Tracheal Diameter and Respiratory Outcome in Infants with Congenital Diaphragmatic Hernia Treated by Fetal Endoscopic Tracheal Occlusion.

AIM: To evaluate tracheal diameters and their clinical impact in patients with congenital diaphragmatic hernia (CDH) after fetal endoscopic tracheal occlusion (FETO). METHODS: Patients born with CDH between January 2012 and August 2016 were divided into two groups: noFETO and FETO. Tracheal diameters at three levels (T1, carina, and maximum tracheal dilation) on chest X-ray at 1, 3, 6, 12, 24, and 36 months of follow-up, requirements of invasive and noninvasive respiratory support, the incidence of respiratory infections, and results of pulmonary function tests (PFT) were compared. RESULTS: A total of 71 patients with CDH were born in the study period, and there were 34/41 survivors in the no-FETO group (82.9%) and 13/30 in the FETO group (43.3%). The maximum tracheal diameter was significantly greater in the FETO group at all ages. No differences were observed in the diameters at T1 and the carina, in the requirements of invasive and noninvasive respiratory support, and in the incidence respiratory infections. At the PFT (6-12 months), the FETO group presented higher respiratory rates (46.1 ± 6.2 vs. 36.5 ± 10.6, p = 0.02). No differences in PFT results were found between the groups after the 1st year of life. CONCLUSIONS: The FETO procedure leads to persistent tracheomegaly. However, the tracheomegaly does not seem to have a significant clinical impact.

Static and dynamic components of esophageal and central venous pressure during intra-abdominal hypertension.

OBJECTIVE: To investigate the effects of intra-abdominal hypertension on esophageal and central venous pressure considering values obtained at end-expiration (i.e., in static conditions) and during tidal volume delivery (i.e., in dynamic conditions). DESIGN: Retrospective (pigs) and prospective, randomized, controlled (rats) trial. SETTING: Animal laboratory of a university hospital. SUBJECTS: Six female pigs and 15 Sprague Dawley male rats. INTERVENTIONS: During anesthesia and paralysis, animals' abdomens were inflated with helium. MEASUREMENTS AND MAIN RESULTS: Abdominal pressure was measured by intraperitoneal catheter. In pigs, esophageal pressure and central venous pressure were continuously measured while inflating the abdomen together with hemodynamic assessment. In rats, the abdomen was inflated after the random application of three levels of positive end-expiratory pressure. Data are shown as mean +/- SD. At end-expiration, esophageal pressures were similar before and after abdominal inflation (p = .177). In contrast, the dynamic component significantly rose after intra-abdominal hypertension, from 3.2 +/- 0.7 cm H2O to 10.0 +/- 2.3 cm H2O (p < .001), and was correlated with peritoneal pressure (linear regression, R2 = .708, p < .001). Positive end-expiratory pressure significantly influenced static esophageal pressure during intra-abdominal hypertension (p = .002) but not dynamic pressures. Static central venous pressure rose with intra-abdominal hypertension from 4.1 +/- 1.5 cm H2O to 6.7 +/- 1.8 cm H2O (p = .043), more so the dynamic component (from 2.9 +/- 0.8 cm H2O to 9.3 +/- 3.1 cm H2O, p = .02). Dynamic changes of esophageal pressures correlated with dynamic changes of central venous pressure (linear regression, R2 = .679, p < .001). Mean values of central venous pressure significantly increased with intra-abdominal hypertension from 7.7 +/- 1.5 cm H2O to 12.7 +/- 2.6 cm H2O (p = .006), whereas transmural central venous pressure and intrathoracic blood volume did not change significantly. CONCLUSIONS: Dynamic changes of esophageal pressure occurred during intra-abdominal hypertension, whereas end-expiratory pressure was affected by high positive end-expiratory pressure levels. Provided that central venous pressure changes reflect esophageal pressure, central venous pressure itself cannot be relied on to guide resuscitation in patients with intra-abdominal hypertension, particularly when abdominal pressures are changing over short periods of time.

Prone position delays the progression of ventilator-induced lung injury in rats: does lung strain distribution play a role?

