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Peter M. Suter

Researcher at University of Geneva

Publications -  149
Citations -  13791

Peter M. Suter is an academic researcher from University of Geneva. The author has contributed to research in topics: Intensive care & ARDS. The author has an hindex of 49, co-authored 147 publications receiving 13360 citations.

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The prevalence of nosocomial infection in intensive care units in Europe. Results of the European Prevalence of Infection in Intensive Care (EPIC) Study. EPIC International Advisory Committee.

TL;DR: ICU-acquired infection is common and often associated with microbiological isolates of resistant organisms, and the potential effects on outcome emphasize the importance of specific measures for infection control in critically ill patients.
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Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: a randomized controlled trial.

TL;DR: Mechanical ventilation can induce a cytokine response that may be attenuated by a strategy to minimize overdistention and recruitment/derecruitment of the lung, and these physiological improvements are associated with improvements in clinical end points.
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Diagnosis of Ventilator-associated Pneumonia by Bacteriologic Analysis of Bronchoscopic and Nonbronchoscopic “Blind” Bronchoalveolar Lavage Fluid

TL;DR: A good correlation between clinical score and quantitative bacteriology was observed and patients with pulmonary infection could be distinguished by a BI greater than or equal to 5 with a sensitivity of 93% and a specificity of 100% (B-BAL).
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Candida colonization and subsequent infections in critically ill surgical patients.

TL;DR: The intensity of Candida colonization assessed by systematic screening helps predicting subsequent infections with identical strains in critically ill patients, and offers opportunity for intervention strategies.
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Effect of Mechanical Ventilation on Inflammatory Mediators in Patients with Acute Respiratory Distress Syndrome: A Randomized Controlled Trial

TL;DR: Mechanical ventilation can induce a cytokine response that may be attenuated by a strategy to minimize overdistention and recruitment/derecruitment of the lung and whether these physiological improvements are associated with improvements in clinical end points should be determined.