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Objectives: We evaluated the retention of pediatric and neonatal intubation performance abilities of clinicians trained on a simulated or live tissue model at 3 intervals after initial training to assess competency degradation related to either training modality or retention interval., Methods: We implemented a quasi-experimental design with purposive sampling to assess performance differences between 171 subjects randomly assigned to 1 of 3 intervals after initial training: 6 weeks, 18 weeks, or 52 weeks. Training followed the American Heart Association Pediatric Advanced Life Support and Neonatal Resuscitation Program protocols with hands-on practice using 1 of 2 models (live feline or simulated feline). Assessment data were captured using validated instruments and analyzed using analysis of variance with repeated measures (statistical significance set at P < 0.05)., Results: Cognitive retention scores decreased significantly (P = 0.000) from posttraining cognitive scores. There were no significant differences between posttraining and retention scores for pediatric and neonatal performances. Both affect and self-efficacy retention scores decreased significantly (P = 0.000) from posttraining scores at 18 and 52 weeks, but remained constant at 6 weeks. Retention scores for all dimensions showed a significant difference between subjects with varying amounts of experience performing pediatric and neonatal intubation, such that those with more experience scored higher those with less (P < 0.003)., Conclusions: Retention performance outcomes decreased sufficiently from posttraining scores to suggest that training refreshment could serve to maintain posttraining competency in the ability to perform pediatric and neonatal intubation. Retraining intervals may be best aligned with provider experience levels. Future research focusing on the effect of variable interval refresher training on retention in pediatric and neonatal intubation is merited.

Sepsis/septic shock and multiple organ failure are important causes of morbidity and mortality. Our objective was to study sepsis and organ failure in a fluid-resuscitated septic model. Males S-D rats were anesthetized with halothane, the jugular vein catheterized, and CLP performed. Each rat was maintained in a metabolism cage on continuous intravenous fluid (3 mL/rat). Urine rate and [creatinine]urine were measured daily. At day 5, serum creatinine with chemistry profile, complete blood count, clotting times, and wet lung/body weight ratios were also measured. Glomerular filtration rate (GFR) was measured according to the principle of endogenous creatinine clearance. GFR was correlated with the product of urine rate x [creatinine]urine (R = .79), so that product was used as a daily indicator of GFR. Urine output remained > or = normal during sepsis. Heparin and antithrombin III were tested in this model. The model was associated with 40% mortality, a 60% reduction in platelet count, liver damage, a 75% reduction in renal function, muscle damage, and a normal wet lung/body weight ratio. Treatment with heparin/antithrombin III ameliorated the decrease in GFR (p < .05) observed in the nontreated animals, prevented the septic-induced thrombocytopenia (p < .05), and improved survival (p = .05).

Studies have shown that active hepatocellular function is depressed early after trauma-hemorrhage and persists despite resuscitation with two or three times (x) the volume of maximum bleedout (MB) with lactated Ringer's solution (LR). However, it is not known if a larger volume of fluid resuscitation corrects this dysfunction. To study this, rats were bled to and maintained at a mean arterial pressure of 40 mm Hg until 40% of the MB volume was returned in the form of LR, and then resuscitated with 4x or 5x the volume of MB with LR. Three doses of indocyanine green (ICG) were given intravenously and [ICG] measured in vivo using an in-vivo hemoreflectometer. The initial velocity of the clearance of ICG was calculated. Maximal velocity of the clearance (Vmax: the number of functional ICG receptors) and kinetic constant (Km: the efficiency of the active transport) were determined from the Lineweaver-Burk plot. Vmax decreased during hemorrhage, was restored to control levels at 0-4 hours after resuscitation, but decreased at 4-8 hours after resuscitation despite restoration of cardiac output following resuscitation with 5x LR. This could be the result of increased TNF release. The Km also decreased during hemorrhage, but increased at 0-1.5 hours and remained at control levels even 4-8 hours after resuscitation. Thus the failure of Vmax to remain at control levels following adequate fluid resuscitation may form the basis of cellular dysfunction and multiple organ failure after severe hemorrhagic shock.