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Background: Delirium is one of the most common complications in critically ill children. Once delirium occurs, it will cause physical and psychological distress in children and increase the length of their ICU stay and hospitalization costs. Understanding the risk factors for delirium in critically ill children can help develop targeted nursing interventions to reduce the incidence of delirium. Aims: To investigate the incidence and the risk factors of delirium in the paediatric intensive care unit (PICU). Study design: We performed a prospective observational study in critically ill patients in the PICU between February and July 2020. Delirium was diagnosed by the Cornell Assessment of Paediatric Delirium (CAPD) and the Richmond Agitation Sedation Scale and analysed via univariate analysis and multivariate logistic regression to determine the independent risk factors of delirium in critically ill children. Results: The study enrolled 315 patients ranging in age from 1–202 (65.3–54.3) months, with 56.2% (n = 177) being male. The incidence of delirium was 29.2% (n = 92) according to CAPD criteria. Among them, 33 cases (35.9%) were of hyperactive delirium, 16 cases (17.4%) were of hypoactive delirium, and 43 cases (46.7%) were of mixed delirium. By using stepwise logistic regression, the independent risk factors of delirium included mechanical ventilation (odds ratio [OR], 11.470; 95% confidence interval [CI], 4.283–30.721), nervous system disease (OR, 5.596; 95%CI, 2.445 to 12.809), developmental delay (OR, 5.157; 95% CI, 1.990–13.363), benzodiazepine (OR, 3.359; 95% CI 1.278–8.832), number of catheters (OR, 1.918; 95% CI, 1.425 to 2.582), and age (OR, 0.985; 95% confidence interval CI, 0.976–0.993). Conclusions: Delirium is a common complication in the PICU. The independent risk factors include mechanical ventilation, nervous system disease, developmental delay, benzodiazepines, higher number of catheters, and younger age. This study may help develop intervention strategies to reduce the incidence of delirium in critically ill children by targeting modifiable risk factors. Relevance to Clinical Practice: Recommendations for practice include paying attention to high‐risk children in the ICU who are prone to delirium, removing influencing factors as soon as possible, and providing targeted nursing interventions. [ABSTRACT FROM AUTHOR]

Objective: To investigate the changes of serum soluble CD 163 (sCD 163) level, to assess the severity of critical illness and to evaluate the immune status of sepsis or severe sepsis in children., Method: A prospective study was conducted. The sCD 163 was determined in 50 cases with sepsis or severe sepsis in pediatric intensive care unit (PICU) and 23 cases of age- and gender-matched healthy children were enrolled as control during the period from April 2010 to March 2011. Double-antibody sandwich ELISA was used for sCD 163 measurement. The relationship with sCD 163 level and disease severity score (pediatric critical illness score, PCIS; and pediatric risk of mortality III, PRISM III), lymphocyte subsets, C-reactive protein (CRP), tumor necrosis factor α (TNFα) were analyzed., Result: The sCD 163 in sepsis/severe sepsis groups (171.04 ± 177.85) mg/L was significantly higher than that in control group (44.19 ± 86.48) mg/L (P < 0.01).sCD 163 in sepsis group [(105.32 ± 145.87) mg/L] was significantly lower than that of severe sepsis group [(233.32 ± 171.78) mg/L] (P < 0.05). sCD 163 level was significantly higher in lower PCIS score patients. (P < 0.01). The sCD 163 levels was higher in PRISM III ≥ 10 than the PRISM III < 10 group. The sCD 163 levels were higher in death group than the survival group. The sCD 163 was negatively correlated with CD4 +, CD4 +/CD8 + (R = -0.820, P < 0.05; R = -0.839, P < 0.01)., Conclusion: Detection of sCD 163 was helpful in predicting the severity of sepsis and severe sepsis, and sCD 163 may reflect the immune status of critically ill children with sepsis.

