World Journal of Emergency Medicine

Intestinal microcirculation dysfunction in sepsis: pathophysiology, clinical monitoring, and therapeutic interventions

A-ling Tang, Mei-jia Shen, Guo-qiang Zhang

2022, 13(5): 343-348. doi:10.5847/wjem.j.1920-8642.2022.031

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BACKGROUND: Intestinal microcirculation dysfunction is an important factor that causes poor prognosis in sepsis patients and is an important pathophysiological basis for the occurrence and development of sepsis.

DATA RESOURCES: PubMed, Web of Science, and China National Knowledge Infrastructure (CNKI) were searched from inception to August 1, 2021. The search was limited to the English language only. Two reviewers independently identified studies related to intestinal microcirculation dysfunction in sepsis. Exclusion criteria were duplicate articles according to multiple search criteria.

RESULTS: Fifty articles were included, and most of them were animal studies. These studies reported pathogenesis, including endothelial dysfunction, leukocyte recruitment and adhesion, microthrombus formation, microcirculation hypoperfusion, and redistribution of intestinal wall blood flow. The monitoring methods of intestinal microcirculation were also diverse, including handheld microscopes, intravital microscopy (IVM), laser Doppler blood flow instruments, laser speckle contrast imaging, tissue reflectance spectrophotometry, biochemical markers of intestinal ischemia, and histopathological examination. In view of the related pathogenesis of intestinal microcirculation disorder in sepsis, existing studies also have different opinions on its treatment.

CONCLUSIONS: Limited by monitoring, there are few clinical studies on intestinal microcirculation dysfunction in sepsis. Related research mainly focuses on basic research, but some progress has also been made. Therefore, this review may provide a reference for future research on intestinal microcirculation dysfunction in sepsis.

Timing of brain computed tomography for predicting neurological prognosis in comatose cardiac arrest survivors: a retrospective observational study

Gan-nan Wang, Zhong-man Zhang, Wen Chen, Xiao-quan Xu, Jin-song Zhang

2022, 13(5): 349-354. doi:10.5847/wjem.j.1920-8642.2022.080

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BACKGROUND: To assess the association between relevant brain computed tomography (CT) parameters at different time and neurological prognosis in adult comatose survivors after cardiac arrest (CA).

METHODS: A total of 94 CA patients who underwent early and late CT scans (within 24 h and 24 h to 7 d respectively after CA) between January 2018 and April 2020 were enrolled in this retrospective study. According to the Cerebral Performance Category (CPC) score at hospital discharge, the patients were divided into either a good outcome (CPC 1-2) group or a poor-outcome group (CPC 3-5). The grey-to-white matter ratio (GWR) and the proportion of cerebrospinal fluid volume (pCSFV) were measured. In predicting poor outcomes, the prognostic performance of relevant CT parameters was evaluated, and the comparison analysis (expressed as the ratio of parameters in late CT to those in the early CT) of different CT time was conducted.

RESULTS: Totally 26 patients were in the good-outcome group, while 68 patients were in the poor-outcome group. The putamen density, GWR, and pCSFV in late CT were significantly lower in the poor-outcome group (P<0.05). The ratios of GWR and pCSFV in the poor-outcome group were significantly decreased according to comparison analysis of different CT time (P<0.05), while there was no significant difference in the ratio of putamen density. GWR-basal ganglia <1.18 in late CT showed the best predictive value. The ratio of pCSFV <0.98 predicted unfavorable neurological outcomes with a sensitivity of 65.9% and a specificity of 93.8% (P=0.001).

CONCLUSIONS: Brain CT performed >24 h after CA may be a good choice as a neuroimaging approach to evaluating prognosis. To predict neurological prognosis, comparison analysis of different CT time can be used as another promising tool in comatose CA survivors.

Development and evaluation of a predictive nomogram for survival in heat stroke patients: a retrospective cohort study

Fei Shao, Xian Shi, Shu-hua Huo, Qing-yu Liu, Ji-xue Shi, Jian Kang, Ping Gong, Sheng-tao Yan, Guo-xing Wang, Li-jie Qin, Fei Wang, Ke Feng, Feng-ying Chen, Yong-jie Yin, Tao Ma, Yan Li, Yang Wu, Hao Cui, Chang-xiao Yu, Song Yang, Wei Gan, Sai Wang, Liu-ye-zi Du, Ming-chen Zhao, Zi-ren Tang, Shen Zhao

2022, 13(5): 355-360. doi:10.5847/wjem.j.1920-8642.2022.092

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BACKGROUND: This study aimed to establish an effective nomogram to predict the survival of heat stroke (HS) based on risk factors.

METHODS: This was a retrospective, observational multicenter cohort study. We analyzed patients diagnosed with HS, who were treated between May 1 and September 30, 2018 at 15 tertiary hospitals from 11 cities in Northern China.

