Machine Learning Approaches-Driven for Mortality Prediction for Patients Undergoing Craniotomy in ICU.

OBJECTIVES: We aimed to predict the mortality of patients with craniotomy in ICU by using predictive models to extract the high-risk factors leading to the death of patients from a retrospective a study. METHODS: Five machine-learning (ML) algorithms were applied for training on mortality predictive models with the data from a surgical intensive care unit (ICU) database of the Fujian Provincial Hospital in China. The accuracy, precision, recall, f1 score and the area under the receiver operator characteristic curve (AUC) were used to evaluate the performance of different models, and the calibration of the model was evaluated by brier score. RESULTS: We demonstrated that eXtreme Gradient Boosting (XGBoost) was more suitable for the task, demonstrating a AUC of 0.84. We analyzed the feature importance with the Local Interpretable Model-agnostic Explanations (LIME) analysis and further identified the high-risk factors of mortality in ICU through this study. CONCLUSIONS: This study established the mortality predictive model of patients who had undergone craniotomy in ICU. Identification of the factors that had great influence on mortality has the potential to provide auxiliary decision support for clinical medical staff on their practices.

Mst1 deletion reduces septic cardiomyopathy via activating Parkin-related mitophagy.

Cardiomyocyte function and viability are highly modulated by mammalian Ste20-like kinase 1 (Mst1)-Hippo pathway and mitochondria. Mitophagy, a kind of mitochondrial autophagy, is a protective program to attenuate mitochondrial damage. However, the relationship between Mst1 and mitophagy in septic cardiomyopathy has not been explored. In the present study, Mst1 knockout mice were used in a lipopolysaccharide (LPS)-induced septic cardiomyopathy model. Mitophagy activity was measured via immunofluorescence, Western blotting, and enzyme-linked immunosorbent assay. Pathway blocker and small interfering RNA were used to perform the loss-of-function assay. The results demonstrated that Mst1 was rapidly increased in response to LPS stress. Knockout of Mst1 attenuated LPS-mediated inflammation damage, reduced cardiomyocyte death, and improved cardiac function. At the molecular levels, LPS treatment activated mitochondrial damage, such as mitochondrial respiratory dysfunction, mitochondrial potential reduction, mitochondrial ATP depletion, and caspase family activation. Interestingly, in response to mitochondrial damage, Mst1 deletion activated mitophagy which attenuated LPS-mediated mitochondrial damage. However, inhibition of mitophagy via inhibiting parkin mitophagy abolished the protective influences of Mst1 deletion on mitochondrial homeostasis and cardiomyocyte viability. Overall, our results demonstrated that septic cardiomyopathy is linked to Mst1 upregulation which is followed by a drop in the protective mitophagy.

The impact of laryngopharyngeal reflux disease on 95 hospitalized patients with COVID-19 in Wuhan, China: A retrospective study.

Studies have demonstrated that comorbidities, especially cardiovascular and endocrine diseases, correlated with poorer clinical outcomes. However, the impact of digestive system diseases has not been issued. The aim of this study is to determine the impact of laryngopharyngeal reflux disease (LPRD) on hospitalized patients with coronavirus disease 2019 (COVID-19). We extracted clinical data regarding 95 patients in Wuhan Jinyintan Hospital, Wuhan, China, between 26 January and 21 February 2020. The Reflux Symptom Index (RSI) was used to assess the presence and severity of LPRD. An RSI greater than 13 is considered to be abnormal. A total of 95 patients with COVID-19 were enrolled, with 61.1% (58/95), 32.6% (31/95), and 6.3% (6/95) being moderately ill, severely ill, and critically ill, respectively. In this study, 38.9% (37/95) of the patient had an RSI score over 13, which was indicative of LPRD. In univariable analysis, the age and RSI scores of severely or critically ill patients were statistically significantly higher than patients with moderate disease (P = .026 and P = .005, respectively). After controlling for age difference in a multivariable model, the RSI greater than 13, compared to RSI equal to 0, was associated with significantly higher risk of severe infection (P < .001; odds ratio [OR] = 11.411; 95% confidence interval [CI], 2.95-42.09) and critical infection (P = .028; OR= 19.61; 95% CI, 1.38-277.99). Among hospitalized patients with COVID-19, RSI scores greater than 13, indicative of LPRD, correlated with poorer clinical outcomes. The prevalence of LPRD may be higher than the general population, which indicated that COVID-19 can impair the upper esophageal sphincter and aggravate reflux.

