[Prospective, multicenter study of mortality and risk factors in children with acute respiratory distress syndrome in 25 pediatric intensive care units in China].

OBJECTIVE: To investigate the mortality and predictors of outcome of children with acute respiratory distress syndrome (ARDS) in pediatric intensive care unit (PICU). METHODS: ARDS cases were selected from the 12 018 patients admitted in 25 pediatric intensive care units in China from January 1 to December 31, 2004, aged 29 days to 14 years, using the Chinese Pediatric Critical Index of Severity (PCIS) and American Guidelines for Admission and Discharge Policies for PICU. ARDS was diagnosed according to the 1994 American-European Consensus Conference criteria. RESULTS: 105 of the 12 018 patients (1.44%) were diagnosed as with ARDS. The overall mortality of ARDS was 61.0% (64/105), 9 times as high as that of the 7269 severe cases in PICU. Logistic regression analysis showed that infiltration shadows in 2 - 3 quadrants, pediatric critical illness score (PCIS), and partial pressure of carbon dioxide (PaCO2) at the onset of ARDS were independently associated with the mortality. CONCLUSION: ARDS has a high risk of death, and the infiltration shadows in 2-3 quadrants, PCIS, and PaCO2 are independently associated with mortality.

[Protective effects of vasoactive intestinal peptide on intestinal lesions induced by endotoxic shock in rat].

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.

[Cause and mortality analysis of acute intracranial hypertension and cerebral edema in pediatric intensive care unit].

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.

[Dexamethasone regulate the neuropeptide expression in rabbit's brain injury induced by endotoxin].

OBJECTIVE: To investigate whether dexamethasone (DXM) regulate the expression of Calcitonin gene-related peptide (CGRP), Endothelin (ET), Atrial natriuretic peptide (ANP), Angiotensin II (AII) in brain injury induced by endotoxin in rabbit. METHODS: Sixty-five New Zealand white rabbits were randomly divided into 3 subgroups: endotoxin group (A group), endotoxin + DXM group (B group) and normal saline group (C group). 100 microg/kg endotoxin was intracerebroventricularly injected in A group, endotoxin 100 microg/kg + DXM 1 mg/kg in B group and same volume of normal saline in C group as control. Neuropeptide level were detected by radioimmunoassay in variable periods (3 h, 6 h, 12 h, 24 h, 48 h, 72 h after injection) in the plasma, cerebrospinal fluid (CSF) and brain tissue (hippocampus area), and brain water content was measured by dry method. RESULTS: CGRP, ET, ANP, AII concentrations in plasma, CSF and brain tissue changed in variable periods after injection. The higher or the lower neuropeptide levels were emerged on 12 - 24 hours after injection (P < 0.05 or P < 0.01), and changed remarkably in A group (P < 0.05 or P < 0.01). Brain water content were significantly higher and reached to peak level on 24 hours after injection. But there was a significantly increasing in A group compared to that of B group (P < 0.05 or P < 0.01). CONCLUSIONS: The timely changes of CGRP, ET, ANP, AII were related to brain injury and brain edema induced by endotoxin, and DXM regulated the expression of neuropeptides and lighten brain edema.