The performance in catalytic oxidation of benzene was investigated in two different heating modes, microwave heating and conventional electric furnace heating. The effects of copper (Cu)-manganese (Mn) mass ratio, doping dose of cerium (Ce) and calcination temperature on the catalytic activity of Cu-Mn-Ce/molecular sieve catalyst were also checked in catalytic oxidation of benzene with microwave heating, and the catalysts were subsequently characterized by scanning electron microscope (SEM) and X-ray diffraction (XRD). The results showed that the catalyst had better catalytic activity for the oxidation of benzene under microwave heating than electric furnace heating, and high oxidation efficiency for benzene was reached due to the "local hot spots" and dipole polarization effect of microwave and stable bed reaction temperature. Under the conditions of Cu, Mn and Ce mass ratio 1:1:0.33 and calcination temperature 500 degrees C, the catalyst had the optimal catalytic activity for benzene oxidation, and its light-off temperature and complete combustion temperature were 165 degrees C and 230 degrees C, respectively. It was indicated by characteristics of XRD and SEM that the presence of copper and manganese oxides and Cu1.5Mn1.5O4 with spinel crystal improved the catalytic activity of the catalyst, and the doping of Ce promoted the dispersion and regularization of active components. High calcination temperature led to the sintering of the catalyst surface and agglomeration of active components, which decreased the catalytic activity of the catalyst in the catalytic oxidation

Objective: To investigate the efficacy of continuous blood purification(CBP) in the treatment of acute lung injury/acute respiratory distress syndrome (ALI/ARDS) in children., Methods: One hundred and forty seven cases of ALI/ARDS were hospitalized to our pediatric intensive care unit, and 32 cases were treated with continuous blood purification (CBP) from June, 2006 to May, 2011. The model for CBP was continuous veno-venous hemofiltration dialysis (CVVHDF). CBP treatment persisted for at least 8 hours and replacement + dialysis fluid dose was 35 - 100 ml/(kg·h). The clinical outcome measures included the mortality rate at 28th day, respiratory index (FiO2/PO2), dynamic lung compliance (Cdyn), arterial partial pressure of oxygen (PaO2), arterial partial pressure of carbon dioxide (PaCO2), mechanical ventilation parameters, vasoactive drug dose and lung X-ray changes., Results: In totally 147 cases of ALI/ARDS, 89 cases (60.5%) were male and 58 (39.5%) were female, mean age was (43.4 ± 36.7) months. Death occurred in 54 cases, the total mortality was 36.7%. The cause of ALI/ARDS was mainly severe pneumonia, severe sepsis, and leukemia or tumor diseases. There were significant differences in severity of illness between the CBP treatment group and non-CBP treatment group on Pediatric risk of score mortality (PRISM) III score (15.3 vs. 12.7, P < 0.05) and pediatric critical illness score (66.8 ± 19.3 vs. 74.6 ± 17.7, P < 0.05). The average duration of CBP treatment was 52 hours (12 hours to 232 hours). PaO2/FiO2 and Cdyn were improved after 2 hours CBP treatment compared with those before CBP treatment (P < 0.05), mechanical ventilation parameters including fraction of inspired oxygen (FiO2), peak inspiratory pressure (PiP) and positive end expiratory pressure (PEEP) were reduced. The use of vasoactive drugs in patients with MODS and shock gradually declined. The average ventilator-free days of the two groups did not show significant difference (P > 0.05). The mortality on CBP treatment group and non-treatment group were 37.5% and 36.5%, respectively, the difference was not significant (P > 0.05)., Conclusion: CBP adjuvant treatment for ALI/ ARDS could reduce pulmonary edema, improve PaO2/FiO2 and Cdyn, and improve mechanical ventilation parameters. CBP may be a very promising treatment for ALI/ARDS in children.

