A multivariable logistic regression was used to select significant variables associated with persistent AKI. The discriminative power was evaluated by a receiver operating characteristic curve analysis.Result Overall, 102 patients were included, 39 of whom had persistent AKI. Renal RI was higher in the persistent AKI patients than in those without persistent AKI: 0.70 ± 0.05 vs. 0.66 ± 0.05; p = 0.001. The performance of RI to predict persistent AKI was poor, with an area under the receiver operating characteristic curve (AUROC) of 0.699 [95% confidence interval (CI) 0.600–0.786]. A clinical prediction model combining serum creatinine at inclusion and the nonrenal SOFA score showed a better prediction ability for nonrecovery, with an AUROC of 0.877 (95% CI 0.797–0.933, p = 0.0012). The addition of renal RI to this model did not improve the predictive performance.Conclusion The Doppler-based renal resistive index performed poorly in predicting persistent AKI and did not improve the clinical prediction provided by a combination of serum creatinine at inclusion and the nonrenal SOFA score in patients with septic shock.

Rationale: Amniotic fluid embolism (AFE) is a rare obstetrical complication and is a leading cause of maternal death in developed countries. Despite the development of supportive therapeutic measures, the mortality rate remains high. Patient concerns: A 38-year-old nulliparous pregnant woman, who underwent in vitro fertilization-embryo transfer, was admitted for labor at 37 weeks' gestation. Approximately 30 minutes after delivery of the placenta, the puerpera developed postpartum hemorrhage with uterine atony. Soon after, the patient experienced hypotension, repeated cardiac arrest, refectory hypoxia, and disseminated intravascular coagulopathy. Diagnosis: AFE is diagnosed clinically. The pregnant woman in this case fulfilled the diagnostic criteria for AFE: acute hypotension, cardiac arrest, acute hypoxia, and coagulation disorders within approximately 30 minutes after delivery of the placenta. Interventions: The patient was intubated, connected to a ventilator, and was administered a high dose of vasoactive drugs to maintain blood pressure and underwent an emergency hysterectomy. Considering the risk for recurrent cardiac arrest and severe refractory hypoxia, venoarterial extracorporeal membrane oxygenation was initiated and discontinued as soon as cardiac function was restored based on serial bedside ultrasound assessment. Outcomes: The patient stabilized on day 7 in the intensive care unit and was transferred to the obstetrics ward and, 1 week later, was discharged with no complications. Two months later, follow-up revealed that the patient was in good condition. Lesson: Serial bedside ultrasound was crucial for assessing cardiac function and optimal weaning. Timely application of venoarterial extracorporeal membrane oxygenation and weaning was significant to avoid the occurrence of complications and improve long-term outcomes.

长期以来,窒息一直是导致新生儿死亡的主要原因,窒息缺氧常引起神经、心血管、泌尿及消化等多系统器官功能障碍;各器官受影响的程度不同,其中以胃肠道最先受累且程度最重,其发生率为33.69％;窒息程度越重,受损程度越重,出现腹胀、呕吐、奶量减少、胃肠道出血,甚至发生坏死性小肠结肠炎.为避免或减少重度窒息新生儿胃肠功能障碍的发生,必须强化护理干预.

目的探讨个性化健康教育对慢性胃炎患者健康行为依从性的影响。方法将120例慢性胃炎患者随机分为试验组和对照组各60例,分别进行个性化健康教育、常规健康教育。随访3个月,分别进行健康知识了解、健康行为依从性的调查。结果试验组健康知识了解程度、健康行为依从性优于对照组,差异均有统计学意义(P<0.05)。结论个性化健康教育可提高慢性胃炎患者的健康知识水平,提高健康行为的依从性,从而改善患者的预后。

幽门螺杆菌(Hp)感染是小儿慢性胃炎及胃、十二指肠溃疡的重要病因之一[1].感染多发生在年龄较大的儿童,一般在6周岁以上,新生儿幽门螺杆菌感染未见报道.笔者对112例足月窒息新生儿胃液进行了幽门螺杆菌检测,现报道如下.