Somatostatin, integrated in a treatment algorithm, was successful in resolving persistent chylothorax in around 50% of patients. With this strategy, some children may be prevented from undergoing an operation. However, factors predicting successful therapy with somatostatin could not be elicited.

The double sigmoidal nature of the mouse pressure-volume (PV) curve is well recognized but largely ignored. This study systematically examined the effect of inflating the mouse lung to 40 cm H2O transrespiratory pressure (Prs) in vivo. Adult BALB/c mice were anesthetized, tracheostomized, and mechanically ventilated. Thoracic gas volume was calculated using plethysmography and electrical stimulation of the intercostal muscles. Lung mechanics were tracked during inflation-deflation maneuvers using a modification of the forced oscillation technique. Inflation beyond 20 cm H2O caused a shift in subsequent PV curves with an increase in slope of the inflation limb and an increase in lung volume at 20 cm H2O. There was an overall decrease in tissue elastance and a fundamental change in its volume dependence. This apparent "softening" of the lung could be recovered by partial degassing of the lung or applying a negative transrespiratory pressure such that lung volume decreased below functional residual capacity. Allowing the lung to spontaneously recover revealed that the lung required approximately 1 h of mechanical ventilation to return to the original state. We propose a number of possible mechanisms for these observations and suggest that they are most likely explained by the unfolding of alveolar septa and the subsequent redistribution of the fluid lining the alveoli at high transrespiratory pressure.

OBJECTIVES: To present our experience in an interdisciplinary and interprofessional morbidity and mortality conference, with special emphasis on its usefulness in improving patient safety. DESIGN: Retrospective analysis. SETTING: Tertiary interdisciplinary neonatal PICU. PATIENTS: Morbidity and mortality conference minutes on 48 patients (newborns to 17 yr), January 2009 to June 2014. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The authors' PICU implemented a morbidity and mortality conference guideline in 2009 using a system-based approach to identify medical errors, their contributing factors, and possible solutions. In the subsequent 5.5 years, there were 44 mortality conferences (of 181 deaths [27%] over the same period) and four morbidity conferences. The median death/morbidity event-morbidity and mortality conference interval was 90 days (range, 7 d to 1.5 yr). The median age of patients was 4 months (range, newborn to 17 years). In six cases, the primary reason for PICU admission was a treatment complication. Unsafe processes/medical errors were identified and discussed in 37 morbidity and mortality conferences (77%). In seven cases, new autopsy findings prompted the discussion of a possible error. The 48 morbidity and mortality conferences identified 50 errors, including 30 in which an interface problem was a contributing factor. Fifty-four improvements were identified in 34 morbidity and mortality conferences. Four morbidity and mortality conferences discussed specific ethical issues. CONCLUSIONS: From our experience, we have found that the interdisciplinary and interprofessional morbidity and mortality conference has the potential to reveal unsafe processes/medical errors, in particular, diagnostic and communication errors and interface problems. When formatted as a nonhierarchical tool inviting contributions from all staff levels, the morbidity and mortality conference plays a key role in the system approach to medical errors. Originally published at: Frey, Bernhard; Doell, Carsten; Klauwer, Dietrich; Cannizzaro, Vincenzo; Bernet, Vera; Maguire, Christine; Brotschi, Barbara (2016). The morbidity and mortality conference in pediatric intensive care as a means for improving patient safety. Pediatric Critical Care Medicine, 17(1):67-72.

Increased loss of antithrombin is present in children with chylothorax, potentially predisposing these children to an increased risk of thrombosis. Repeated antithrombin substitution should be considered in critically ill children with chylothorax.

Despite decades of research, the mechanisms of ventilator-induced lung injury are poorly understood. We used strain-dependent responses to mechanical ventilation in mice to identify associations between mechanical and inflammatory responses in the lung. BALB/c, C57BL/6, and 129/Sv mice were ventilated using a protective [low tidal volume and moderate positive end-expiratory pressure (PEEP) and recruitment maneuvers] or injurious (high tidal volume and zero PEEP) ventilation strategy. Lung mechanics and lung volume were monitored using the forced oscillation technique and plethysmography, respectively. Inflammation was assessed by measuring numbers of inflammatory cells, cytokine (IL-6, IL-1β, and TNF-α) levels, and protein content of the BAL. Principal components factor analysis was used to identify independent associations between lung function and inflammation. Mechanical and inflammatory responses in the lung were dependent on ventilation strategy and mouse strain. Three factors were identified linking 1) pulmonary edema, protein leak, and macrophages, 2) atelectasis, IL-6, and TNF-α, and 3) IL-1β and neutrophils, which were independent of responses in lung mechanics. This approach has allowed us to identify specific inflammatory responses that are independently associated with overstretch of the lung parenchyma and loss of lung volume. These data provide critical insight into the mechanical responses in the lung that drive local inflammation in ventilator-induced lung injury and the basis for future mechanistic studies in this field.

Copeptin, the C-terminal part of the arginine vasopressin precursor peptide, holds promise as a diagnostic and prognostic plasma biomarker in various acute clinical conditions. Factors influencing copeptin response in the critical care setting are only partially established and have not been investigated systematically. Using an in vivo infant ventilation model (Wistar rats, 14 days old), we studied the influence of commonly occurring stressors in critically ill children. In unstressed ventilated rats basal median copeptin concentration was 22pmol/L. In response to respiratory alkalosis copeptin increased 5-fold, while exposure to hypoxemia, high PEEP, hemorrhage, and psycho-emotional stress produced a more than 10-fold increase. Additionally, we did not find a direct association between copeptin and acidosis, hypercapnia, and hyperthermia. Clinicians working in the acute critical care setting should be aware of factors influencing copeptin plasma concentrations. Moreover, our results do have implications for animal studies in the field of stress research.

The degree to which mechanical ventilation induces ventilator-associated lung injury is dependent on the initial acute lung injury (ALI). Viral-induced ALI is poorly studied, and this study aimed to determine whether ALI induced by a clinically relevant infection is exacerbated by protective mechanical ventilation. Adult female BALB/c mice were inoculated with 10(4.5) plaque-forming units of influenza A/Mem/1/71 in 50 microl of medium or medium alone. This study used a protective ventilation strategy, whereby mice were anesthetized, tracheostomized, and mechanically ventilated for 2 h. Lung mechanics were measured periodically throughout the ventilation period using a modification of the forced oscillation technique to obtain measures of airway resistance and coefficients of tissue damping and tissue elastance. Thoracic gas volume was measured and used to obtain specific airway resistance, tissue damping, and tissue elastance. At the end of the ventilation period, a bronchoalveolar lavage sample was collected to measure inflammatory cells, macrophage inflammatory protein-2, IL-6, TNF-alpha, and protein leak. Influenza infection caused significant increases in inflammatory cells, protein leak, and deterioration in lung mechanics that were not exacerbated by mechanical ventilation, in contrast to previous studies using bacterial and mouse-specific viral infection. This study highlighted the importance of type and severity of lung injury in determining outcome following mechanical ventilation.

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