Exertional heat stroke (EHS) is an emergency with a high mortality rate, characterized by acute onset and identification difficulties. EHS prevention focuses on evaluating the environment by professionals, making preventive measures in advance, identifying internal and external risk factors for the onset of disease, carrying out prior heat adaptation and endurance training, monitoring the status of high risk persons in real time. After occurrence of EHS, the key to success treatment is on-site accurate identification and diagnosis and rapid implementation of effective cooling measures, thus winning time of EHS patients transferred to the hospital for the treatment. This article reviews the current status of EHS prevention and treatment in domestic and foreign from the scene to the hospital. Summarizing the recognition, diagnosis, cooling measures, treatment concepts and principles of EHS, we hope to provide a reference for the rescue of EHS in hospital and outside.

Objective To compare the intensity of cognitive impairment and the level of pathological lesion in hippocampus induced by ischemia or chronic stress for a more valuable guidance in the treatment of post-stroke cognitive impairment(PSCI).Methods Forty male adult SD rats were divided medially into 4 groups:control,stress,ischemia and ischemia plus stress.Animals in 3 treatment groups were subjected respectively to an operation of modified selective middle cerebral artery occlusion or a procedure of continuous 3-week chronic unpredictable mild stress or a combined program of the two treatments.Morris water maze was employed to assess hippocampus-dependent learning and memory function and the brain-derived neurotrophic factor(BDNF)expression was detected by immunohistochemical staining in CA3 area and the mRNA amplification through semi-quantitative reverse transcription polymerase chain reaction(RT-PCR).Results Both chronic stressors and ischemia could significantly decrease the learning and memory function in rats like the escape latency in the performance of the Morris water maze test compared with the controL The stress group was related preferentially to a more severe deterioration in the learning function but not statistically in the memory loss as compared to ischemia group.The cognitive function decreased more markedly in rats when suffered the chronic unpredictable mild stresses plus ischemia,In comparison to control,ischemia significantly increased BDNF+ cells in hippocampal CA3 area (27.0 ±2.5 vs 20.1 ±2.1),while stress markedly reduced the expression of BDNF(15.2 ± 1.8 vs 20.1 ±2.1).Their combined effects still statistically led to a reduction in BDNF expression(8.2 ± 1.5,F =52.87,P ＜0.05).The same tendency was found in BDNF mRNA expression.Conclusions Stress may preferentially and powerfully influence hippocampus-dependent cognitive function compared with ischemia and the combination of focal ischemia and stress leads to the most impairments in cognition and hippocampal BDNF expression.Data suggest that more attention should be given to the strategies to increase the resistance to psychosocial stressors and decrease the depressed symptoms for a full PSCI recovery.

Objective To explore effects and cause of fluid overload on infant following cardiac surgery.Methods This is a single center,(ICU,the Great Wall Affiliated Hospital of Nanchang University)retrospective study,between April 2012 and April 2016,176 infants who aged less than 6 months undergoing pediatric cardiac surgery were included.During consecutive postoperative 7 days,comprehensive treatment strategy for infants following cardiac surgery was adopted,collecting clinical outcomes and calculating data of fluid overload;ROC curve analysising postoperative optimal cutoff value of fluid overload.Hospitalization mortality and the second clinical outcome including low cardiac output syndrome,days on mechanical ventilation,ICU length of stay and hospital length of stay were compared to find risk factors of fluid overload.Results 176 cases of infants included in the study.ROC curves for postoperative seven consecutive days time point of Fo determined the optimal cutoff values of 7.8 ％ for FO (A UC =0.69).The mortality and hospital length of stay is not significant difference between fluid overload above 7.8％ and below or equal to 7.8％,however,the incidence of low cardiac output syndrome was higher in infants with fluid overload above 7.8％,and longer duration of mechanical ventilation,ICU residence time.After multivariable analysis,the postoperative adverse outcomes was associated with low cardiac output syndrome and peak serum creatinine (P ＜ 0.05),and cumulative higher fluid overload on the second day after surgery was associated with postoperative acute kidney injury and low cardiac output syndrome(P ＜ 0.05,respectively).Conclusion Postoperative adverse outcomes in infants with congenital heart disease are associated with peak serum creatinine and low cardiac output syndrome;postoperative acute kidney injury and low cardiac output syndrome are the main causes of fluid overload.Shortening cardiopulmonary bypass time and maintaining fluid overload of postoperative day 2 below 7.8％ will help to the postoperative complications.

Objective:To assess the predictive value of atrial natriuretic peptide, b-type natriuretic peptide(BNP), cardiac troponin I(cTn-I) and central venose oxygen saturation(ScvO 2)as indicators of low cardiac output syndrome(LCOS) in children with congenital heart disease undergoing cardiopulmonary bypass(CPB). Methods:After corrective surgery for congenital heart disease under CPB, 70 children(aged 5 days to 160 months) were enrolled in a prospective observational pilot study during 1-year period from April 2017 to March 2018. The patients were classified according to whether they developed low cardiac output syndrome. Biomarker levels were measured at 2, 12, 24, and 48 h post-CPB. The clinical data and outcome variables were analyzed by a multiple logistic regression model. Results:Twenty-two(31.4%) patients developed low cardiac output syndrome(group 1) and the remaining 48(68.6%) patients were included in group 2. cTn-I levels >13 ng/ml at 2 hours after CPB( OR=40.2, 95% CI: 9.4-171.4, P<0.001) and ScvO 2 levels<0.37 at 12 hours following CPB( OR=124.7, 95% CI: 28.7-538.2, P<0.001) were independent predictors of low cardiac output syndrome. Conclusion:Our results suggest that cTn-I at 2 h and ScvO 2 levels at 12 h post-CPB are evident early predictors of low cardiac output syndrome. This predictive capacity is, moreover, reinforced when cTn-I combined with ScvO 2 following CPB. These 2 cardiac biomarkers would aid in therapeutic decision-making in clinical practice and would also enable clinicians to modify the type of support to be used in the pediatric intensive care unit.