RESULTS: Among the 175 patients, 32 patients (18.29%) died before hospital discharge. After the univariate analysis, mechanical ventilation, initial mean arterial pressure <70 mmHg, maximum heart rate, lab results on day 1 (white blood cell count, alanine aminotransferase, creatinine), and Glasgow admission prediction score were included in multivariate analysis. Multivariate Cox regression showed that invasive ventilation, initial mean arterial pressure <70 mmHg (1 mmHg=0.133 kPa), and Glasgow admission prediction score were independent risk factors for HS. The nomogram was established for predicting 7-d and 14-d survival in the training cohort. The nomogram exhibited a concordance index (C-index) of 0.880 (95% confidence interval [95% CI] 0.831-0.930) by bootstrapping validation (B=1,000). Furthermore, the nomogram performed better when predicting 14-d survival, compared to 7-d survival. The prognostic index cut-off value was set at 2.085, according to the operating characteristic curve for overall survival prediction. The model showed good calibration ability in the internal and external validation datasets.

CONCLUSION: A novel nomogram, integrated with prognostic factors, was proposed; it was highly predictive of the survival in HS patients.

Analysis of imaging characteristics of blunt traumatic aortic dissection: an 8-year experience

Li Li, Li-ying Lin, Yuan-qiang Lu

2022, 13(5): 361-366. doi:10.5847/wjem.j.1920-8642.2022.091

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BACKGROUND: Traumatic aortic dissection (TAD) has a low incidence but extremely high mortality. It always presents atypical clinical manifestations that are easily missed or misdiagnosed. This study mainly aims to describe the imaging characteristics and management of TAD patients.

METHODS: A retrospective analysis of 27 blunt TAD patients was performed between 2013 and 2020. Demographic features, imaging characteristics, and management were analyzed.

RESULTS: Twenty-seven patients with type B aortic dissection (age 56.04±16.07 years, 20 men) were included. Aortic intimal tears were mostly initiated from the aortic isthmus. The sizes of the proximal intimal tears in the greater curvature were larger than those in the lesser curvature (1.78±0.56 cm vs. 1.24±0.52 cm, P=0.031). Compared with those in the control group, the maximum diameters of the aortic arch, thoracic aorta, and abdominal aorta in the TAD patients were all significantly widened (all P<0.050). Multivariate logistic regression analysis showed that the maximum diameter of the thoracic aorta was an independent risk factor for TAD, with a predictive value with an area under the receiver operating characteristic curve (AUC) of 0.673. Finally, 26 patients successfully underwent delayed thoracic endovascular aortic repair (TEVAR), and the remaining one patient was treated conservatively. No progression of aortic dissection or death occurred during the six-month follow-up period.

CONCLUSIONS: In blunt trauma, the aortic isthmus is the most common site of proximal intimal tears. An accurate diagnosis of TAD requires an overall consideration of medical history and imaging characteristics. Delayed TEVAR might be an effective therapeutic option for TAD.

Is rosuvastatin protective against sepsis-associated encephalopathy? A secondary analysis of the SAILS trial

Shi-yuan Yu, Zeng-zheng Ge, Jun Xiang, Yan-xia Gao, Xin Lu, Joseph Harold Walline, Mu-bing Qin, Hua-dong Zhu, Yi Li

2022, 13(5): 367-372. doi:10.5847/wjem.j.1920-8642.2022.072

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BACKGROUND: Sepsis is a common cause of death in emergency departments and sepsis-associated encephalopathy (SAE) is a major complication. Rosuvastatin may play a neuroprotective role due to its protective effects on the vascular endothelium and its anti-inflammatory functions. Our study aimed to explore the potential protective function of rosuvastatin against SAE.

METHODS: Sepsis patients without any neurological dysfunction on admission were prospectively enrolled in the “Rosuvastatin for Sepsis-Associated Acute Respiratory Distress Syndrome” study (SAILS trial, ClinicalTrials.gov number: NCT00979121). Patients were divided into rosuvastatin and placebo groups. This is a secondary analysis of the SAILS dataset. Baseline characteristics, therapy outcomes, and adverse drug events were compared between groups.

RESULTS: A total of 86 patients were eligible for our study. Of these patients, 51 were treated with rosuvastatin. There were significantly fewer cases of SAE in the rosuvastatin group than in the placebo group (32.1% vs. 57.1%, P=0.028). However, creatine kinase levels were significantly higher in the rosuvastatin group than in the placebo group (233 [22-689] U/L vs. 79 [12-206] U/L, P=0.034).

CONCLUSION: Rosuvastatin appears to have a protective role against SAE but may result in a higher incidence of adverse events.

Arctigenin attenuates paraquat-induced human lung epithelial A549 cell injury by suppressing ROS/p38 mitogen-activated protein kinases-mediated apoptosis

Chao Liu, Zhao-rui Sun, Meng-meng Wang, Zhi-zhou Yang, Wei Zhang, Yi Ren, Xiao-qin Han, Rui Liu, Quan Li, Shi-nan Nie

2022, 13(5): 373-378. doi:10.5847/wjem.j.1920-8642.2022.086

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BACKGROUND: Paraquat (PQ)-induced acute lung injury (ALI) and pulmonary fibrosis are common diseases with high mortality but without effective antidotes in emergency medicine. Our previous study has proved that arctigenin suppressed pulmonary fibrosis induced by PQ. We wondered whether arctigenin could also have a protective effect on PQ-induced ALI.

METHODS: A PQ-induced A549 cell injury model was used, and the effect of arctigenin was determined by a cell counting kit-8 (CCK-8) cell viability assay. In addition, terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labelling (TUNEL) staining assays and mitochondrial membrane potential assays were performed to evaluate the level of cell apoptosis. The generation of reactive oxygen species (ROS) was reflected by dihydroethidium (DHE) staining and a 2’,7’-dichlorodihydrofluorescein diacetate (DCFH-DA) assay. Moreover, immunoblotting studies were used to assess the expression of mitogen-activated protein kinases (MAPKs) and p38 MAPK.

RESULTS: Arctigenin attenuated PQ-induced inhibition of A549 cell viability in a dose-dependent manner. Arctigenin also significantly reduced PQ-induced A549 cell apoptosis, as reflected by the TUNEL assay and mitochondrial membrane potential assay, which may result from suppressed ROS/p38 MAPK signaling because we found that arctigenin dramatically suppressed ROS generation and p38 MAPK phosphorylation.

CONCLUSION: Arctigenin could attenuate PQ-induced lung epithelial A549 cell injury in vitro by suppressing ROS/p38 MAPK-mediated cell apoptosis, and arctigenin might be considered a potential candidate drug for PQ-induced ALI.

Hepatocellular carcinoma-derived exosomal miRNA-761 regulates the tumor microenvironment by targeting the SOCS2/JAK2/STAT3 pathway

Xiao-hu Zhou, Hao Xu, Chang Xu, Ying-cai Yan, Lin-shi Zhang, Qiang Sun, Wei-lin Wang, Yan-jun Shi

2022, 13(5): 379-385. doi:10.5847/wjem.j.1920-8642.2022.089

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BACKGROUND: Exosomes and exosomal microRNAs have been implicated in tumor occurrence and metastasis. Our previous study showed that microRNA-761 (miR-761) is overexpressed in hepatocellular carcinoma (HCC) tissues and that its inhibition affects mitochondrial function and inhibits HCC metastasis. The mechanism by which exosomal miR-761 modulates the tumor microenvironment has not been elucidated.

METHODS: Exosomal miR-761 was detected in six cell lines. Cell counting kit-8 (CCK-8) and transwell migration assays were performed to determine the function of exosomal miR-761 in HCC cells. The luciferase reporter assay was used to analyze miR-761 target genes in normal fibroblasts (NFs). The inhibitors AZD1480 and C188-9 were employed to determine the role of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway in the transformation of cancer-associated fibroblasts (CAFs).

RESULTS: In this study, we characterized the mechanism by which miR-761 reprogrammed the tumor microenvironment. We found that HCC-derived exosomal miR-761 was taken up by NFs. Moreover, HCC exosomes affected the tumor microenvironment by activating NFs via suppressor of cytokine signaling 2 (SOCS2) and the JAK2/STAT3 signaling pathway.

CONCLUSIONS: These results demonstrated that exosomal miR-761 modulated the tumor microenvironment via SOCS2/JAK2/STAT3 pathway-dependent activation of CAFs. Our findings may inspire new strategies for HCC prevention and therapy.

Impact of different waves of COVID-19 on emergency medical services and out-of-hospital cardiopulmonary arrest in Madrid, Spain

Jose-María Navalpotro-Pascual, Diana Monge Martín, Manuel-José González León, Fernando Neria Serrano, Carlos Alonso Blas, Belén Muñoz Isabel, Yago Muñecas Cuesta, Alfredo Carrillo Moya, Juan Les González, Alonso Mateos Rodríguez

2022, 13(5): 386-389. doi:10.5847/wjem.j.1920-8642.2022.085

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The role of the perfusion index in patients with thoracic trauma

İsmail Uzkuç, Ekim Saglam Gurmen, Cumhur Murat Tulay

2022, 13(5): 390-392. doi:10.5847/wjem.j.1920-8642.2022.077

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Posterior lamellar tarsorrhaphy in the early treatment of severe eyelid trauma/burns

Neelam Pushker, Deepsekhar Das, Sujeeth Modaboyina, Pallavi Singh, Sahil Agrawal