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Despite the established success of surfactant application in neonates, the use of surfactant in older children is still a matter of discussion. We hypothesized that surfactant application in children with acute respiratory distress syndrome (ARDS) secondary to a pulmonary or systemic disease or after cardiac surgery improves pulmonary function. We also asked whether repeated treatment could further improve pulmonary function. To answer these questions, we measured oxygenation index (OI) and hypoxemia score after the first and after a second application of surfactant (50-100 mg/kg body wt) at least 24 h later. We enrolled 19 children (older than 4 weeks) for a retrospective chart review study, and six of them underwent cardiac surgery. Demographic data were extracted. OI and hypoxemia score were estimated before and 2 and 24 h after surfactant application. Lung injury score was calculated before and 24 h after surfactant application. Outcome measures included survival, duration of mechanical ventilation, and pediatric ICU and hospital stay. The median patient age was 9.0 (quarter percentile 3.7/25) months. The median weight was 8.4 (4.1/11.5) kg. The median lung injury score before the first surfactant application was 2.3 (2.3/2.6). Hospital duration and pediatric ICU stay for all patients was 31.0 (20.0/49.5) days and 27.0 (15.5/32.5) days, respectively. The duration of mechanical ventilation was 24.0 (18.5/31.0) days. The overall mortality was 53%. Twenty-four hours after the first surfactant application, pulmonary function significantly improved. The median OI was 14 (5.5/26) before and 7 (4.5/14.5) 24 h after surfactant application (P= 0.027). The hypoxemia score was 91.7 (69.9/154.2) before and 148.4 (99.2/167.6) 24 h after surfactant application (P = 0.0026). Seven children received a second application, which did not further improve pulmonary function. The lung injury score was not influenced by either surfactant application. We conclude that a single surfactant application improves pulmonary function in children with ARDS. A second application of surfactant showed no further benefit. Outcome was not affected in our study population.

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Critical Care 2017, 21(Suppl 1):P349 Introduction Imbalance in cellular energetics has been suggested to be an important mechanism for organ failure in sepsis and septic shock. We hypothesized that such energy imbalance would either be caused by metabolic changes leading to decreased energy production or by increased energy consumption. Thus, we set out to investigate if mitochondrial dysfunction or decreased energy consumption alters cellular metabolism in muscle tissue in experimental sepsis. Methods We submitted anesthetized piglets to sepsis (n = 12) or placebo (n = 4) and monitored them for 3 hours. Plasma lactate and markers of organ failure were measured hourly, as was muscle metabolism by microdialysis. Energy consumption was intervened locally by infusing ouabain through one microdialysis catheter to block major energy expenditure of the cells, by inhibiting the major energy consuming enzyme, N+/K + -ATPase. Similarly, energy production was blocked infusing sodium cyanide (NaCN), in a different region, to block the cytochrome oxidase in muscle tissue mitochondria. Results All animals submitted to sepsis fulfilled sepsis criteria as defined in Sepsis-3, whereas no animals in the placebo group did. Muscle glucose decreased during sepsis independently of N+/K + -ATPase or cytochrome oxidase blockade. Muscle lactate did not increase during sepsis in naïve metabolism. However, during cytochrome oxidase blockade, there was an increase in muscle lactate that was further accentuated during sepsis. Muscle pyruvate did not decrease during sepsis in naïve metabolism. During cytochrome oxidase blockade, there was a decrease in muscle pyruvate, independently of sepsis. Lactate to pyruvate ratio increased during sepsis and was further accentuated during cytochrome oxidase blockade. Muscle glycerol increased during sepsis and decreased slightly without sepsis regardless of N+/K + -ATPase or cytochrome oxidase blocking. There were no significant changes in muscle glutamate or urea during sepsis in absence/presence of N+/K + -ATPase or cytochrome oxidase blockade. ConclusionsThese results indicate increased metabolism of energy substrates in muscle tissue in experimental sepsis. Our results do not indicate presence of energy depletion or mitochondrial dysfunction in muscle and should similar physiologic situation be present in other tissues, other mechanisms of organ failure must be considered. , and long-term follow up has shown increased fracture risk [2]. It is unclear if these changes are a consequence of acute critical illness, or reduced activity afterwards. Bone health assessment during critical illness is challenging, and direct bone strength measurement is not possible. We used a rodent sepsis model to test the hypothesis that critical illness causes early reduction in bone strength and changes in bone architecture. Methods 20 Sprague-Dawley rats (350 ± 15.8g) were anesthetised and randomised to receive cecal ligation and puncture (CLP) (50% cecum length, 18G needle single pass through anterior and posterior wa...

Aortopulmonary collateral arteries sometimes complicate cyanotic congenital heart defects. Combined with a relevant left-right shunt, this could result in massive airway bleeding during and after corrective surgery. A preoperatively diagnosed 1.2 mm small aortopulmonary collateral artery in a newborn suffering from transposition of the great arteries caused life-threatening airway bleeding during surgery. Postoperative extracorporeal membrane oxygenation (ECMO) was necessary, and coil embolization was performed on ECMO to terminate pulmonary bleeding.