A novel mutation Gly222Arg in PROS1 causing protein S deficiency in a patient with pulmonary embolism.

BACKGROUND: Thrombophilia is becoming a more frequently reported disorder these years. Hereditary protein S deficiency is one of the anticoagulant deficiencies that eventually results in thrombophilia. CASE PRESENTATION: A 24-year-old male patient was suffering from unexplained thrombosis for the second time with a family history of deep venous thrombosis. Screening tests for anticoagulant proteins found the activity of protein S markedly lowered (5.0%). The patient was discharged after anticoagulation treatment. Four years later, the review still showed the activity of protein S in his plasma decreased (16.0%). Molecular genetic analysis revealed him homozygous for a missense mutation, c.664G>A, in the exon7 of PROS1. The mutation discovered here is the first mutation affecting the codon 222 of PROS1. This mutation results in the replacement of the glycine at the codon 222 of protein S with arginine, leading to a reduction of protein S function. CONCLUSIONS: The finding of this mutation may help with the understanding of the mechanism of protein S deficiency, especially in the Chinese population.

Resveratrol Protects the Myocardium in Sepsis by Activating the Phosphatidylinositol 3-Kinases (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Pathway and Inhibiting the Nuclear Factor-κB (NF-κB) Signaling Pathway.

BACKGROUND Sepsis combined with myocardial injury is an important cause of septic shock and multiple organ failure. However, the molecular mechanism of sepsis-induced myocardial dysfunction has not yet been thoroughly studied. Resveratrol has been an important research topic due its organ-protection function, but the specific mechanism is unclear. The purpose of this study was to explore the mechanism of organ injury in sepsis and to investigate the molecular mechanism of resveratrol in myocardial protection in sepsis. MATERIAL AND METHODS A classical Sprague-Dawley rat model of sepsis peritonitis was constructed for further experiments. The PI3K inhibitor LY294002 and resveratrol were used to intervene in a rat model of cardiomyopathy. HE staining was used to observe pathological changes. Cardiomyocyte apoptosis was detected by TUNEL assay. Western blot analysis was used to detect the level of maker proteins. RESULTS The PI3K inhibitors could promote cardiac abnormalities and apoptosis, but resveratrol showed the opposite effect. The upregulation function of the PI3K inhibitor on the expression of NF-kappaB, IL-6, IL-1ß, and TLR4 in LPS rats was not obvious, but the expression of TNF-a in LPS+LY294002 rats was increased by 22.85% compared with that in LPS rats (P<0.05). Compared with the LPS group, the expression of NF-kappaB, TNF-alpha, IL-6, IL-1ß, and TLR4 in the LPS+resveratrol group was decreased. The expression of p-PI3K, p-AKT, and p-mTOR in LPS+LY294002 was reduced. The expression p-PI3K, p-AKT, and p-mTOR in the myocardium of the LPS+resveratrol group was increased. CONCLUSIONS Resveratrol can protect the myocardium in sepsis by activating the PI3K/AKT/mTOR signaling pathway and inhibiting the NF-kappaB signaling pathway and related inflammatory factors.

Intracranial pressure responsiveness to positive end-expiratory pressure is influenced by chest wall elastance: a physiological study in patients with aneurysmal subarachnoid hemorrhage.

BACKGROUND: Respiratory system elastance (ERS) is an important determinant of the responsiveness of intracranial pressure (ICP) to positive end-expiratory pressure (PEEP). However, lung elastance (EL) and chest wall elastance (ECW) were not differentiated in previous studies. We tested the hypothesis that patients with high ECW or a high ECW/ERS ratio have greater ICP responsiveness to PEEP. METHODS: An esophageal balloon catheter was placed to measure esophageal pressure. PEEP was increased from 5 to 15 cmH2O. Airway pressure and esophageal pressure were measured and EL, ECW and ERS were calculated at the two PEEP levels. Patients were classified into either an ICP responder group or a non-responder group based on whether the change of ICP after PEEP adjustment was greater than or less than the median of the overall study population. RESULTS: The magnitude of the increase in esophageal pressure (median [interquartile range]) at end-expiratory occlusion was significantly increased in the responder group compared with that in the non-responder group (4.1 [2.7-4.1] versus 2.7 [0.0-2.7] cmH2O, p = 0.033) after PEEP adjustment. ECW and the ECW/ERS ratio were significantly higher in ICP responders than in non-responders at both low PEEP (p = 0.021 and 0.017) and high PEEP (p = 0.011 and 0.025) levels. No significant differences in ERS and EL were noted between the two groups at both PEEP levels. CONCLUSIONS: Patients with greater ICP responsiveness to increased PEEP exhibit higher ECW and a higher ECW/ERS ratio, suggesting the importance of ECW monitoring.

Research progress on correlations between trace element levels and epilepsy.

Research investigating the correlation between human trace element levels and disease alterations is growing. Epilepsy, a common nervous system disease, has also been found to be closely related to abnormal levels of trace elements. Studies continue to explore mechanisms of various trace elements involved in epileptic seizures through experimental animal models of epilepsy. Thus, we reviewed the research progress on the correlation between trace element levels and epilepsy in recent years and found that the trace elements most closely related to epilepsy are mainly metal ions such as selenium, iron, copper, zinc, and manganese. These results indicate that the changes in some trace elements are closely related to the increase in epilepsy susceptibility. In addition, after treatment with drugs and a ketogenic diet, the concentration of trace elements in the serum of patients with epilepsy changes. In other words, the abnormality of trace element concentrations is of great significance in the occurrence and development of epilepsy. This article is a literature update on the potential role of trace element imbalance in the development of epilepsy, providing new references for the subsequent prevention and treatment of epilepsy.

Risk factors for disease severity in COVID-19 patients: A single-center retrospective study.

Background: The outbreak of coronavirus disease 2019 (COVID-19) has posed a huge threat to human health. However, little is known regarding the risk factors associated with COVID-19 severity. We aimed to explore early-stage disease risk factors associated with eventual disease severity. Methods: This study enrolled 486 hospitalized, non-intensive care unit (ICU)-admitted adult patients with COVID-19 (age ≥ 18 years) treated at Wuhan Jinyintan Hospital, who were divided into three groups according to disease severity. The demographic, clinical, and laboratory data at admission and clinical outcomes were compared among severity groups, and the risk factors for disease severity were identified by multiple regression analysis. Results: Of 486 patients with COVID-19, 405 (83.33%) were discharged, 33 (6.71%) died outside of the ICU, and 48 (7.20%) were still being treated in the ICU by the time the study period ended. Significant differences in age, lymphocyte counts, and the levels of procalcitonin, aspartate aminotransferase, and D-dimer (P < 0.001 for all) among the three groups. Further analysis showed that older age, decreased lymphocyte counts, and increased procalcitonin, aspartate aminotransferase, and D-dimer levels were significantly associated with disease progression. Conclusion: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may impair the immune system, the blood coagulation system, and hepatic and cardiac function. Some clinical characteristics and laboratory findings can help identify patients with a high risk of disease severity, which can be significant for appropriate resource allocation during the COVID-19 pandemic.

[Study of multimodal monitoring in neurocritical care patients].

