Pediatric Specialty Transport Teams Are Not Associated With Decreased 48-Hour Pediatric Intensive Care Unit Mortality: A Propensity Analysis of the VPS, LLC Database.

OBJECTIVE: The purpose of this study was to determine if pediatric specialty pediatric team (SPT) interfacility-transported children from community emergency departments to a pediatric intensive care unit (PICU) have improved 48-hour mortality. METHODS: This is a multicenter, historic cohort analysis of the VPS, LLC PICU clinical database (VPS, LLC, Los Angeles, CA) for all PICU directly admitted pediatric patients ≤ 18 years of age from January 1, 2007, to March 31, 2009. Categoric variables were analyzed by the chi-square and Mann-Whitney tests for non-normally distributed continuous variables. The propensity score was determined by multiple logistic regression analysis. Nearest neighbor matching developed emergency medical services SPT pairs by similar propensity score. Multiple regression analyses of the matched pairs determined the association of SPT with 48-hour PICU mortality. P values < .05 were considered significant. RESULTS: This study included 3,795 PICU discharges from 12 hospitals. SPT-transported children were more severely ill, younger in age, and more likely to have a respiratory diagnosis (P < .0001). Unadjusted 48-hour PICU mortality was statistically significantly higher for SPT transports (2.04% vs. 0.070%, P = .0028). Multiple regressions adjusted for propensity score, illness severity, and PICU site showed no significant difference in 48-hour PICU mortality. CONCLUSION: No significant difference in adjusted 48-hour PICU mortality for children transported by transport team type was discovered.

Acute Pancreatitis in the Pediatric Intensive Care Unit.

AIM: The aim of this study is to describe the demographics and outcomes of children with a discharge diagnosis of acute pancreatitis (AP) from the pediatric intensive care unit (PICU). METHODS: Data for this retrospective cohort study were obtained from a multisite, clinical PICU database. PICU discharges with a primary or secondary diagnosis of AP (SAP) between 2009 and 2013 from 113 centers were reviewed. We also obtained the Pediatric Index of Mortality 2 Risk of Mortality (PIM2ROM), an indicator of the severity of illness. RESULTS: Of 360,162 PICU discharges, 2026 with a diagnosis of AP were analyzed further (0.56%)-331 had a primary diagnosis of AP, whereas 1695 had a SAP. Among children with primary AP, median PIM2ROM was 1.0% (interquartile range [IQR] 0.8%-1.4%). Fifty-five children with primary AP (16.6%) required mechanical ventilation (MV) for a median of 3.8 days (IQR 1.0-9.3). The length of stay (LOS) in PICU was a median of 2.95 days (IQR 1.53-5.90). Only 1 patient died (mortality 0.3%). Among children with secondary AP, median PIM2ROM was 1.1% (IQR 0.8%-4.0%). A total of 711 children (42.0%) with secondary AP required MV for a median of 5.8 days (IQR 1.8-14.0). PICU LOS was a median of 4.43 days (IQR 1.84-11.22). There were 115 deaths in this group (mortality 6.8%). Median PIM2ROM, PICU LOS, mortality (all P < 0.001), and length of MV (P = 0.035) were significantly greater in children with secondary AP than with primary AP. CONCLUSIONS: Unlike in adult series, children with AP rarely die. Patients with secondary AP experience more morbidity and mortality than patients with primary AP.

Can utilization review criteria be used to determine appropriate pediatric patient placement for a critical care bed expansion?

The rising trend in critical care utilization has led to the expansion of critical care beds in many hospitals across the country. Traditional models of estimating bed capacity requirements use administrative data such as inpatient admissions, length of stay, and case mix index. The use of such data has been limited in quantifying the complexities of demand variables in critical care bed needs. Mathematical modeling is another method for estimating numbers of beds required. It captures the dynamic changes in the management of critically ill patients that occur when units become full. Depending on data analysis methods used, bed need underestimation or overestimation can occur. In our study, we used utilization review criteria to understand changes in level of care (LOC) during the course of patients' stays and to validate critical care bed expansion needs. Using LOC criteria, we studied the proportion of our intermediate care patients in an acute care unit that met acute, intermediate, or critical care criteria. We also evaluated whether these proportions were related to specific factors such as census ratios, staffing proportions, or severity of illness. Using LOC criteria was helpful in validating our critical care bed projection, which was previously derived from mathematical modeling. The findings also validated our assessment for additional specialty acute care beds.

Treatment of pediatric restless legs syndrome.

