The AirView Study: Comparison of Intubation Conditions and Ease between the Airtraq-AirView and the King Vision.

We conducted a study assessing the quality and speed of intubation between the Airtraq with its new iPhone AirView app and the King Vision in a manikin. The primary endpoint was reduction of time needed for intubation. Secondary endpoints included times necessary for intubation. 30 anaesthetists randomly performed 3 intubations with each device on a difficult airway manikin. Participants had a professional experience of 12 years: 60.0% possessed the Airtraq in their hospital, 46.7% the King Vision, and 20.0% both. Median time difference [IQR] to identify glottis (1.1 [-1.3; 3.9] P = 0.019), for tube insertion (2.1 [-2.6; 9.4] P = 0.002) and lung ventilation (2.8 [-2.4; 11.5] P = 0.001), was shorter with the Airtraq-AirView. Median time for glottis visualization was significantly shorter with the Airtraq-AirView (5.3 [4.0; 8.4] versus 6.4 [4.6; 9.1]). Cormack Lehane before intubation was better with the King Vision (P = 0.03); no difference was noted during intubation, for subjective device insertion or quality of epiglottis visualisation. Assessment of tracheal tube insertion was better with the Airtraq-AirView. The Airtraq-AirView allows faster identification of the landmarks and intubation in a difficult airway manikin, while clinical relevance remains to be studied. Anaesthetists assessed the intubation better with the Airtraq-AirView.

Impact of a Dedicated Noninvasive Ventilation Team on Intubation and Mortality Rates in Severe COPD Exacerbations.

BACKGROUND: Compared with usual care, noninvasive ventilation (NIV) lowers the risk of intubation and death for subjects with respiratory failure secondary to COPD exacerbations, but whether administration of NIV by a specialized, dedicated team improves its efficiency remains uncertain. Our aim was to test whether a dedicated team of respiratory therapists applying all acute NIV treatments would reduce the risk of intubation or death for subjects with COPD admitted for respiratory failure. METHODS: We carried out a retrospective study comparing subjects with COPD admitted to the ICU before (2001-2003) and after (2010-2012) the creation of a dedicated NIV team in a regional acute care hospital. The primary outcome was the risk of intubation or death. The secondary outcomes were the individual components of the primary outcome and ICU/hospital stay. RESULTS: A total of 126 subjects were included: 53 in the first cohort and 73 in the second. There was no significant difference in the demographic characteristics and severity of respiratory failure. Fifteen subjects (28.3%) died or had to undergo tracheal intubation in the first cohort, and only 10 subjects (13.7%) in the second cohort (odds ratio 0.40, 95% CI 0.16-0.99, P = .04). In-hospital mortality (15.1% vs 4.1%, P = .03) and median stay (ICU: 3.1 vs 1.9 d, P = .04; hospital: 11.5 vs 9.6 d, P = .04) were significantly lower in the second cohort, and a trend for a lower intubation risk was observed (20.8% vs 11% P = .13). CONCLUSIONS: The delivery of NIV by a dedicated team was associated with a lower risk of death or intubation in subjects with respiratory failure secondary to COPD exacerbations. Therefore, the implementation of a team administering all NIV treatments on a 24-h basis should be considered in institutions admitting subjects with COPD exacerbations.

Automatic Mallampati Classification Using Active Appearance Models

Difficult tracheal intubation assessment is an important research topic in anesthesia as failed intubations are important causes of mortality in anesthetic practice. The modified Mallampati score is widely used, alone or in conjunction with other criteria, to predict the difficulty of intubation. This work presents an automatic method to assess the modified Mallampati score from an image of a patient with the mouth wide open. For this purpose we propose an active appearance models (AAM) based method and use linear support vector machines (SVM) to select a subset of relevant features obtained using the AAM. This feature selection step proves to be essential as it improves drastically the performance of classification, which is obtained using SVM with RBF kernel and majority voting. We test our method on images of 100 patients undergoing elective surgery and achieve 97.9% accuracy in the leave-one-out crossvalidation test and provide a key element to an automatic difficult intubation assessment system.

First Report of a Newborn Rat Ventilation Model for Bronchopulmonary Dysplasia Permitting Evaluation of Long-Term Outcome

Background: Bronchopulmonary dysplasia (BPD) remains the leading cause of chronic pulmonary morbidity among preterm neonates. However, the exact pathophysiology is still unknown. Here we present the first results from a new model inteAbstracts, 25th International Workshop on Surfactant Replacement 400 Neonatology 2010;97:395-400 grating the most common risk factors for BPD (lung immaturity, inflammation, mechanical ventilation (MV), oxygen), which allows long-term outcome evaluation due to a non-traumatic intubation procedure. Objectives: To test the feasibility of a new rat model by investigating effects of MV, inflammation and oxygen applied to immature lungs after a ventilation-free interval. Methods: On day 4, 5, or 6 newborn rats were given an intraperitoneal injection of lipopolysaccharides to induce a systemic inflammation. 24 h later they were anesthetized, endotracheally intubated and ventilated for 8 h with 60% oxygen. After weaning of anesthesia and MV the newborn rats were extubated and returned to their mothers. Two days later they were killed and outcome measurements were performed (histology, quantitative RT-PCR) and compared to animals investigated directly after MV. Results: Directly after MV, histological signs of ventilator-induced lung injury were found. After 48 h, the first signs of early BPD were seen with delayed alveolar formation. Expression of inflammatory genes was only transiently increased. After 48 h genes involved in alveolarization, such as matrix metalloproteinase-9 and tropoelastin, showed a significant change of their expression. Conclusion: For the first time we can evaluate in a newborn rat model the effects of MV after a ventilation-free interval. This allows discrimination between immediate response genes and delayed changes of expression of more structural genes involved in alveolarization.

Hyperoxemia in newborn infants: detection by pulse oximetry.

Pulse oximetry has been proposed as a noninvasive continuous method for transcutaneous monitoring of arterial oxygen saturation of hemoglobin (tcSO2) in the newborn infant. The reliability of this technique in detecting hyperoxemia is controversial, because small changes in saturation greater than 90% are associated with relatively large changes in arterial oxygen tension (PaO2). The purpose of this study was to assess the reliability of pulse oximetry using an alarm limit of 95% tcSO2 in detecting hyperoxemia (defined as PaO2 greater than 90 mm Hg) and to examine the effect of varying the alarm limit on reliability. Two types of pulse oximeter were studied alternately in 50 newborn infants who were mechanically ventilated with indwelling arterial lines. Three arterial blood samples were drawn from every infant during routine increase of inspired oxygen before intratracheal suction, and PaO2 was compared with tcSO2. The Nellcor N-100 pulse oximeter identified all 26 hyperoxemic instances correctly (sensitivity 100%) and alarmed falsely in 25 of 49 nonhyperoxemic instances (specificity 49%). The Ohmeda Biox 3700 pulse oximeter detected 13 of 35 hyperoxemic instances (sensitivity 37%) and alarmed falsely in 7 of 40 nonhyperoxemic instances (specificity 83%). The optimal alarm limit, defined as a sensitivity of 95% or more associated with maximal specificity, was determined for Nellcor N-100 at 96% tcSO2 (specificity 38%) and for Ohmeda Biox 3700 at 89% tcSO2 (specificity 52%). It was concluded that pulse oximeters can be highly sensitive in detecting hyperoxemia provided that type-specific alarm limits are set and a low specificity is accepted.

Continuous monitoring of liver oxygenation with near infrared spectroscopy during naso-gastric tube feeding in neonates.

