Prediction of fluid responsiveness using respiratory variations in left ventricular stroke area by transoesophageal echocardiographic automated border detection in mechanically ventilated patients.

BackgroundLeft ventricular stroke area by transoesophageal echocardiographic automated border detection has been shown to be strongly correlated to left ventricular stroke volume. Respiratory variations in left ventricular stroke volume or its surrogates are good predictors of fluid responsiveness in mechanically ventilated patients. We hypothesised that respiratory variations in left ventricular stroke area (DeltaSA) can predict fluid responsiveness.MethodsEighteen mechanically ventilated patients undergoing coronary artery bypass grafting were studied immediately after induction of anaesthesia. Stroke area was measured on a beat-to-beat basis using transoesophageal echocardiographic automated border detection. Haemodynamic and echocardiographic data were measured at baseline and after volume expansion induced by a passive leg raising manoeuvre. Responders to passive leg raising manoeuvre were defined as patients presenting a more than 15% increase in cardiac output.ResultsCardiac output increased significantly in response to volume expansion induced by passive leg raising (from 2.16 +/- 0.79 litres per minute to 2.78 +/- 1.08 litres per minute; p < 0.01). DeltaSA decreased significantly in response to volume expansion (from 17% +/- 7% to 8% +/- 6%; p < 0.01). DeltaSA was higher in responders than in non-responders (20% +/- 5% versus 10% +/- 5%; p < 0.01). A cutoff DeltaSA value of 16% allowed fluid responsiveness prediction with a sensitivity of 92% and a specificity of 83%. DeltaSA at baseline was related to the percentage increase in cardiac output in response to volume expansion (r = 0.53, p < 0.01).ConclusionDeltaSA by transoesophageal echocardiographic automated border detection is sensitive to changes in preload, can predict fluid responsiveness, and can quantify the effects of volume expansion on cardiac output. It has potential clinical applications

Ability of pleth variability index to detect hemodynamic changes induced by passive leg raising in spontaneously breathing volunteers

IntroductionPleth Variability Index (PVI) is a new algorithm that allows continuous and automatic estimation of respiratory variations in the pulse oximeter waveform amplitude. Our aim was to test its ability to detect changes in preload induced by passive leg raising (PLR) in spontaneously breathing volunteers.MethodsWe conducted a prospective observational study. Twenty-five spontaneously breathing volunteers were enrolled. PVI, heart rate and noninvasive arterial pressure were recorded. Cardiac output was assessed using transthoracic echocardiography. Volunteers were studied in three successive positions: baseline (semirecumbent position); after PLR of 45 degrees with the trunk lowered in the supine position; and back in the semirecubent position.ResultsWe observed significant changes in cardiac output and PVI during changes in body position. In particular, PVI decreased significantly from baseline to PLR (from 21.5 +/- 8.0% to 18.3 +/- 9.4%; P < 0.05) and increased significantly from PLR to the semirecumbent position (from 18.3 +/- 9.4% to 25.4 +/- 10.6 %; P < 0.05). A threshold PVI value above 19% was a weak but significant predictor of response to PLR (sensitivity 82%, specificity 57%, area under the receiver operating characteristic curve 0.734 +/- 0.101).ConclusionPVI can detect haemodynamic changes induced by PLR in spontaneously breathing volunteers. However, we found that PVI was a weak predictor of fluid responsiveness in this setting

Effect of cardiopulmonary bypass on activated partial thromboplastin time waveform analysis, serum procalcitonin and C-reactive protein concentrations

Abstract Introduction Systemic inflammatory response syndrome (SIRS) is a frequent condition after cardiopulmonary bypass (CPB) and makes conventional biological tests fail to detect postoperative sepsis. Biphasic waveform (BPW) analysis is a new biological test derived from activated partial thromboplastin time that has recently been proposed for sepsis diagnosis. The aim of this study was to investigate the accuracy of BPW to detect sepsis after cardiac surgery under CPB. Methods We conducted a prospective study in American Society of Anesthesiologists' (ASA) physical status III and IV patients referred for cardiac surgery under CPB. Procalcitonin (PCT) and BPW were recorded before surgery and every day during the first week following surgery. Patients were then divided into three groups: patients presenting no SIRS, patients presenting with non-septic SIRS and patients presenting with sepsis. Results Thirty two patients were included. SIRS occurred in 16 patients (50%) including 5 sepsis (16%) and 11 (34%) non-septic SIRS. PCT and BPW were significantly increased in SIRS patients compared to no SIRS patients (0.9 [0.5-2.2] vs. 8.1 [2.0-21.3] ng/l for PCT and 0.10 [0.09-0.14] vs. 0.29 [0.16-0.56] %T/s for BPW; P < 0.05 for both). We observed no difference in peak PCT value between the sepsis group and the non-septic SIRS group (8.4 [7.5-32.2] vs. 7.8 [1.9-17.5] ng/l; P = 0.67). On the other hand, we found that BPW was significantly higher in the sepsis group compared to the non-septic SIRS group (0.57 [0.54-0.78] vs. 0.19 [0.14-0.29] %T/s; P < 0.01). We found that a BPW threshold value of 0.465%T/s was able to discriminate between sepsis and non-septic SIRS groups with a sensitivity of 100% and a specificity of 93% (area under the curve: 0.948 +/- 0.039; P < 0.01). Applying the previously published threshold of 0.25%T/s, we found a sensitivity of 100% and a specificity of 72% to discriminate between these two groups. Neither C-reactive protein (CRP) nor PCT had significant predictive value (area under the curve for CRP was 0.659 +/- 0.142; P = 0.26 and area under the curve for PCT was 0.704 +/- 0.133; P = 0.15). Conclusions BPW has potential clinical applications for sepsis diagnosis in the postoperative period following cardiac surgery under CPB

Treatment of intracranial dural fistulas with Onyx : a prospective cohort, systematic review, and meta-analysis

BACKGROUND Onyx is important embolic material in the endovascular treatment of intracranial dural arteriovenous fistula (DAVF). However, its impact on DAVF occlusion rates, morbidity, mortality, and complication rates is not fully examined. OBJECTIVE To improve understanding of safety and effectiveness profiles associated with transarterial endovascular treatment using Onyx for intracranial DAVF METHODS We analyzed data from our prospective clinical registry and conducted a systematic review of all previous transarterial embolization studies using Onyx published between January 2005 and December 2015 in MEDLINE and EMBASE. RESULTS In the prospective study, 41 transarterial procedures were performed in 33 consecutive patients harboring 36 DAVFs. Complete initial exclusion was obtained in 32 of 36 (88.9%) fistulas; 31 fistulas were followed up showing 4 (12.9%) recurrences. Procedure-related morbidity and mortality were 3% and 0%, respectively. The literature review identified 19 studies involving a total of 425 patients with 463 DAVFs. Meta-analysis, including our registry data, showed an initial complete occlusion rate of 82% (95% confidence interval [CI]: 74%, 88%; I2, 70.6%), and recurrence rate at midterm of 2% (95% CI: 0%, 5%; I2, 21.5%). Pooled postoperative neurological deficit, procedure-related morbidity, and mortality rates were 4% (95% CI: 2%, 6%; I2, 0%), 3% (95% CI: 1%, 5%; I2, 0%), and 0%, respectively. CONCLUSION This meta-analysis suggests that transarterial embolization with Onyx is a safe treatment modality for DAVFs. Although Onyx showed a low recurrence rate at midterm, the long-term risk is poorly addressed in our study and should warrant a longer follow-up

Estimating Attributable Mortality Due to Nosocomial Infections Acquired in Intensive Care Units

Background. The strength of the association between intensive care unit (ICU)-acquired nosocomial infections (NIs) and mortality might differ according to the methodological approach taken. Objective. TO assess the association between ICU-acquired NIs and mortality using the concept of population-attributable fraction (PAF) for patient deaths caused by ICU-acquired NIs in a large cohort of critically ill patients. Setting. Eleven ICUs of a French university hospital. Design. We analyzed surveillance data on ICU-acquired NIs collected prospectively during the period from 1995 through 2003. The primary outcome was mortality from ICU-acquired NI stratified by site of infection. A matched-pair, case-control study was performed. Each patient who died before ICU discharge was defined as a case patient, and each patient who survived to ICU discharge was denned as a control patient. The PAF was calculated after adjustment for confounders by use of conditional logistic regression analysis. Results. Among 8,068 ICU patients, a total of 1,725 deceased patients were successfully matched with 1,725 control Patients. The adjusted PAF due to ICU-acquired NI for patients who died before ICU discharge was 14.6% (95% confidence interval [CI], 14.4%—14.8%). Stratified by the type of infection, the PAF was 6.1% (95% CI, 5.7%-6.5%) for pulmonary infection, 3.2% (95% CI, 2.8%-3.5%) for central venous catheter infection, 1.7% (95% CI, 0.9%-2.5%) for bloodstream infection, and 0.0% (95% CI, -0.4% to 0.4%) for urinary tract infection. Conclusions. ICU-acquired NI had an important effect on mortality. However, the statistical association between ICU-acquired NI and mortality tended to be less pronounced in findings based on the PAF than in study findings based on estimates of relative risk. Therefore, the choice of methods does matter when the burden of NI needs to be assesse

