Introduction: Invasive mechanical ventilation contributes to ventilator-induced diaphragmatic dysfunction, delaying extubation and increasing mortality in adults. Despite the possibility of having a higher impact in paediatrics, this dysfunction is not routinely monitored. Diaphragm ultrasound has been proposed as a safe and non-invasive technique for this purpose. The aim of this study was to describe the evolution of diaphragmatic morphology and functional measurements by ultrasound in ventilated children.Material and Methods: Prospective exploratory study. Children admitted to Paediatric Intensive Care Unit requiring mechanical ventilation > 48 hours were included. The diaphragmatic thickness, excursion and the thickening fraction were assessed by ultrasound.Results: Seventeen cases were included, with a median age of 42 months. Ten were male, seven had comorbidities and three in seventeen had malnutrition at admission. The median time under mechanical ventilation was seven days. The median of the initial and minimum diaphragmatic thickness was 2.3 mm and 1.9 mm, respectively, with a median decrease in thickness of 13% under pressure-regulated volume control. Diaphragmatic atrophy was observed in 14/17 cases. Differences in the median thickness variation were found between patients with sepsis and without (0.70 vs 0.25 mm; p = 0.019). During pressure support ventilation there was a tendency to increase diaphragmatic thickness and excursion. Extubation failure occurred for diaphragmatic thickening fraction ≤ 35%.Discussion: Under pressure-regulated volume control there was a tendency for a decrease in diaphragmatic thickness. In the pre-extubation stage under pressure support, there was a tendency for it to increase. These results suggest that, by titrating ventilation using physiological levels of inspiratory effort, we can reduce the diaphragmatic morphological changes associated with ventilation.Conclusion: The early recognition of diaphragmatic changes may encourage a targeted approach, namely titration of ventilation, in order to reduce ventilator-induced diaphragmatic dysfunction and its clinical repercussions.

Introduction: Invasive mechanical ventilation contributes to ventilator-induced diaphragmatic dysfunction, delaying extubation and increasing mortality in adults. Despite the possibility of having a higher impact in paediatrics, this dysfunction is not routinely monitored. Diaphragm ultrasound has been proposed as a safe and non-invasive technique for this purpose. The aim of this study was to describe the evolution of diaphragmatic morphology and functional measurements by ultrasound in ventilated children. Material and Methods: Prospective exploratory study. Children admitted to Paediatric Intensive Care Unit requiring mechanical ventilation > 48 hours were included. The diaphragmatic thickness, excursion and the thickening fraction were assessed by ultrasound. Results: Seventeen cases were included, with a median age of 42 months. Ten were male, seven had comorbidities and three in seventeen had malnutrition at admission. The median time under mechanical ventilation was seven days. The median of the initial and minimum diaphragmatic thickness was 2.3 mm and 1.9 mm, respectively, with a median decrease in thickness of 13% under pressure-regulated volume control. Diaphragmatic atrophy was observed in 14/17 cases. Differences in the median thickness variation were found between patients with sepsis and without (0.70 vs 0.25 mm; p = 0.019). During pressure support ventilation there was a tendency to increase diaphragmatic thickness and excursion. Extubation failure occurred for diaphragmatic thickening fraction ≤ 35%. Discussion: Under pressure-regulated volume control there was a tendency for a decrease in diaphragmatic thickness. In the pre-extubation stage under pressure support, there was a tendency for it to increase. These results suggest that, by titrating ventilation using physiological levels of inspiratory effort, we can reduce the diaphragmatic morphological changes associated with ventilation. Conclusion: The early recognition of diaphragmatic changes may encourage a targeted approach, namely titration of ventilation, in order to reduce ventilator-induced diaphragmatic dysfunction and its clinical repercussions.

Introduction Aspiration of gastric contents is one of-the most found complications of general anesthesia and is known to bean important cause of the adult respiratory distress syndrome (ARDS). Hydrochloric seid (HCL) damages the alveolar-capillary membrane leading to intn-alveolar hemorrhage and accumulation of plasma proteins. It is known that these proteins inhibit nomul surfactant function in a dose-dependentway A study was designed to investigate the effect of different treatment strategies with an exogenous surfactant preparation on lung function of nits suffering from respiratory failure after intratracheal HCL instillation. Methods The studies were performed in 34 male adult Sprague-Dawley rats (body weight: 300-350 g). The animals were anesthetized, tracheotomized, paralyzed and ventilated by a Siemens Servo ventilator 900C at the following ventilator setting.: pressureconlrolled ventilation, FiO2=1.0, ventilation frequency= 30/ndn, peak airway pressure (Ppeak)=14 cm H2O, PEEP=2 cm H2O and I/E ratio= 12.After reaching steady state (P.O2>500 mmHg) all rats received HCL intntncheelly (0.1 N; 3 ml/kg). PEEP was increased to 6 cm H2O and Ppeak to 26 cm H20. After Ps02 decreased < 200 mmHg, the animals were divided into 5 groups: Group I (n=7) was only ventilated; Group II (n=8) received surfacunt iröntecheally; Group HI (n=7) was lavageil with saline followed by intrstracheal surfaclant instillation; Group IV and V (n =6 in both groups) were laysged with saline or a diluted surfactant suspension, respectively. The amount of saline used for all bronchoalveolarlavagea was 30 M/kg at 37 C; the amount of surfactant in the diluted surfactant suspensions was 100 mg/kg. The surfactant concentration for intratracheal instillation (Groups Hand V) was at a dose of 200 mg/kg. Blood samples for measurement of Pe02 were taken from the carotid artery of each animal before intratracheal HCL instillation, every 15 min post-instillation and 5, 30 and 60 min after treatment. Results lust before treatment (after HCL instillation) there were no significant differences in Pa02 values between all groups (mean t SD: 139.4 t 39.7 mmHg). Five minutes after treatment there was a significant increase in Pa02 values in Groups M and IV (288.1 ± 111.1 and 338.2 ± 61.6 mmHg, respectively). There was a further decrease in Pa02 values in Groups laud IV (103:6 t 25.8 and 86.3 ± 41.9 mmHg, respectively). The Pa02 values in Group 11 did riot increase significantly (168.6 ± 46.2 mmHg). Cooelusioo These results demonstrate that gas exchange can be improved by lavaging the lungs with saline, followed by surfactant instillation, or'by lavaging lungs with a diluted surfactant suspension. An explanation is that by means of lavage, plasma proteins, which are known to be potent surfactant inhibitors [1.21, are removed from the alveoli. Theo results should be considered for treatment with surfactant of patients suffering from respiratory failure after HCL aspiration.

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