Near infrared spectroscopy (NIRS) is a non-invasive method of estimating the haemoglobin concentration changes in certain tissues. It is frequently used to monitor oxygenation of the brain in neonates. At present it is not clear whether near infrared spectroscopy of other organs (e.g. the liver as a corresponding site in the splanchnic region, which reacts very sensitively to haemodynamic instability) provides reliable values on their tissue oxygenation. The aim of the study was to test near infrared spectroscopy by measuring known physiologic changes in tissue oxygenation of the liver in newborn infants during and after feeding via a naso-gastric tube. The test-retest variability of such measurements was also determined. On 28 occasions in 25 infants we measured the tissue oxygenation index (TOI) of the liver and the brain continuously before, during and 30 minutes after feeding via a gastric tube. Simultaneously we measured arterial oxygen saturation (SaO2), heart rate (HR) and mean arterial blood pressure (MAP). In 10 other newborn infants we performed a test-retest analysis of the liver tissue oxygenation index to estimate the variability in repeated intra-individual measurements. The tissue oxygenation index of the liver increased significantly from 56.7 +/- 7.5% before to 60.3 +/- 5.6% after feeding (p < 0.005), and remained unchanged for the next 30 minutes. The tissue oxygenation index of the brain (62.1 +/- 9.7%), SaO2 (94.4 +/- 7.1%), heart rate (145 +/- 17.3 min-1) and mean arterial blood pressure (52.8 +/- 10.2 mm Hg) did not change significantly. The test-retest variability for intra-individual measurements was 2.7 +/- 2.1%. After bolus feeding the tissue oxygenation index of the liver increased as expected. This indicates that near infrared spectroscopy is suitable for monitoring changes in tissue oxygenation of the liver in newborn infants.

Asthme aigu sévère [Severe acute asthma]

Acute severe asthma is defined by the occurrence of an acute exacerbation resistant to the initial medical treatment, complicated by life-threatening respiratory distress due to severe lung hyperinflation. The conventional therapeutic approach is based on oxygen therapy and on the combined treatment of inhaled beta2-agonists at repeated doses and systemic corticosteroids. Inhaled or systemic magnesium sulfate is also recommended. The unresponsiveness to the initial bronchodilating therapy and the development of respiratory distress requiring intubation significantly increases mortality, due to the complications induced by mechanical ventilation. In these situations, a ventilatory strategy, including controlled hypoventilation with permissive hypercapnia, aiming at preventing lung hyperinflation, is indicated. Non-invasive ventilation may be successful in certain patients and represents an effective alternative to intubation. In ventilated patients, helium-oxygen mixtures can be considered as adjunctive therapies. After having reviewed the basic pathophysiological principles, this article will focus on the current medical treatment and of the modalities of mechanical ventilation in acute severe asthma.

Persistent pulmonary arterial hypertension in the newborn (PPHN): a frequent manifestation of TMEM70 defective patients.

INTRODUCTION: Mutations in the TMEM70 are the most common cause of nuclear ATP synthase deficiency resulting in a distinctive phenotype characterized by severe neonatal hypotonia, hypertrophic cardiomyopathy (HCMP), facial dysmorphism, severe lactic acidosis, hyperammonemia and 3-methylglutaconic aciduria (3-MGA). METHODS AND RESULTS: We collected 9 patients with genetically confirmed TMEM70 defect from 8 different families. Six were homozygous for the c.317-2A>G mutation, 2 were compound heterozygous for mutations c.317-2A>G and c.628A>C and 1 was homozygous for the novel c.701A>C mutation. Generalized hypotonia, lactic acidosis, hyperammonemia and 3-MGA were present in all since birth. Five patients presented acute respiratory distress at birth requiring intubation and ventilatory support. HCMP was detected in 5 newborns and appeared a few months later in 3 additional children. Five patients showed a severe and persistent neonatal pulmonary hypertension (PPHN) requiring Nitric Oxide (NO) and/or sildenafil administration combined in 2 cases with high-frequency oscillatory (HFO) ventilation. In 3 of these patients, echocardiography detected signs of HCMP at birth. CONCLUSIONS: PPHN is a life-threatening poorly understood condition with bad prognosis if untreated. Pulmonary hypertension has rarely been reported in mitochondrial disorders and, so far, it has been described in association with TMEM70 deficiency only in one patient. This report further expands the clinical and genetic spectrum of the syndrome indicating PPHN as a frequent and life-threatening complication regardless of the type of mutation. Moreover, in these children PPHN appears even in the absence of an overt cardiomyopathy, thus representing an early sign and a clue for diagnosis.

