Target-controlled inhalation induction with sevoflurane in children: a prospective pilot study.

BACKGROUND: Target-controlled inhalation induction (TCII) with sevoflurane is becoming possible with new anesthesia platforms. Although TCII has already been performed in adults, it remains to be evaluated in children. METHODS: In a prospective study, we compared TCII using the Felix AInOC anesthetic station (Taema, Anthony, France) to our standard protocol inhalation induction in children scheduled for elective surgery under general anesthesia. After preoxygenation, sevoflurane induction was performed in both groups without priming of the circuit. Sufentanil was administered after venous line placement. RESULTS: In the TCII group, no overdosage or underdosage was observed except in two children where TCII failed owing to high agitation, and the number of adjustments was lower compared with our standard protocol inhalation induction (1(1-2.5[0-5]) vs 6(5-6[4-10]) respectively). Moreover, the delay to obtain target end-tidal sevoflurane concentration was shorter in the TCII group (2(1.6-2.7[1.3-4]) min vs 3.4(2.5-3.8[2.3-6.5]) min respectively). No significant difference in the delay of loss of consciousness or in the conditions for intubation or laryngeal mask placement was observed between the groups. CONCLUSION: The Felix AInOC allows TCII to be performed satisfactorily in children. Manual inhalation induction induced a higher number of adjustments and overdosages.

PEEP titration in moderate to severe ARDS: plateau versus transpulmonary pressure.

BACKGROUND: Although lung protection with low tidal volume and limited plateau pressure (Pplat) improves survival in acute respiratory distress syndrome patients (ARDS), the best way to set positive end-expiratory pressure (PEEP) is still debated. METHODS: This study aimed to compare two strategies using individual PEEP based on a maximum Pplat (28-30 cmH2O, the Express group) or on keeping end-expiratory transpulmonary pressure positive (0-5 cmH2O, PLexpi group). We estimated alveolar recruitment (Vrec), end-expiratory lung volume and alveolar distension based on elastance-related end-inspiratory transpulmonary pressure (PL,EL). RESULTS: Nineteen patients with moderate to severe ARDS (PaO2/FiO2 < 150 mmHg) were included with a baseline PEEP of 7.0 ± 1.8 cmH2O and a PaO2/FiO2 of 91.2 ± 31.2 mmHg. PEEP and oxygenation increased significantly from baseline with both protocols; PEEP Express group was 14.2 ± 3.6 cmH2O versus 16.7 ± 5.9 cmH2O in PLexpi group. No patient had the same PEEP with the two protocols. Vrec was higher with the latter protocol (299 [0 to 875] vs. 222 [47 to 483] ml, p = 0.049) and correlated with improved oxygenation (R2 = 0.45, p = 0.002). Two and seven patients in the Express and PL,expi groups, respectively, had PL,EL > 25 cmH2O. CONCLUSIONS: There is a great heterogeneity of PLexpi when Pplat is used to titrate PEEP but with limited risk of over-distension. A PEEP titration for a moderate positive level of PLexpi might slightly improve alveolar recruitment and oxygenation but increases the risk of over-distension in one-third of patients.

PDZRN3 destabilizes endothelial cell-cell junctions through a PKCζ-containing polarity complex to increase vascular permeability.

Endothelial cells serve as a barrier between blood and tissues. Maintenance of the endothelial cell barrier depends on the integrity of intercellular junctions, which is regulated by a polarity complex that includes the ζ isoform of atypical protein kinase C (PKCζ) and partitioning defective 3 (PAR3). We revealed that the E3 ubiquitin ligase PDZ domain-containing ring finger 3 (PDZRN3) regulated endothelial intercellular junction integrity. Endothelial cell-specific overexpression of Pdzrn3 led to early embryonic lethality with severe hemorrhaging and altered organization of endothelial intercellular junctions. Conversely, endothelial-specific loss of Pdzrn3 prevented vascular leakage in a mouse model of transient ischemic stroke, an effect that was mimicked by pharmacological inhibition of PKCζ. PDZRN3 regulated Wnt signaling and associated with a complex containing PAR3, PKCζ, and the multi-PDZ domain protein MUPP1 (Discs Lost-multi-PDZ domain protein 1) and targeted MUPP1 for proteasomal degradation in transfected cells. Transient ischemic stroke increased the ubiquitination of MUPP1, and deficiency of MUPP1 in endothelial cells was associated with decreased localization of PKCζ and PAR3 at intercellular junctions. In endothelial cells, Pdzrn3 overexpression increased permeability through a PKCζ-dependent pathway. In contrast, Pdzrn3 depletion enhanced PKCζ accumulation at cell-cell contacts and reinforced the cortical actin cytoskeleton under stress conditions. These findings reveal how PDZRN3 regulates vascular permeability through a PKCζ-containing complex.

Guidelines on the use of ultrasound guidance for vascular access.

Insertion of vascular access is a common procedure with potential for iatrogenic events, some of which can be serious. The spread of ultrasound scanners in operating rooms, intensive care units and emergency departments has made ultrasound-guided catheterisation possible. The first guidelines were published a decade ago but are not always followed in France. The French Society of Anaesthesia and Intensive Care has decided to adopt a position on this issue through its Guidelines Committee in order to propose a limited number of simple guidelines. The method used was the GRADE(®) method using the most recently published meta-analyses as the source of references. The level of evidence found ranged from low to high and all the positive aspects associated with ultrasound guidance, i.e. fewer traumatic complications at puncture, probably or definitely outweigh the potential adverse consequences regardless of whether an adult or child is involved and regardless of the site of insertion.

Clinical utility of coronary calcium scoring after nonischemic myocardial perfusion imaging.

BACKGROUND: Coronary artery calcium (CAC) scoring is increasingly being used after myocardial perfusion imaging (MPI) to detect preclinical coronary artery disease (CAD). However, there are few data to support this approach. METHODS AND RESULTS: We reviewed 200 consecutive patients without known CAD who were referred for CAC scoring shortly after nonischemic MPI. Of these, 13 (6.5%) had CAC scores greater than 400, indicating significant CAD; 22 (11%) had CAC scores of 101 to 400; 27 had CAC scores of 11 to 100; and the remainder (n = 138) has CAC scores of 1 to 10. Traditional risk factors and patient characteristics were not significant predictors of CAC scores of 101 or greater. However, age and the Framingham risk score were predictors of CAC scores greater than 0. At follow-up, significantly more patients with CAC scores of 101 or greater had been given the advice to take lipid-lowering medication and aspirin compared with those with CAC scores of 0. CONCLUSIONS: Of patients referred for CAC scoring after nonischemic MPI, 17.5% were identified as having CAD based on a CAC score greater than 100, allowing intervention with aggressive medical therapy. Patients who were reclassified were not easily identifiable by traditional risk factors, but Framingham risk score did predict the presence of CAC. Clinicians modified medical therapy based on the results of CAC scoring.