OBJECTIVE: To explore the significance of multimodal monitoring in the monitoring and treatment of neurocritical care patients. METHODS: 104 neurocritical care patients admitted to the department of Critical Care Medicine of Fujian Provincial Hospital from March 2019 to January 2020 were enrolled. Patients were randomly assigned into two groups, with 52 in each group. In the routine monitoring treatment group, heart rate, blood pressure, respiratory rate and the changes in consciousness and pupils were monitored after operation. The patients were treated with routine medicine to reduce intracranial pressure (ICP), maintain proper cerebral perfusion pressure (CPP), balance fluid intake and output, and maintain the airway clear. Patients in the multimodal monitoring treatment group were treated with invasive ICP monitoring, ultrasound to assess brain structure, ultrasound to measure optic nerve sheath diameter (ONSD), transcranial color doppler (TCCD), internal jugular venous blood oxygen saturation monitoring, near-infrared spectroscopy (NIRS), non-invasive cerebral blood oxygen saturation monitoring and quantitative electroencephalogram monitoring. According to the monitoring results, the patients were given targeted treatment with the goal of controlling ICP and improving brain metabolism. The length of intensive care unit (ICU) stay, the incidences of neurological complications (secondary cerebral infarction, cerebral hemorrhage, high intracranial pressure, etc.), and the incidences of poor prognosis [6 months after the onset of Glasgow outcome score (GOS) 1 to 3] were compared between the two groups. Spearman rank correlation analysis of the correlation between invasive ICP and the ICP value which was calculated by TCCD. The receiver operating characteristic (ROC) curve of invasive ICP and pulsatility index of middle cerebral artery (PIMCA) were used to predict poor prognosis. RESULTS: The length of ICU stay in the multimodal monitoring treatment group was significantly shorter than that of the routine monitoring treatment group (days: 6.27±3.81 vs. 9.61±5.09, P < 0.01), and the incidence of neurological complications was significantly lower than that in the routine monitoring treatment group (9.62% vs. 25.00%, P < 0.05). In the multimodal monitoring treatment group, 37 cases had a good prognosis and 15 cases had a poor prognosis, while the routine monitoring treatment group had a good prognosis in 27 cases and a poor prognosis in 25 cases. The incidence of poor prognosis in the multimodal monitoring treatment group was lower than that of the routine monitoring treatment group (28.85% vs. 48.08%, P < 0.05). In the multimodal monitoring treatment group, the invasive ICP and PIMCA of patients with good prognosis were significantly lower than those of patients with poor prognosis [invasive ICP (mmHg, 1 mmHg = 0.133 kPa): 16 (12, 17) vs. 22 (20, 24), PIMCA: 0.90±0.33 vs. 1.39±0.58, both P < 0.01]. There was no significant difference in resistance index of the middle cerebral artery (RIMCA) between the good prognosis group and the poor prognosis group (0.63±0.12 vs. 0.66±0.15, P > 0.05). There was a positive correlation between the invasive ICP and the ICP value which was calculated by TCCD (r = 0.767, P < 0.001). ROC curve analysis showed that the area under ROC curve (AUC) of invasive ICP for poor prognosis prediction was 0.906, the best cut-off value was ≥ 18 mmHg, the sensitivity was 86.49%, and the specificity was 86.67%. The AUC of PIMCA for poor prognosis prediction was 0.759, the best cut-off value was ≥ 1.12, the sensitivity was 81.08%, and the specificity was 60.00%. The AUC of invasive ICP was greater than PIMCA (Z = 2.279, P = 0.023). CONCLUSIONS: Comprehensive analysis of multimodal monitoring indicators for neurocritical care patients to guide clinical treatment can reduce the length of hospital stay, and reduce the risk of neurosurgery complications and disability; invasive ICP can predict poor prognosis of neurocritical care patients.

Investigation of Penetration Performance of Zr-based Amorphous Alloy Liner Compared with Copper.

Zr-based amorphous alloy is a new type of metastable energetic material, which has been exploringly used to design shaped charge (SC) liners by scholars of the military industry. In order to know well how the stand-off distance influences jet penetration performance of liners made by such energetic materials against metal targets, SC static explosion tests were conducted under the same initiation and target conditions but different stand-off distances compared with copper liners. Test results indicate that the jet depth of penetration (DOP) of Zr-based amorphous alloy liners firstly increases slowly and then decreases sharply as the stand-off becomes larger. The optimum stand-off distance is 3.5 times of charge diameter (CD) and the corresponding maximum DOP is about 2.68 CD against the 45# steel plate. The perforation area varies with the stand-off distance. It reaches the maximum when the stand-off is 3.5 CD and the corresponding perforation diameter is about 42mm, also the penetration hole is nearly circular. The jet DOP of Zr-based amorphous alloy liner is smaller than that of copper liner's while the perforation area is the opposite. The former DOP is about 55.7% of the latter and the former perforation area is about 2.8 times of latter when the stand-off distance is 3.5 CD.

SRV2 promotes mitochondrial fission and Mst1-Drp1 signaling in LPS-induced septic cardiomyopathy.