Coating carbon nanotubes with a polystyrene-based polymer protects against pulmonary toxicity.

BACKGROUND: carbon nanotubes (CNT) can have adverse effects on health. Therefore, minimizing the risk associated with CNT exposure is of crucial importance. The aim of this work was to evaluate if coating multi-walled CNT (MWCNT) with polymers could modify their toxicity, thus representing a useful strategy to decrease adverse health effects of CNT. We used industrially-produced MWCNT uncoated (NT1) or coated (50/50 wt%) with acid-based (NT2) or polystyrene-based (NT3) polymer, and exposed murine macrophages (RAW 264.7 cell line) or Balb/c mice by intratracheal administration. Biological experiments were performed both in vitro and in vivo, examining time- and dose-dependent effects of CNT, in terms of cytotoxicity, expression of genes and proteins related to oxidative stress, inflammation and tissue remodeling, cell and lung tissue morphology (optical and transmission electron microscopy), and bronchoalveolar lavage fluid content analysis.RESULTS: extensive physico-chemical characterization of MWCNT was performed, and showed, although similar dimensions for the 3 MWCNT, a much smaller specific surface area for NT2 and NT3 as compared to NT1 (54.1, 34 and 227.54 m(2)/g respectively), along with different surface characteristics. MWCNT-induced cytotoxicity, oxidative stress, and inflammation were increased by acid-based and decreased by polystyrene-based polymer coating both in vitro in murine macrophages and in vivo in lung of mice monitored for 6 months.CONCLUSIONS: these results demonstrate that coating CNT with polymers, without affecting their intrinsic structure, may constitute a useful strategy for decreasing CNT toxicity, and may hold promise for improving occupational safety and that of general the user.

Urokinase receptor (uPAR, CD87) is a platelet receptor important for kinetics and TNF-induced endothelial adhesion in mice.

BACKGROUND: Urokinase plasminogen activator receptor (uPAR, CD87) is a widely distributed 55-kD, glycoprotein I-anchored surface receptor. On binding of its ligand uPA, it is known to increase leukocyte adhesion and traffic. Using genetically deficient mice, we explored the role of uPAR in platelet kinetics and TNF-induced platelet consumption. METHODS AND RESULTS: Anti-uPAR antibody stained platelets from normal (+/+) but not from uPAR-/- mice, as seen by fluorescence-activated cell sorter analysis. 51Cr-labeled platelets from uPAR-/- donors survived longer than those from +/+ donors when injected into a +/+ recipient. Intratracheal TNF injection induced thrombocytopenia and a platelet pulmonary localization, pronounced in +/+ but absent in uPAR-/- mice. Aprotinin, a plasmin inhibitor, decreased TNF-induced thrombocytopenia. TNF injection markedly reduced the survival and increased the pulmonary localization of 51Cr-labeled platelets from +/+ but not from uPAR-/- donors, indicating that it is the platelet uPAR that is critical for their response to TNF. As seen by electron microscopy, TNF injection increased the number of platelets and polymorphonuclear neutrophils (PMNs) in the alveolar capillaries of +/+ mice, whereas in uPAR-/- mice, platelet trapping was insignificant and PMN trapping was slightly reduced. Platelets within alveolar capillaries of TNF-injected mice were activated, as judged from their shape, and this was evident in +/+ but not in uPAR-/- mice. CONCLUSIONS: These results demonstrate for the first time the critical role of platelet uPAR for kinetics as well as for activation and endothelium adhesion associated with inflammation.