Background: In cases of severe sepsis and septic shock, a series of pathophysiological changes lead to multiple organ dysfunction syndrome. This study aimed to investigate the expression of glucocorticoid receptor mRNA in the rat lung following endotoxin (LPS) induced shock., Methods: Totally 56 SD rats were randomly divided into 4 groups: LPS shock group (n=16), LPS+vasoactive intestinal peptide group(VIP) group, (n=16), LPS+VIP+ glucocorticoid (GC) group, (n=16),and control group (n=8). LPS shock was induced by intravenous injection of LPS (10 mg/kg) in rats. Within 15 minutes after LPS injection, rats in the treatment groups received VIP (5 nmol/kg) or VIP and methylprednisolone (3 mg/kg). The control group was given normal saline instead of LPS. The rats of the four groups were sacrificed at 6 hours,24 hours after injection respectively, and the lung tissues were collected. Pathological changes of the lungs were examined by light microscopy and electron microscopy. GRmRNA expression in the lung tissues was evaluated by RT-PCR., Results: In the LPS shock group, lung histopathology demonstrated destruction of the alveolar space,widening of the inter-alveolar space, inflammatory cell infiltration and interstitial edema. However,pathological changes in the LPS+ VIP group and LPS+ VIP+GC group were milder than those in the LPS shock group. Six hours after LPS injection, GR mRNA expression was down-regulated in the LPS group (0.72± 0.24) and LPS+ VIP group (0.88±0.27) (P<0.05) as compared with the control group (1.17±0.22). The LPS shock group showed a more significant down-regualtion than the LPS+VIP group, but the difference was not statistically significant (P>0.05). In contrast, GRmRNA expression in the LPS+ VIP+GC group was significantly up-regulated at 6 hours and further at 24 hours (1.45±0.32 and 1.91±0.46 respectively) (P<0.05)., Conclusion: GrmRNA expression decreased in LPS induced lung injury in rats. Combined treatment with VIP and GC mitigated lung injury ang inflammation. The mechanism may be related to up-regulation of GR mRNA expression.

Background: Hand-foot-mouth disease has become a major public health issue in children in China. In the present prospective study we investigated the clinical characteristics and emergency management of children with severe encephalitis associated with NPE caused by enterovirus 71., Methods: The study was conducted in 2 pediatric intensive care units (PICUs) over a 2-month period. Clinical records were reviewed of critically ill children with severe encephalitis associated with NPE caused by EV71 who were admitted to PICUs during the period of May to June 2008 in Fuyang., Results: We reviewed the complete records of 36 children, of whom 23 (63.9%) were male and 13 (36.1%) female. Their age ranged from 4 to 48 months, with an average of 15.8 months. All children except one were under 3 years of age. The overall mortality in these children was 19.4%. The average duration of critical life threatening signs and symptoms was 2.1 days (12 hours-5 days). Nervous system diseases included brainstem encephalitis in 27 children (75%), brainstem encephalitis associated with myelitis in 6 children (16.7%), and general encephalitis in 3 chidren (8.3%), respectively. In 12 patients of NPE (33.3%) pink or bloody bubble sputum and asymmetric pulmonary edema or hemorrhage was the primary manifestation but no typical exanthema was observed. Five children died of acute onset of NPE and / or pulmonary hemorrhage with rapid progression of cardiopulmonary failure within hours after admission. Therapeutic management consisted of mechanical ventilation and administration of mannitol, methylprednisolone, intravenous immunoglobulin (IVIG) and vasoactive drugs, associated with the need of fluid volume resuscitation in 9 (25%) of the 36 children., Conclusions: In children less than 3 years of age found to be affected by severe EV71 encephalitis associated with NPE, one fifth may die. The major organ systems infected by severe EV71 include the central nervous system, the respiratory system, and the cardiovascular system. Early diagnosis and evaluation, respiratory support, treatment of intracranial hypertension, and mainttenance of function of the cardiovascular system are the most important therapeutic measures.

Objective: Vasoactive intestinal peptide (VIP) is a neuro-peptide that can modulate immunity. Previous studies indicated that VIP can attenuate the deleterious consequences of severe sepsis and septic shock by regulating production of inflammatory cytokines in immune activated cells. The signaling induced by bacterial components occurs primarily through Toll like receptors (TLRs). TLRs have been recognized to play a key role in pathogen recognition and innate immunity. It was convincingly demonstrated that lung is one of early suffered disaster organ and may trigger multiple organ dysfunction syndrome in sepsis. The present study was conducted to investigate the effects of VIP on TLR2/4 mRNA expressions on acute lung injury of endotoxic shock induced by lipopolysaccharide (LPS) in rat., Method: Forty Sprague-Dawley rats were randomly divided into 3 groups, i.e., LPS shock group (n = 16), LPS + VIP group (n = 16), and control group (n = 8). LPS shock model was established by LPS (E. coli O(55)B(5) 10 mg/kg) with tail intravenous injection. The rats in LPS + VIP group were given a bolus of 5 nmol VIP intravenous injection follow by LPS. The rats in control group were given normal saline. The rats were sacrificed at 6 h, 24 h after being injected. The lung tissues were collected. The TLR2 mRNA and TLR4 mRNA expressions were detected by RT-PCR from the lung tissues. Pathological changes of the lungs were observed by light microscope and electron microscope 24 h after LPS injection., Result: (1) Lung histopathology: the alveolar space was full with leukocyte, necrotic cells, segmental hemorrhage and protein effusion. Partial alveolar space was enlarged, lung interstitial edema were observed in LPS shock group. However, pathological changes of LPS + VIP group were milder than those in LPS shock group. (2) The expressions of TLR2 mRNA and TLR4 mRNA were significantly higher in LPS shock group compared with those of the control group (F = 16.638, P = 0.000; t = 5.876, P = 0.000), TLR2 mRNA and TLR4 mRNA expression on 24 h was down-regulated in LPS + VIP shock subgroup than those in LPS shock subgroup (F = 16.676, P = 0.000; t = 3.946, P < 0.001)., Conclusion: Expressions of TLR2 mRNA and TLR4 mRNA were up-regulated on LPS induced lung injury in rats. VIP mitigated lung injury induced by LPS, which may be related to TLR2 mRNA and TLR4 mRNA down-regulation of expression. The effect of VIP may suggest a protective mechanism in sepsis. VIP may play a potential protective role in severe infection.

Objective: Sepsis and septic shock remain a common problem that results in significant mortality and morbidity in pediatric intensive care units (PICU). According to literature, the use of more physiologic steroid replacement therapy is associated with hemodynamic and survival benefits in adult patients with relative adrenal insufficiency (RAI) and catecholamine-resistant septic shock. But little information is available in children. The aim of the current prospective study was to determine the prevalence of adrenal insufficiency in children with sepsis and septic shock using a low-dose adrenocorticotropic hormone (ACTH) stimulation test (1 microg/1.73 m2) in children., Methods: The authors performed cortisol estimation at baseline and after low-dose (1 microg/1.73 m2) ACTH stimulation at 30 mins in children during the first 24 hours in patients with sepsis or septic shock admitted to our PICU. Adrenal insufficiency was defined as a response < or = 90 microg/L. Absolute adrenal insufficiency (AAI) was further defined as baseline cortisol (T0) < 200 microg/L and RAI insufficiency by T0 > or = 200 microg/L., Results: Sixty-two consecutive cases with sepsis and septic shock admitted to PICU of Shanghai Jiaotong University Affiliated Children's Hospital from April, 2006 to March, 2007. The median age was 37.6 months (range, 2 - 168 months), and their gender distribution was 42 (67.7%) males and 20 (32.3%) females, 53 cases had sepsis (85.5%) and 9 had septic shock (14.5%). The mean pediatric critical illness score (PCIS) was 79.3 +/- 9.2 and median pediatric risk of mortality score (PRMSIII) 11.3 (5 - 19), respectively. Overall mortality of sepsis and septic shock was 27.42%. The evaluation of adrenal insufficiency was conducted as follows. (1) The mean cortisol levels at baseline (T0) and 30 mins after ACTH stimulation (T1) were (318.6 +/- 230.4) microg/L, (452.3 +/- 230.7) microg/L and (454.7 +/- 212.7) microg/L, (579.3 +/- 231.9) microg/L in patients with severe sepsis and septic shock group, respectively. There were no significant difference between the two groups (P > 0.05). (2) The proportion of patients with adrenal insufficiency in the study population was 40.3% as defined by a response < or = 90 microg/L post test. The proportion of patients with adrenal insufficiency in sepsis and septic shock were 39.6% and 44.4%, respectively (chi2) = 0.073, P > 0.05). (3) The serum T0 and T1 levels were (320.5 +/- 223.9) microg/L, (462.3 +/- 212.0) microg/L and (384.3 +/- 258.3) microg/L, (500.7 +/- 470.6) microg/L, respectively, and the proportion of patients with adrenal insufficiency were 37.8% and 47.1% in the survivors and the dead (P > 0.05). The levels of T0 and T1 were related to the PCIS (P < 0.05). The morbidity of adrenal insufficiency was not related to the PCIS, PRISMIII, and number of organ that developed functional insufficiency (P > 0.05)., Conclusions: Adrenal insufficiency may occur in patients with sepsis and septic shock in children. ACTH stimulation test may be helpful to determine whether corticosteroid therapy has a survival benefit in patients with relative adrenal insufficiency. A low-dose ACTH stimulation test can be used to evaluate the adrenal function status of severe sepsis and septic shock in children.

Objective: Vasoactive intestinal peptide (VIP) is a neuro-peptide that can modulate immunity in several aspects. Previous reports showed that VIP attenuates the deleterious consequences of severe infection and septic shock by regulating production of inflammatory cytokines in immune activated cells. Intestine is one of the major organ of immune system and it may trigger multiple organ dysfunction syndrome in sepsis. The present study was planned to study the change of serum TNF-alpha, IL-1beta, IL-10 level and histopathological alteration of intestinal tract, and protective effects of VIP on endotoxic shock in rat., Methods: Twenty eight SD rats were randomly divided into 3 groups, including control group (8 rats), LPS shock group (10 rats), and LPS + VIP group (10 rats). Endotoxic shock model was established by administration of a single dose of 10 mg/kg LPS in LPS shock group, a bolus of 5 nmol VIP intravenous injection following LPS in LPS + VIP group. The rats in the control group were given the same volume of normal saline injection. Blood samples were taken at time points of 1, 2, 4, and 6 hours after intervention from each group for measuring the level of TNF-alpha, IL-1beta and IL-10 by ELISA. Pathological changes of the intestine were observed by light microscope and electron microscope at the animals death or at the end of the experiment., Results: Serum TNF-alpha, IL-1beta and IL-10 levels elevated at each time point in LPS shock group and LPS + VIP group (P < 0.05 or P < 0.01). TNF-alpha concentration reached the peak level 2 h after LPS injection; IL-1beta and IL-10 increased continuously till the end of the experiment. In LPS + VIP group, TNF-alpha and IL-1beta elevated slightly and IL-10 increased significantly as compared with LPS shock group (P < 0.01). Leukocyte infiltration, ischemia, segmental hemorrhage or necrosis appeared in intestine under light microscope and cell swelling, cytoplasmic vacuoles and organelle damage were observed under electron microscope. However, pathological changes in LPS + VIP group were milder than those in LPS group., Conclusions: VIP improved endotoxic shock-associated histopathological alteration of intestine, down-regulated pro-inflammatory cytokines production and up-regulated anti-inflammatory cytokines. These effects may suggest a protective mechanism of VIP in septic shock. VIP is a potential immunoregulatory substance in treatment of septic shock.

Objective: Acute intracranial hypertension/cerebral edema (ICH/CE) is an increase in brain volume caused by an absolute increase in cerebral tissue water content. Severe ICH/CE is often associated with a higher mortality and higher neurological consequence rate in intensive care unit. However, little relevant information is available on critical condition of central nervous system in children. The aim of this survey was to study the causes, clinical epidemiology and risk factors of critical illness with ICH/CE in pediatric intensive care unit (PICU)., Methods: Case records of critically ill patients with ICH/CE admitted to PICU in Children's Hospital Affiliated to Shanghai Jiaotong University during the period from January, 1999 to December, 2003 were reviewed for causes, case fatality rate, prognosis and relationship with multiple organ dysfunction syndrome (MODS). Univariate analyses were performed to identify risk factors associated with ICH/CE., Results: During the 5 years, 1446 cases with critical illnesses were admitted and ICH/CE developed in 216 patients. The leading causes of ICH/CE were central nervous system infection (27.8%), accidental injuries (22.4%), and sepsis (10.2%). The overall mortality of the patients with ICH/CE was 29.2%. The mortality showed no significant change during the years from 1999 to 2003 (chi(2) = 0.371, P = 0.985). There was no significant difference in mortality of patients with ICH/CE between those with and without neurological diseases (chi(2) = 0.546, P = 0.460). Univariate analyses involving 12 factors indicated the following risk factors: younger age, number of failed organ, lower pediatric critical illness score, underlying diseases, abnormal respiration and change in size of pupil (P < 0.05 or < 0.001). The following factors were not associated with higher risk of death from ICH/CE: sex, organ of primary disease, Glasgow coma score ( 7) on admission, elevated blood pressure and anterior fontanelle change (P > 0.05)., Conclusions: The mortality of ICH/CE remains high since 1999. Central nervous system infection, accidental injuries, and sepsis were leading causes of ICH/CE in PICU of the hospital. Children who had ICH/CE due to younger age, lower pediatric critical illness score, and complicated with MODS had a higher mortality rate.