Mitochondrial fission is associated with cardiomyocyte death and myocardial depression, and suppressor of ras val-2 (SRV2) is a newly discovered pro-fission protein. In this study, we examined the mechanisms of SRV2-mediated mitochondrial fission in septic cardiomyopathy. Western blotting, ELISA, and immunofluorescence were used to evaluate mitochondrial function, oxidative balance, energy metabolism and caspase-related death, and siRNA and adenoviruses were used to perform loss- and gain-of-function assays. Our results demonstrated that increased SRV2 expression promotes, while SRV2 knockdown attenuates, cardiomyocyte death in LPS-induced septic cardiomyopathy. Mechanistically, SRV2 activation promoted mitochondrial fission and physiological abnormalities by upregulating oxidative injury, ATP depletion, and caspase-9-related apoptosis. Our results also demonstrated that SRV2 promotes mitochondrial fission via a Mst1-Drp1 axis. SRV2 knockdown decreased Mst1 and Drp1 levels, while Mst1 overexpression abolished the mitochondrial protection and cardiomyocyte survival-promoting effects of SRV2 knockdown. SRV2 is thus a key novel promotor of mitochondrial fission and Mst1-Drp1 axis activity in septic cardiomyopathy.

Sepsis-related myocardial injury is associated with Mst1 upregulation, mitochondrial dysfunction and the Drp1/F-actin signaling pathway.

LPS-induced septic cardiomyopathy has been found to be connected with mitochondrial stress through unknown mechanisms. Mitochondrial fission is an early event in mitochondrial dysfunction. The aim of our study was to determine the role and regulatory mechanism of mitochondrial fission in the progression of LPS-induced septic cardiomyopathy, with a particular focus on Mst1 and F-actin. Our data demonstrated that Mst1 expression was rapidly upregulated in LPS-treated hearts and that increased Mst1 promoted cardiomyocyte death by inducing mitochondrial stress. Mechanistically, elevated expression of Mst1 upregulated Drp1, and the latter initiated mitochondrial fission. Excessive mitochondrial fission caused mitochondrial oxidative injury, mitochondrial membrane potential reduction, mitochondrial proapoptotic element translocation into the cytoplasm/nucleus, mitochondrial energy dysfunction and mitochondrial apoptosis activation. Inhibition of mitochondrial fission sustained mitochondrial function and favored cardiomyocyte survival. Furthermore, we identified F-actin degradation as an apparent downstream event of mitochondrial fission activation in the context of LPS-induced septic cardiomyopathy. Stabilization of F-actin attenuated fission-mediated cardiomyocyte death. Altogether, our results define the Mst1/Drp1/mitochondrial fission/F-actin axis as a new signaling pathway that mediates LPS-related septic cardiomyopathy by inducing mitochondrial stress and cardiomyocyte death. Therefore, Mst1 expression, mitochondrial fission modification and F-actin stabilization may serve as potential therapeutic targets for sepsis-related myocardial injury.

Dendritic cells and Th17/Treg ratio play critical roles in pathogenic process of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a common disorder of respiratory system. This study aimed to evaluate changes of mature dendritic cells (DCs) and regulatory T cells (Treg) in lung tissues and peripheral blood of COPD patients. For lung tissue analysis, patients were divided into no-smoking and no-COPD (CS-COPD-), smoking and no-COPD (CS + COPD-) and COPD group. For peripheral blood analysis, patients were divided into CS-COPD-, CS + COPD-, stable COPD (SCOPD) and acute exacerbation of COPD (AECOPD) group. Hematoxylin and eosin (HE) staining was used to evaluate inflammation of lung tissues. Immunohistochemistry assay was employed to examine CD80, CCR6, IL-17 A, FoxP3 in lung tissues. DCs and Treg cells were isolated from lung tissues and peripheral blood. Levels of CD80, FoxP3+ Treg, CCR6 and IL-17 A were detected by using flow cytometry. Results showed that FEV%, FVC% and FEV1/FVC were significantly reduced and Bosken scores were remarkably increased in COPD patients compared to non-COPD patients (p < 0.05). CD80 and FoxP3 levels were lower, and CCR6 and IL-17A levels were higher obviously in COPD compared to non-COPD patients (p < 0.05). COPD patients illustrated reduced mDCs levels and enhanced imDCs levels. COPD patients exhibited remarkably higher Th17 levels compared to no-smoking patients (p < 0.05). COPD patients illustrated obviously lower Treg levels and significantly higher Th17/Treg ratio compared to non-smoking patients (p < 0.05). Th17% (Th17/Treg) negatively and Treg% was positively correlated with FEV1%, FEVC%, FEV1/FEVC (p < 0.05). In conclusion, dendritic cells and Th17/Treg ratio play critical roles for pathogenic process of chronic obstructive pulmonary disease.

