Heparin-free adventitia pulmonary oxygenation in the treatment of trauma complicated with severe pulmonary infection: a case report.

The application of Venovenous (VV) extracorporeal membrane oxygenation (ECMO) in trauma and patients with severe bleeding tendency has been controversial. However, VV ECMO without anticoagulation contributes to reducing the risk of bleeding during ECMO maintenance. VV ECMO serves critical roles in therapy of patients with severe pulmonary infection and failure in conventional therapy. The common peripheral catheterization approach for VV ECMO is femoral vein-internal jugular vein catheterization, and bilateral femoral vein catheterization can also achieve the purpose of respiratory support for patients with limited cervical catheterization. In this case report, we described a patient with post-traumatic cervical spinal cord injury and severe pulmonary infection who was successfully treated with heparin-free intravenous ECMO.

Hypothermia prevents hippocampal oxidative stress and apoptosis via the GSK-3ß/Nrf2/HO-1 signaling pathway in a rat model of cardiac arrest-induced brain damage.

OBJECTIVES: The present study was undertaken to investigate the effects and related mechanisms of hypothermia on oxidative stress and apoptosis caused by cardiac arrest (CA)-induced brain damage in rats. METHODS: The CA/CPR model was initiated by asphyxia. Body temperature in the normothermia and hypothermia groups was maintained at 37°C ± 0.2°C and 34°C ± 0.2°C, respectively, by surface cooling with an ice pack. First, neurological deficit scores (NDSs) were assessed, and then hippocampus samples were collected at 24 and 72 h after return of spontaneous circulation (ROSC). RESULTS: The NDSs of rats were significantly reduced after CA, and hypothermia ameliorated neurological deficits. Varying degrees of changes in cellular nuclei and mitochondria were observed in the hippocampus following CA; however, morphological changes became less apparent after therapeutic hypothermia. Malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were higher in the hippocampus at 24 h after ROSC. In contrast, hypothermia did not alter MDA content, while SOD activity further increased. Furthermore, hypothermia reversed the caspase-3 enhancement observed in the normothermia group at 24 h after ROSC. CA also inhibited GSK-3ß phosphorylation, promoted Nrf2 translocation to the nucleus, and downregulated HO-1 expression. However, hypothermia significantly reversed these CA-induced changes in GSK-3ß phosphorylation, Nrf2 translocation, and HO-1 expression. CONCLUSION: Hypothermia attenuated CA-induced neurological deficits and hippocampal morphology changes in rats. The protective effect of hypothermia following CA may have been related to inhibition of oxidative stress and apoptosis, and its underlying mechanisms may have been due, at least in part, to activation of the GSK-3ß/Nrf2/HO-1 pathway.

Hypothermia protects neurons against ischemia/reperfusion-induced pyroptosis via m6A-mediated activation of PTEN and the PI3K/Akt/GSK-3ß signaling pathway.

Cerebral ischemia/reperfusion (I/R) injury often leads to irreversible neuronal injury and even death, and hypothermia is the only therapeutic method that has been proven to be effective. However, the molecular mechanisms underlying the effect of hypothermia treatment on I/R injury have not been fully elucidated. In the present study, we aimed to evaluate the neuroprotective effects and mechanisms of hypothermia against hypoxia/reoxygenation (H/R)-induced neuronal damage. Primary hippocampal neurons were exposed to H/R and were then treated with hypothermia. We observed that hypothermia significantly increased cellular viability, downregulated the expression of pyroptosis-related proteins-including NLR pyrin domain containing 3 (NLRP3), apoptotic speck-like protein containing CARD (ASC), cleaved Caspase-1, and Gasdermin-D (GsdmD) p30-and reduced secretion of the pro-inflammatory cytokines, IL-1ß and IL-18. Additionally, pretreatment with MCC950, a specific small-molecule inhibitor of the NLRP3 inflammasome, yielded a protective effect on cellular viability that was comparable to that of hypothermia treatment. Furthermore, hypothermia also significantly elevated the expression level of phosphatase and tensin homologous protein (PTEN) and activated the phosphorylation levels of protein kinase B (Akt) and glycogen synthase kinase-3ß (GSK-3ß). These protective effects of hypothermia on pyroptosis-related proteins and pro-inflammatory cytokines were partially reversed by the specific PI3K/Akt inhibitor, LY294002. Moreover, the methylated level of PTEN mRNA was elevated in hippocampal neurons upon H/R, whereas this level remained stable in the hypothermia group. Therefore, our findings suggest that hypothermia protects neurons against neuronal H/R-induced pyroptosis, and that m6A-mediated activation of PTEN and the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/Akt/GSK-3ß signaling pathway may play crucial roles during this process.