OBJECTIVE: To investigate if prone position delays the progression of experimental ventilator-induced lung injury, possibly due to a more homogeneous distribution of strain within lung parenchyma. DESIGN: Prospective, randomized, controlled trial. SETTING: Animal laboratory of a university hospital. SUBJECTS: Thirty-five Sprague Dawley male rats (weight 257 +/- 45 g). INTERVENTIONS: Mechanical ventilation in either supine or prone position and computed tomography scan analysis. MEASUREMENTS: : Animals were ventilated in supine (n = 15) or prone (n = 15) position until a similar ventilator-induced lung injury was reached. To do so, experiments were interrupted when respiratory system elastance was 150% of baseline. Ventilator-induced lung injury was assessed as lung wet-to-dry ratio and histology. Time to reach lung injury was considered as a main outcome measure. In five additional animals, computed tomography scans (GE Light Speed QX/I, thickness 1.25 mm, interval 0.6 mm, 100 MA, 100 Kv) were randomly taken at end-expiration and end-inspiration in both positions, and quantitative analysis was performed. Data are shown as mean +/- sd. MEASUREMENTS AND MAIN RESULTS: Similar ventilator-induced lung injury was reached (respiratory system elastance, wet-to-dry ratio, and histology). The time taken to achieve the target ventilator-induced lung injury was longer with prone position (73 +/- 37 mins vs. 112 +/- 42, supine vs. prone, p = .011). Computed tomography scan analysis performed before lung injury revealed that at end-expiration, the lung was wider in prone position (p = .004) and somewhat shorter (p = .09), despite similar lung volumes (p = .455). Lung density along the vertical axis increased significantly only in supine position (p = .002). Lung strain was greater in supine as opposed to prone position (width strain, 7.8 +/- 1.8% vs. 5.6 +/- 0.9, supine vs. prone, p = .029). CONCLUSIONS: Prone position delays the progression of ventilator-induced lung injury. Computed tomography scan analysis suggests that a more homogeneous distribution of strain may be implicated in the protective role of prone position against ventilator-induced lung injury.

Positive end-expiratory pressure delays the progression of lung injury during ventilator strategies involving high airway pressure and lung overdistention.

OBJECTIVE: Many studies have investigated the protective role of positive end-expiratory pressure (PEEP) on ventilator-induced lung injury. Most assessed lung injury in protocols involving different ventilation strategies applied for the same length of time. This study, however, set out to investigate the protective role of PEEP with respect to the time needed to reach similar levels of lung injury. DESIGN: Prospective, randomized laboratory animal investigation. SETTING: The University Laboratory of Ospedale Maggiore, Milano, IRCCS. SUBJECTS: Anesthetized, paralyzed, and mechanically ventilated Sprague-Dawley rats. INTERVENTIONS: Three groups of five Sprague-Dawley rats were ventilated using zero end-expiratory pressure ZEEP (PEEP of 0 cm H(2)O) and PEEP of 3 and 6 cm H(2)O and a similar index of lung overdistension (Paw(p)/P(100) congruent with 1.1; where Paw(p) is peak airway pressure and P(100) is the pressure corresponding to total lung capacity). To obtain this, tidal volume was reduced depending on the PEEP. To reach similar levels of lung injury, we measured respiratory system elastance while ventilating the animals and killed them when respiratory system elastance was 150% of baseline. Once target respiratory system elastance was reached, the lung wet-to-dry ratio was obtained. RESULTS: Rats were ventilated with comparable high airway pressure (Paw(p) of 42.8 +/- 3.1, 43.5 +/- 2.6, and 46.2 +/- 4.4, respectively, for PEEP 0, 3, and 6) obtaining similar overdistension (Paw(p)/P(100) - index of overdistension: 1.17 +/- 0.2, 1.06 +/- 0.1, and 1.19 +/- 0.2). The respiratory system elastance target was reached and wet-to-dry ratio was not different in the three groups, suggesting a similar degree of lung damage. The time taken to achieve the target respiratory system elastance was three times longer with PEEP 3 and 6 (55 +/- 14 mins and 60 +/- 17) as compared with zero end-expiratory pressure (18 +/- 3 mins, p <.001). CONCLUSION: These findings confirm that PEEP is protective against ventilator-induced lung injury and may enable the clinician to "buy time" in the progression of lung injury.