Didier Ledoux

Surv Anesthesiol 2016;60(2):51–53 The implementation of ventilator-associated pneumonia (VAP) bundles in intensive care units (ICUs) has led to a reduction in VAP rate, but the discrepancy between VAP rates in ICUs in the United States and Europe merits further investigation. Focusing on ventilator-associated events involving quantitative evidence of deteriorating respiration (worsening oxygenation) has been proposed to obtain fast and reliable surveillance definitions of VAP.

Résumé L’hypertension intracrânienne (HTIC) est l’une des causes majeures de lésions secondaires survenant dans les suites d’un traumatisme crânien grave. Dans cet article, nous présentons une revue des thérapies actuellement disponibles pour le traitement de l’HTIC réfractaire, définie comme une HTIC ne répondant pas aux thérapies de première ligne. Les thérapies de seconde ligne disponibles pour le traitement de l’HTIC réfractaire sont : l’hypothermie induite, le contrôle de la pression de perfusion cérébrale, l’hyperventilation transitoire, les barbituriques et la crâniectomie décompressive. Mise à part la crâniectomie décompressive, ces traitements font l’objet de recommandations par la Brain Trauma Foundation (BTF). Malheureusement, le niveau d’évidence scientifique supportant ces traitements est généralement faible à modéré. Cette relative faiblesse des données de la littérature s’explique probablement pour partie par le fait que les traumatismes crâniens graves sont extrêmement hétérogènes et nécessitent une approche multimodale et individualisée, ce qui rend la conduite d’études cliniques randomisées très compliquée. Néanmoins, les études en cours, telles que celles menées sur l’hypothermie induite (EUROTHEM3235) et sur la crâniectomie décompressive (RESCUEicp), pourraient ouvrir de nouvelles perspectives pour la prise en charge de l’HTIC réfractaire.

To validate the SAPS 3 admission score in an independent general intensive care case mix and to compare its performances with the APACHE II and the SAPS II scores. Cohort observational study. A 26-bed general ICU from a Tertiary University Hospital. Eight hundred and fifty-one consecutive patients admitted to the ICU over an 8-month period. Of these patients, 49 were readmissions, leaving 802 patients for further analysis. None. APACHE II, SAPS II and SAPS 3 variables were prospectively collected; scores and their derived probability of death were calculated according to their original manuscript description. The discriminative power was assessed using the area under the ROC curve (AUROC) and calibration was verified with the Hosmer–Lemeshow goodness-of-fit test. The AUROC of the APACHE II model (AUROC = 0.823) was significantly lower than those of the SAPS II (AUROC = 0.850) and SAPS 3 models (AUROC = 0.854) (P = 0.038). The calibration of the APACHE II model (P = 0.037) and of the SAPS 3 global model (P = 0.035) appeared unsatisfactory. On the contrary, both SAPS II model and SAPS 3 model customised for Central and Western Europe had a good calibration. However, in our study case mix, SAPS II model tended to overestimate the probability of death. In this study, the SAPS 3 admission score and its prediction model customised for Central and Western Europe was more discriminative and better calibrated than APACHE II, but it was not significantly better than the SAPS II.

We thank Dr Lambermont et al. for their comments on the GFR estimation from the serum cystatin C level. The issue raised by these authors is indeed of some interest. However, we think that they did not focus on the right problem. It is correct that, as for serum creatinine measurement, different methods exist for the measurement of serum Cystatin C. However it has been shown that agreement between particle enhanced nephelometric immunoassay (PENIA) and particle enhanced turbidimetric immunoassay (PETIA) methods is good.¹ There are to date at least 10 published equations for GFR estimation from cystatin C. These equations lead to GFR estimations that vary not only according to the used assay. As other authors already pointed,² we think that the discrepancy (Table 1) between these published equations is due, for a large part, to the patients casemix differences, to the use of different gold standard measurements for GFR and to the small sample size of these studies. Therefore one should rather stress the need for the construction of a proper cystatin C based GFR equation relying on a large patient cohort as it was the case for the creatinine based MDRD GFR equation.³

Pre-operative renal dysfunction is a known risk factor for mortality and morbidity after heart surgery. Despite limited accuracy, serum creatinine is widely used to estimate glomerular filtration rate (GFR). Cystatin C is more accurate for assessing GFR. The aim of the present study was to assess associations between GFR estimated from serum cystatin C levels before heart surgery and hospital mortality, hospital morbidity, and 1 year mortality. In a prospective single-centre observational study, clinical risk factors for morbidity and mortality were recorded and serum creatinine and cystatin C levels were measured in patients admitted for heart surgery. Hospital mortality and morbidity and 1 year mortality were recorded. Over an 8 month period, 499 patients were screened, among whom 376 (74.5%) were included in the study. Hospital mortality was 5.6% (21 patients) and 1 year mortality was 10.2%. Hospital morbidity, defined by a length of stay above the 75th percentile, was 22.1% (83 patients). In the multivariable analysis, GFR estimated from serum cystatin C, but not GFR estimated from serum creatinine, was an independent risk factor for hospital morbidity/mortality (odds ratio per 10 mL/min of GFR decrease, 1.20 (1.07–1.34), P = 0.001) and for 1 year mortality (hazards ratio per 10 mL/min of GFR decrease, 1.26 (1.09–1.46), P = 0.002). Pre-operative GFR estimation from serum cystatin C may provide a better risk assessment than pre-operative GFR estimation from serum creatinine in patients scheduled for heart surgery.

Introduction: Combination antibiotic therapy for ventilator associated pneumonia (VAP) is often used to broaden the spectrum of activity of empirical treatment. The relevance of such synergy is commonly supposed but poorly supported. The aim of the present study was to compare the clinical outcome and the course of biological variables in patients treated for a VAP, using a monotherapy with a beta-lactam versus a combination therapy. Methods: Patients with VAP were prospectively randomised to receive either cefepime alone or cefepime in association with amikacin or levofloxacin. Clinical and inflammatory parameters were measured on the day of inclusion and thereafter. Results: Seventy-four mechanically ventilated patients meeting clinical criteria for VAP were enrolled in the study. VAP was microbiologically confirmed in 59 patients (84%). Patients were randomised to receive cefepime (C group, 20 patients), cefepime with amikacin (C-A group, 19 patients) or cefepime with levofloxacin (C-L group, 20 patients). No significant difference was observed regarding the time course of temperature, leukocytosis or C-reactive protein level. There were no differences between length of stay in the intensive care unit after infection, nor in ventilator free days within 28 days after infection. No difference in mortality was observed. Conclusion: Antibiotic combination using a fourth generation cephalosporin with either an aminoside or a fluoroquinolone is not associated with a clinical or biological benefit when compared to cephalosporin monotherapy against common susceptible pathogens causing VAP.