Use of Platelet Indices for Determining Illness Severity and Predicting Prognosis in Critically Ill Patients.

BACKGROUND: Decreased platelet (PLT) count is one of the independent risk factors for mortality in intensive care unit (ICU) patients. This study was to investigate the relationship between PLT indices and illness severity and their performances in predicting hospital mortality. METHODS: Adult patients who admitted to ICU of Changzheng Hospital from January 2011 to September 2012 and met inclusion criteria were included in this study. Univariate analysis was used to identify potential independent risk factors for mortality. Multiple logistic regression analysis was used to calculate adjusted odds ratio for mortality in patients with normal or abnormal PLT indices. The relationship between PLT indices and illness severity were assessed by the Acute Physiology and Chronic Health Evaluation II (APACHE II) scores or sequential organ failure assessment (SOFA) scores in patients with normal and abnormal PLT indices. The performances of PLT indices in predicting mortality were assessed by receiver operating curves and diagnostic parameters. The survival curves between patients with normal and abnormal PLT indices were compared using Kaplan-Meier method. RESULTS: From January 2011 to September 2012, 261 of 361 patients (204 survivors and 57 nonsurvivors) met the inclusion criteria. After adjustment for clinical variables, PLT count <100 × 10 12 /L (P = 0.011), plateletcrit (PCT) <0.108 (P = 0.002), mean platelet volume (MPV) >11.3 fL (P = 0.023) and platelet distribution width (PDW) percentage >17% (P = 0.009) were identified as independent risk factors for mortality. The APACHE II and SOFA scores were 14.0 (9.0-20.0) and 7.0 (5.0-10.5) in the "low PLT" tertile, 13.0 (8.0-16.0) and 7.0 (4.0-11.0) in the "low PCT" tertile, 14.0 (9.3-19.0) and 7.0 (4.0-9.8) in the "high MPV" tertile, 14.0 (10.5-20.0) and 7.0 (5.0-11.0) in the "high PDW" tertile, all of which were higher than those in patients with normal indices. Patients with decreased PLT and PCT values (all P < 0.001), or increased MPV and PDW values (P = 0.007 and 0.003, respectively) had shortened length of survival than those with normal PLT indices. CONCLUSIONS: Patients with abnormally low PLT count, high MPV value, and high PDW value were associated with more severe illness and had higher risk of death as compared to patients with normal PLT indices.

[Prognostic value of arterial lactate content combined with base excess in patients with sepsis: a retrospective study].

OBJECTIVE: To study the prognostic value of arterial lactate combined with base excess (BE) in sepsis patients. METHODS: Clinical data of patients admitted to intensive care unit (ICU) from July 2009 to December 2012 were retrospectively analyzed. Patients were divided into survivor group and non-survivor group, and the arterial blood lactate and BE concentrations were compared between groups. The receiver operating characteristic curve (ROC curve) was drawn and area under the ROC curve (AUC) was calculated to analyze the function of arterial lactate, BE and their combination in judging the prognosis of sepsis. The best cut-off values of arterial lactate and BE for sepsis prognosis were searched. RESULTS: One hundred and eighteen patients were enrolled with 75 in survivor group and 43 in non-survivor group. There were significant differences in arterial lactate [1.20(0.90) mmol/L, 2.30(1.90) mmol/L] and BE (0.44 ± 5.13 mmol/L, -4.35 ± 4.86 mmol/L) between two groups (both P=0.000). The AUC for mortality prediction was 0.805, 0.755 and 0.822 for arterial blood lactate, BE, and their combination respectively. Using arterial lactate higher than 1.7 mmol/L and BE lower than -3 mmol/L as cut-off values, a better sensitivity (79.1% and 69.8%) and positive predictive value (3.955 and 2.493) can be obtained. CONCLUSION: Combination of arterial lactate and BE can be a better indicator of prognosis in sepsis patients.