Effects of increased positive end-expiratory pressure on intracranial pressure in acute respiratory distress syndrome: a protocol of a prospective physiological study.

INTRODUCTION: There are concerns that the use of positive end-expiratory pressure (PEEP) in patients with brain injury may potentially elevate intracranial pressure (ICP). However, the transmission of PEEP into the thoracic cavity depends on the properties of the lungs and the chest wall. When chest wall elastance is high, PEEP can significantly increase pleural pressure. In the present study, we investigate the different effects of PEEP on the pleural pressure and ICP in different respiratory mechanics. METHODS AND ANALYSIS: This study is a prospective, single-centre, physiological study in patients with severe brain injury. Patients with acute respiratory distress syndrome with ventricular drainage will be enrolled. An oesophageal balloon catheter will be inserted to measure oesophageal pressure. Patients will be sedated and paralysed; airway pressure and oesophageal pressure will be measured during end-inspiratory occlusion and end-expiratory occlusion. Elastance of the chest wall, the lungs and the respiratory system will be calculated at PEEP levels of 5, 10 and 15 cm H2O. We will classify each patient based on the maximal ΔICP/ΔPEEP being above or below the median for the study population. 2 groups will thus be compared. ETHICS AND DISSEMINATION: The study protocol and consent forms were approved by the Institutional Review Board of Fujian Provincial Hospital. Study findings will be disseminated through peer-reviewed publications and conference presentations. TRIAL REGISTRATION NUMBER: NCT02670733; pre-results.

The Effect of Esmolol on Tissue Perfusion and Clinical Prognosis of Patients with Severe Sepsis: A Prospective Cohort Study.

Purpose. This study was aimed at investigating the effect of esmolol on tissue perfusion and the clinical prognosis of patients with severe sepsis. Materials and Methods. One hundred fifty-one patients with severe sepsis were selected and divided into the esmolol group (n = 75) or the control group (n = 76), who received conventional antiseptic shock treatment. The esmolol group received a continuous infusion of esmolol via a central venous catheter, and their heart rate (HR) was maintained at 70-100 bpm over 72 hours. Results. The HR of all patients reached the target level within 72 hours of treatment for both groups. The effect of esmolol on PvaCO2 was only significant at 48 hours (P < 0.05). ScvO2 increased in the esmolol group and decreased in the control group (P < 0.01). Lac showed a linear downward trend over the treatment time, but the reduction was more significant in the control group at 48 hours (P < 0.05) between the two groups. Kaplan-Meier analysis showed a significantly shorter duration of mechanical ventilation in the esmolol group than in the control group (P < 0.05). Conclusions. Esmolol reduced the duration of mechanical ventilation in patients with severe sepsis, with no significant effect on circulatory function or tissue perfusion.

Better short-term efficacy of treating severe flail chest with internal fixation surgery compared with conservative treatments.

BACKGROUND: The objective of the study is to provide evidence for selecting the best treatment approach for severe flail chest by comparing surgical and conservative treatments. METHODS: This is a retrospective study in which 32 patients with severe flail chest were treated in the Fujian Provincial Hospital (China) between July 2007 and July 2012 with surgical internal rib fixation (n = 17) or conservative treatments (n = 15). Mechanical ventilation time, intensive care unit (ICU) stay time, pulmonary infection, antibiotic treatment duration, acute physiology and chronic health evaluation II (APACHE II) scores 7 and 14 days after trauma, rate of tracheostomy, and rate of endotracheal re-intubation were compared. RESULTS: One patient died in the conservative treatment group. Better short-term outcomes were observed in the surgery group, such as total mechanical ventilation time (10.5 ± 3.7 vs. 13.7 ± 4.4 days, P = 0.03), ICU stay (15.9 ± 5.0 vs. 19.6 ± 5.0 days, P = 0.05), pulmonary infection rate (58.8 % vs. 93.3 %, P = 0.02), and APACHE II scores on the 14th day (6.5 ± 3.8 vs. 10.1 ± 4.7, P = 0.02). No difference was observed in the therapeutic time of antibiotics, rate of tracheostomy, and the rate of endotracheal re-intubation between the two groups. CONCLUSIONS: Results suggest that internal fixation surgery resulted in better outcomes in the management of severe flail chest compared with conservative treatments.