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      Polymicrobial intensive care unit-acquired pneumonia: prevalence, microbiology and outcome

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          Abstract

          Background

          Microbial aetiology of intensive care unit (ICU)-acquired pneumonia (ICUAP) determines antibiotic treatment and outcomes. The impact of polymicrobial ICUAP is not extensively known. We therefore investigated the characteristics and outcomes of polymicrobial aetiology of ICUAP.

          Method

          Patients with ICUAP confirmed microbiologically were prospectively compared according to identification of 1 (monomicrobial) or more (polymicrobial) potentially-pathogenic microorganisms. Microbes usually considered as non-pathogenic were not considered for the etiologic diagnosis. We assessed clinical characteristics, microbiology, inflammatory biomarkers and outcome variables.

          Results

          Among 441 consecutive patients with ICUAP, 256 (58 %) had microbiologic confirmation, and 41 (16 %) of them polymicrobial pneumonia. Methicillin-sensitive Staphylococcus aureus, Haemophilus influenzae, and several Enterobacteriaceae were more frequent in polymicrobial pneumonia. Multi-drug and extensive-drug resistance was similarly frequent in both groups. Compared with monomicrobial, patients with polymicrobial pneumonia had less frequently chronic heart disease (6, 15 % vs . 71, 33 %, p = 0.019), and more frequently pleural effusion (18, 50 %, vs . 54, 25 %, p = 0.008), without any other significant difference. Appropriate empiric antimicrobial treatment was similarly frequent in the monomicrobial (185, 86 %) and the polymicrobial group (39, 95 %), as were the initial response to the empiric treatment, length of stay and mortality. Systemic inflammatory response was similar comparing monomicrobial with polymicrobial ICUAP.

          Conclusion

          The aetiology of ICUAP confirmed microbiologically was polymicrobial in 16 % cases. Pleural effusion and absence of chronic heart disease are associated with polymicrobial pneumonia. When empiric treatment is frequently appropriate, polymicrobial aetiology does not influence the outcome of ICUAP.

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          Most cited references32

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          A new Simplified Acute Physiology Score (SAPS II) based on a European/North American multicenter study.

          To develop and validate a new Simplified Acute Physiology Score, the SAPS II, from a large sample of surgical and medical patients, and to provide a method to convert the score to a probability of hospital mortality. The SAPS II and the probability of hospital mortality were developed and validated using data from consecutive admissions to 137 adult medical and/or surgical intensive care units in 12 countries. The 13,152 patients were randomly divided into developmental (65%) and validation (35%) samples. Patients younger than 18 years, burn patients, coronary care patients, and cardiac surgery patients were excluded. Vital status at hospital discharge. The SAPS II includes only 17 variables: 12 physiology variables, age, type of admission (scheduled surgical, unscheduled surgical, or medical), and three underlying disease variables (acquired immunodeficiency syndrome, metastatic cancer, and hematologic malignancy). Goodness-of-fit tests indicated that the model performed well in the developmental sample and validated well in an independent sample of patients (P = .883 and P = .104 in the developmental and validation samples, respectively). The area under the receiver operating characteristic curve was 0.88 in the developmental sample and 0.86 in the validation sample. The SAPS II, based on a large international sample of patients, provides an estimate of the risk of death without having to specify a primary diagnosis. This is a starting point for future evaluation of the efficiency of intensive care units.
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            Statistical evaluation of ventilator-free days as an efficacy measure in clinical trials of treatments for acute respiratory distress syndrome.

            Trials of potential new therapies in acute lung injury are difficult and expensive to conduct. This article is designed to determine the utility, behavior, and statistical properties of a new primary end point for such trials, ventilator-free days, defined as days alive and free from mechanical ventilation. Describing the nuances of this outcome measure is particularly important because using it, while ignoring mortality, could result in misleading conclusions. To develop a model for the duration of ventilation and mortality and fit the model by using data from a recently completed clinical trial. To determine the appropriate test statistic for the new measure and derive a formula for power. To determine a formula for the probability that the test statistic will reject the null hypothesis and mortality will simultaneously show improvement. To plot power curves for the test statistic and determine sample sizes for reasonable alternative hypotheses. Intensive care units. Patients with acute respiratory distress syndrome or acute lung injury as defined by the American-European Consensus Conference. The proposed model fit the clinical data. Ventilator-free days were improved by lower tidal volume ventilation, but the improvement was mostly caused by the improved mortality rate, so trials that expected similar effects would only have modest increase in power if they used ventilator-free days as their primary end point rather than 28-day mortality. Similar results were obtained using the model in two groups segregated by low or high Acute Physiology and Chronic Health Evaluation score. On the other hand, if patients are divided into two groups on the basis of the lung injury score, both the duration of ventilation and mortality are lower in the low lung injury score group. A trial of a treatment that had a similar clinical effect would have a large increase in power, allowing for a reduction in the required sample size. Use of ventilator-free days as a trial end point allows smaller sample sizes if it is assumed that the treatment being tested simultaneously reduces the duration of ventilation and improves mortality. It is unlikely that a treatment that led to higher mortality could lead to a statistically significant improvement in ventilator-free days. This would be especially true if the treatment were also required to produce a nominal improvement in mortality.
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              Ventilator-associated pneumonia caused by potentially drug-resistant bacteria.

              To determine risk factors for ventilator-associated pneumonia (VAP) caused by potentially drug-resistant bacteria such as methicillin-resistant Staphylococcus aureus, Pseudomonas aeruginosa, