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Pediatric interfacility transport teams facilitate access to subspecialty care, and physicians often guide management remotely as transport medical control (TMC). Pediatric subspecialty fellows frequently perform TMC duties, but tools assessing competency are lacking. Our objective was to develop content validity for the items required to assess pediatric subspecialty fellows’ TMC skills.We conducted a modified Delphi process among transport and fellow education experts in pediatric critical care medicine, pediatric emergency medicine, neonatal-perinatal medicine, and pediatric hospital medicine. The study team generated an initial list of items on the basis of a literature review and personal experience. A modified Delphi panel of transport experts was recruited to participate in 3 rounds of anonymous, online voting on the importance of the items using a 3-point Likert scale (marginal, important, essential). We defined consensus for inclusion as ≥80% agreement that an item was important/essential and consensus for exclusion as ≥80% agreement that an item was marginal.The study team of 20 faculty drafted an initial list of items. Ten additional experts in each subspecialty served on the modified Delphi panel. Thirty-six items met the criteria for inclusion, with widespread agreement across subspecialties. Only 1 item, “discussed bed availability,” met the criteria for inclusion among some subspecialties but not others. The study team consolidated the final list into 26 items for ease of use.Through a consensus-based process among transport experts, we generated content validity for the items required to assess pediatric subspecialty fellows’ TMC skills.

To determine whether the receipt of more than or equal to 30 mL/kg of intravenous fluid in the first hour after emergency department (ED) arrival is associated with sepsis-attributable mortality among children with hypotensive septic shock.

AbstractObjectivesOur institution relocated to a new facility 3.5 miles from our original location in Chicago on June 9, 2012. We describe the tools we developed to prepare, execute, and manage our evacuation and relocation.MethodsTools developed for the planned evacuation included the following: level of acuity and team composition classification, patient departure checklist, evacuation handoff tool, and a patient tracking system within the electronic health record. Incident Command structure was utilized.ResultsMonthly census tracking exercises were held beginning 12 months before the evacuation. Simulation drills began 6 months before the evacuation. The entire evacuation took less than 14 hours and there were no safety issues. A total of 127 patients were transported to the new facility: 45 patients were moved via the Neonatal/Pediatric Critical Care Transport Team, and the rest were moved with various team configurations.ConclusionDocuments developed for a planned evacuation can be used for any planned or unplanned evacuation. We believe the tools we used to prepare, execute, and manage our evacuation and relocation would assist any health care facility to be better prepared to safely and efficiently evacuate patients in the event of a disaster, or to create surge capacity, and relocate them to another facility. (Disaster Med Public Health Preparedness. 2017;11:479–486)

We previously reported that neuronal nitric oxide synthase (nNOS) is the predominant NOS in the intestine. Inducible NOS (iNOS), an enzyme involved in the inflammatory response, is regulated by cytokines via the transcriptional factor NF‐κB. We examined a new mechanism of intestinal iNOS regulation with respect to the role of nNOS and its effect on NF‐κB. Young Sprague‐Dawley rats were treated for 4 days with 1)saline, 2)7‐nitroindazole (7‐NI, specific nNOS inhibitor), 3)7‐NI + pyrrolidine dithiocarbam‐ate (PDTC, NF‐κB inhibitor), or 4)PDTC. Intestinal iNOS mRNA, NF‐κB activity, and the tissue content of the regulatory IκBα were examined. We found that 7‐NI‐treated animals had higher intestinal NF‐κB (p50‐p65) activity, lower IκBαcontent, and increased intestinal iNOS mRNA, iNOS protein, and iNOS activity compared with controls. All of these changes were abolished when PDTC was given together with 7‐NI. PDTC alone had no effect. 7‐NI induces a delayed increase in intestinal myeloperoxidase activity (after elevation in NF‐κB and iNOS), which could be abrogated by PDTC. We conclude that in normal rat small intestine, nNOS suppresses the gene expression of iNOS through NF‐κB down‐regulation and that nNOS suppression leads to IκBα degradation, NF‐κB activation, and iNOS expression.—Qu, X.‐w., Wang, H., De Plaen, I. G., Rozenfeld, R. A., Hsueh, W. Neuronal nitric oxide synthase (NOS) regulates the expression of inducible NOS in rat small intestine via modulation of nuclear factor kappa B. FASEB J.15, 439‐446 (2001)

1We studied endotoxin (lipopolysaccharide, LPS)‐induced platelet‐activating factor (PAF) production in various visceral organs, and the effect of PAF antagonists or splenectomy on LPS‐induced changes.2PAF production in response to LPS was highest in the spleen, followed by ileum, heart, lung and kidneys. None was found in the liver. The splenic response was rapid, reaching 10 times the basal level at 30 min. The increased PAF content in each organ was unrelated to the enzyme activity of either macrophages or neutrophils.3LPS‐induced hypotension and haemoconcentration were largely prevented by PAF antagonists and splenectomy.4Plasma volume fell, and plasma atrial natriuretic peptide (ANP) rose, after LPS administration. Splenectomy or pretreatment with PAF antagonists almost completely prevented these LPS‐induced changes at 30 min, but only partially reversed them at 90 min.5These results suggest that during endotoxaemia: (a) the spleen is the site of the highest endogenous PAF production; (b) the initial release of ANP is dependent on the production of endogenous PAF, and a PAF‐ANP interaction mediates the early plasma volume reduction; (c) plasma volume reduction as well as ANP release depend on the spleen; (d) PAF mediated the hypotensive response and its action in the spleen; and (e) sequestered neutrophils are probably not the main source of PAF in the spleen.

Dysoxia can be defined as ATP flux decreasing in proportion to O2availability with preserved ATP demand. Hepatic venous β-hydroxybutyrate-to-acetoacetate ratio (β-OHB/AcAc) estimates liver mitochondrial NADH/NAD and may detect the onset of dysoxia. During partial dysoxia (as opposed to anoxia), however, flow may be adequate in some liver regions, diluting effluent from dysoxic regions, thereby rendering venous β-OHB/AcAc unreliable. To address this concern, we estimated tissue ATP while gradually reducing liver blood flow of swine to zero in a nuclear magnetic resonance spectrometer. ATP flux decreasing with O2availability was taken as O2uptake (V˙o2) decreasing in proportion to O2delivery (Q˙o2); and preserved ATP demand was taken as increasing Pi/ATP.V˙o2, tissue Pi/ATP, and venous β-OHB/AcAc were plotted againstQ˙o2to identify critical inflection points. Tissue dysoxia required meanQ˙o2for the group to be critical for bothV˙o2and for Pi/ATP. CriticalQ˙o2values forV˙o2and Pi/ATP of 4.07 ± 1.07 and 2.39 ± 1.18 (SE) ml ⋅ 100 g−1⋅ min−1, respectively, were not statistically significantly different but not clearly the same, suggesting the possibility that dysoxia might have commenced after V˙o2began decreasing, i.e., that there could have been “O2conformity.” CriticalQ˙o2for venous β-OHB/AcAc was 2.44 ± 0.46 ml ⋅ 100 g−1⋅ min−1(P= NS), nearly the same as that for Pi/ATP, supporting venous β-OHB/AcAc as a detector of dysoxia. All issues considered, tissue mitochondrial redox state seems to be an appropriate detector of dysoxia in liver.