OBJECTIVE: The primary aim was to determine if iron supplementation effectively treats children with restless legs syndrome (RLS), the time to improvement or resolution of symptoms, and patient characteristics (family history of RLS, secondary sleep disorders, medical diagnoses, and/or mental health diagnoses) that may affect outcome. METHODS.: This was a retrospective chart review of children between 5 and 18 years old who were diagnosed with RLS at the pediatric sleep disorders clinic at Children's Hospital of Wisconsin in Milwaukee, Wisconsin. Documented RLS treatment approaches included supplemental iron, nonpharmacologic interventions, melatonin, gabapentin, clonidine, and dopamine agonists (pramipexole and ropinirole). RESULTS: Ninety-seven children were diagnosed with RLS; 60.8% of children were between 5 and 11 years old. Most children (65%) received iron either as monotherapy or in combination with other treatments. Approximately 80% of the children who received iron and had follow-up had improvement or resolution of their symptoms. The median baseline ferritin level was 22.7 ng/mL, and 71% of children had a ferritin level less than 30 ng/mL. The median time to improvement or resolution of symptoms was 3.8 months. CONCLUSIONS: Supplemental iron as monotherapy or in combination with other treatments is effective in treating pediatric RLS. A prospective study could help determine if the initial ferritin level and degree of change in the ferritin level impact response to iron treatment. It is also important to study the long-term outcomes in these patients.

Transcriptome profiling of the newborn mouse lung response to acute ozone exposure.

Ozone pollution is associated with adverse effects on respiratory health in adults and children but its effects on the neonatal lung remain unknown. This study was carried out to define the effect of acute ozone exposure on the neonatal lung and to profile the transcriptome response. Newborn mice were exposed to ozone or filtered air for 3h. Total RNA was isolated from lung tissues at 6 and 24h after exposure and was subjected to microarray gene expression analysis. Compared to filtered air-exposed littermates, ozone-exposed newborn mice developed a small but significant neutrophilic airway response associated with increased CXCL1 and CXCL5 expression in the lung. Transcriptome analysis indicated that 455 genes were down-regulated and 166 genes were up-regulated by at least 1.5-fold at 6h post-ozone exposure (t-test, p < .05). At 24h, 543 genes were down-regulated and 323 genes were up-regulated in the lungs of ozone-exposed, compared to filtered air-exposed, newborn mice (t-test, p < .05). After controlling for false discovery rate, 50 genes were identified as significantly down-regulated and only a few (RORC, GRP, VREB3, and CYP2B6) were up-regulated at 24h post-ozone exposure (q < .05). Gene ontology enrichment analysis revealed that cell cycle-associated functions including cell division/proliferation were the most impacted pathways, which were negatively regulated by ozone exposure, an adverse effect that was associated with reduced bromo-deoxyuridine incorporation. These results demonstrate that acute ozone exposure alters cell proliferation in the developing neonatal lung through a global suppression of cell cycle function.

Early enteral nutrition is associated with lower mortality in critically ill children.

BACKGROUND: The purpose of this study was to examine the association of early enteral nutrition (EEN), defined as the provision of 25% of goal calories enterally over the first 48 hours of admission, with mortality and morbidity in critically ill children. METHODS: We conducted a multicenter retrospective study of patients in 12 pediatric intensive care units (PICUs). We included patients aged 1 month to 18 years who had a PICU length of stay (LOS) of ≥96 hours for the years 2007-2008. We obtained patients' demographics, weight, Pediatric Index of Mortality-2 (PIM2) score, LOS, duration of mechanical ventilation (MV), mortality data, and nutrition intake data in the first 4 days after admission. RESULTS: We identified 5105 patients (53.8% male; median age, 2.4 years). Mortality was 5.3%. EEN was achieved by 27.1% of patients. Children receiving EEN were less likely to die than those who did not (odds ratio, 0.51; 95% confidence interval, 0.34-0.76; P = .001 [adjusted for propensity score, PIM2 score, age, and center]). Comparing those who received EEN to those who did not, adjusted for PIM2 score, age, and center, LOS did not differ (P = .59), and the duration of MV for those receiving EEN tended to be longer than for those who did not, but the difference was not significant (P = .058). CONCLUSIONS: EEN is strongly associated with lower mortality in patients with PICU LOS of ≥96 hours. LOS and duration of MV are slightly longer in patients receiving EEN, but the differences are not statistically significant.

Active tissue factor pathway inhibitor is expressed on the surface of coated platelets.

The incorporation of blood-borne forms of tissue factor (TF) into a growing blood clot is necessary for normal fibrin generation and stabilization of the blood clot. Tissue factor pathway inhibitor (TFPI) is the primary physiologic inhibitor of tissue factor and is present within platelets. Expression of TFPI on the platelet surface may be the optimal location for it to abrogate blood-borne TF activity that incorporates within the blood clot, balancing the need for adequate hemostasis while preventing development of occlusive thrombosis. TFPI is produced by megakaryocytes but is not expressed on the platelet surface. Activation of platelets with thrombin receptor activation peptide does not cause release or surface expression of TFPI, demonstrating that TFPI is not stored within platelet alpha granules. TFPI is expressed on the platelet surface following dual-agonist activation with convulxin plus thrombin to produce coated platelets. In association with its expression on the surface of coated platelets TFPI is also released in microvesicles or as a soluble protein.