Publications (216) View all
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Article: Nosocomial Infections in Adult Cardiogenic Shock Patients Supported by Venoarterial Extracorporeal Membrane Oxygenation.
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ABSTRACT: Background. Incidence and impact on adult patients' outcomes of nosocomial infections (NIs) occurring during venoarterial extracorporeal membrane oxygenation (VA-ECMO) support for refractory cardiogenic shock have rarely been described.Methods. We retrospectively reviewed the charts of a large series of patients who received VA-ECMO in our intensive care unit (ICU) from January 2003 through December 2009. Incidence, types, risk factors, and impact on outcomes of NIs occurring during ECMO support were analyzed.Results. Among 220 patients (49 ± 16 years old, simplified acute physiology score (SAPS) II 61 ± 20) who underwent ECMO support for >48 hours for a total of 2942 ECMO days, 142 (64%) developed NIs. Ventilator-associated pneumonia (VAP), bloodstream infections, cannula infections, and mediastinitis infections occurred in 55%, 18%, 10% and 11% of the patients, respectively. More critical condition at ICU admission, but not antibiotics at the time of ECMO cannulation, was associated with subsequently developing NIs (hazard ratio, 0.73; 95% confidence interval [CI], .50-1.05; P = .09). Infected patients had longer durations of mechanical ventilation, ECMO support, and hospital stays. Independent predictors of death were infection with severe sepsis or septic shock (odds ratio, 1.93; 95% CI, 1.26-2.94; P = .002) and SAPS II, whereas immunosuppression and myocarditis as the reason for ECMO support were associated with better outcomes.Conclusions. Cardiogenic shock patients who received the latest generation VA-ECMO still had a high risk of developing NIs, particularly VAP. Strategies aimed at preventing these infections may improve the outcomes of these critically ill patients.Clinical Infectious Diseases 09/2012; · 9.15 Impact Factor -
Article: Safety and pharmacokinetics of an anti-PcrV PEGylated monoclonal antibody fragment in mechanically ventilated patients colonized with Pseudomonas aeruginosa: a randomized,double-blind, placebo-controlled trial.
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ABSTRACT: The type III secretion system is an important Pseudomonas aeruginosa-virulence determinant in animal models of infection and in humans. Antibody-mediated inhibition of the PcrV protein, an essential component of this system, might abrogate the Pseudomonas aeruginosa ability to damage epithelial cells, neutrophils, and macrophages, thereby limiting its pathogenicity. The objective of the trial was to determine the safety, pharmacokinetics, and ability to prevent Pseudomonas aeruginosa ventilator-associated pneumonia of KB001, a recombinant, PEGylated, engineered, human Fab' fragment that specifically binds to a Pseudomonas aeruginosa PcrV epitope and blocks its function. Multicenter, randomized, placebo-controlled, double-blind, phase-2a trial. Ten intensive care units across France. Thirty-nine Pseudomonas aeruginosa-colonized, but not infected, mechanically ventilated patients. Patients were randomized 1:1:1 to receive a single intravenous infusion of KB001, 3 mg/kg (n=13) or 10 mg/kg (n=14), or placebo (n=12). The primary end points were KB001 safety and tolerability, assessed as treatment-related adverse-event frequency and severity. Secondary end points included serum and lung KB001 pharmacokinetics, and Pseudomonas aeruginosa pneumonia rate within 28 days of its infusion. KB001 was well tolerated and not immunogenic. The 3- and 10-mg/kg groups had respective maximum serum concentrations of 52,811-88,660 and 121,857-285,454 ng/mL, with mean elimination half-lives of 8.1 and 9.3 days. KB001 was detected in endotracheal aspirates from all patients receiving it, as early as day 1 and up to 28 days. Respective mean endotracheal aspirate/serum concentration ratios were 0.092 and 0.085 for the 3- and 10-mg/kg groups, who developed Pseudomonas aeruginosa pneumonia less frequently (33% and 31%, respectively) than placebo recipients (60%). KB001 was safe and well tolerated in this study, with a favorable pharmacokinetic profile and promising potential for reducing Pseudomonas aeruginosa pneumonia incidence in intensive care unit mechanically ventilated patients colonized with this bacterium.Critical care medicine 05/2012; 40(8):2320-6. · 6.37 Impact Factor -
Article: Hemodynamic monitoring in shock and implications for management
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ABSTRACT: ObjectiveShock is asevere syndrome resulting in multiple organ dysfunction and ahigh mortality rate. The goal of this consensus statement is to provide recommendations regarding the monitoring and management of the critically ill patient with shock. MethodsAn international consensus conference was held in April 2006 to develop recommendations for hemodynamic monitoring and implications for management of patients with shock. Evidence-based recommendations were developed, after conferring with experts and reviewing the pertinent literature, by ajury of 11persons representing five critical care societies. Data synthesisAtotal of 17recommendations were developed to provide guidance to intensive care physicians monitoring and caring for the patient with shock. Topics addressed were as follows: (1) What are the epidemiologic and pathophysiologic features of shock in the ICU? (2) Should we monitor preload and fluid responsiveness in shock? (3) How and when should we monitor stroke volume or cardiac output in shock? (4) What markers of the regional and micro-circulation can be monitored, and how can cellular function be assessed in shock? (5) What is the evidence for using hemodynamic monitoring to direct therapy in shock? One of the most important recommendations was that hypotension is not required to define shock, and as aresult, importance is assigned to the presence of inadequate tissue perfusion on physical examination. Given the current evidence, the only bio-marker recommended for diagnosis or staging of shock is blood lactate. The jury also recommended against the routine use of (1) the pulmonary artery catheter in shock and (2) static preload measurements used alone to predict fluid responsiveness. ConclusionsThis consensus statement provides 17 different recommendations pertaining to the monitoring and caring of patients with shock. There were some important questions that could not be fully addressed using an evidence-based approach, and areas needing further research were identified.Intensive Care Medicine 04/2012; 33(4):575-590. · 5.40 Impact Factor -
Article: Reply to Taccone et al, Wolff, and Masuta and Iwata.
Clinical Infectious Diseases 03/2012; · 9.15 Impact Factor -
Article: Two-dimensional strain rate and Doppler tissue myocardial velocities: analysis by echocardiography of hemodynamic and functional changes of the failed left ventricle during different degrees of extracorporeal life support.
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ABSTRACT: To evaluate hemodynamic and functional changes of the failed left ventricle by Velocity Vector Imaging (VVI) and tissue Doppler, 22 patients with cardiogenic shock supported by extracorporeal life support (ECLS) were imaged during ECLS output variations inducing severe load manipulations. The following data were acquired: (1) mean arterial pressure, aortic Doppler velocity-time integral, left ventricular end-diastolic volume, and mitral Doppler E wave; (2) tissue Doppler systolic (Sa) and early diastolic (Ea) velocities; and (3) systolic peak velocity (Sv), strain, and strain rate using VVI. Load variations were documented by a significant decrease in afterload (mean arterial pressure, -21%), an increase in preload (left ventricular end-diastolic volume, +12%; E, +46%; E/Ea ratio, +22%), and an increase in the velocity-time integral (+45%). VVI parameters increased (Sv, +36%; strain, +81%; and strain rate, +67%; P < .05), unlike tissue Doppler systolic velocities (+2%; P = NS). Whatever the ECLS flow, Sa was higher in patients who survived. VVI parameters are not useful in characterizing the failed left ventricle with rapidly varying load conditions. Tissue Doppler systolic velocities appear to be load independent and thus could help in the management of ECLS patients.Journal of the American Society of Echocardiography: official publication of the American Society of Echocardiography 03/2012; 25(6):632-40. · 2.98 Impact Factor