Change in Sleep Quality of Residents the Night Before High-Fidelity Simulation: Results From a Prospective 1-Year National Survey.

peer reviewed[en] OBJECTIVE: The stress level of participants in high-fidelity simulation stems from various factors but may result in anticipatory anxiety causing sleep disturbances during the night prior to simulation. The objective of this survey was to determine the change in sleep quality of residents during the night prior to the simulation. METHODS: The survey was proposed for 1 year to all residents at the beginning of the simulation, in 10 simulation centres. The questionnaire combined demographics and the Leeds Sleep Evaluation Questionnaire using visual analogue scales divided into 4 sleep qualitative domains. The primary outcome was the prevalence of sleep disturbance (>10 mm on 1 domain). Secondary outcomes were the prevalence of severe sleep disturbance (>25 mm), as well as qualitatively and quantitatively reported explanatory sleep parameters. RESULTS: Among respondents, 66% [95% CI: 63 to 69] of residents had more than 10 mm and 27% [95% CI: 24 to 30] had more than 25 mm of sleep disturbance. Residents with a sleep disturbance of more than 10 mm had fewer hours of sleep (6.4 [standard deviation=1.8] vs 7.3 [standard deviation=1.3], difference: -0.9 [95% CI: -1.1 to -0.7]; P < .0001), with a higher number of night-time awakenings (1.3 [standard deviation=1.5] vs 0.7 [standard deviation=0.9], difference: 0.6 [95% CI: 0.4 to 0.8]; P < .0001). CONCLUSION: Among residents participating in the simulation, a high prevalence of change in sleep quality during the night before the simulation was noted. Strategies to help residents achieve better sleep prior to simulation should be explored

Préconditionnement et postconditionnement myocardiques induits par les agents anesthésiques halogénés

Volatile anesthetics protect myocardium against reversible and irreversible ischemic injury. Using a rabbit in vivo model, we compared the potency of four different halogenated to induce preconditioning. We shown that brain death induced catecholamines storm retains the ability to protect the heart by isoflurane inhalation. A new emulsified formulation of halogenated administered intravenously induces acute and delayed preconditioning. Mitochondrial adenosine triphosphate-sensitive potassium channels and mechanogated channels are involved in halogenated-induced acute preconditioning. Desflurane-induced preconditioning improved the resistance of the mitochondrial permeability transition pore to calcium-induced opening. Endothelial nitric oxide synthase is a trigger and mediator of delayed preconditioning by isoflurane. Isoflurane acts during early reperfusion by activation of the phosphatidylinositol-3-kinase signallingLes agents anesthésiques halogénés peuvent induire un préconditionnement myocardique. A partir d un modèle expérimental de lapin in vivo, nous avons comparé les effets protecteurs des différents halogénés et démontré par ailleurs la persistance de ce préconditionnement après mort encéphalique. Une nouvelle formulation de ces agents anesthésiques, présentés en émulsion lipidique, induit un préconditionnement précoce et tardif après administration intra-veineuse. Le préconditionnement précoce met en jeu l ouverture des canaux potassiques ATP dépendants mitochondriaux ainsi que les canaux stretch et se traduit par un retard à l ouverture du pore de transition de perméabilité mitochondriale induit par une surcharge calcique. Les halogénés induisent un préconditionnement tardif dont la signalisation passe par le monoxyde d azote. Ces agents sont enfin capables d induire un postconditionnement lorsqu ils sont administrés dès les premiers instants de la reperfusion myocardiqueLYON1-BU.Sciences (692662101) / SudocSudocFranceF

Anesthésie vigile par remifentanil pour endartériectomie carotidienne (étude clinique préliminaire)

LYON1-BU Santé (693882101) / SudocPARIS-BIUM (751062103) / SudocPARIS-Bib. Serv.Santé Armées (751055204) / SudocSudocFranceF

Endoprothèses coronaires et anesthésie (résultats de l'étude POSTENT (Prospective Observational STENT study))

LYON1-BU Santé (693882101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

LES INSUFFISANCES AORTIQUES AIGUES POST-TRAUMATIQUES (REVUE DE LA LITTERATURE ; A PROPOS D'UN CAS CHEZ UN POLYTRAUMATISE)

LYON1-BU Santé (693882101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF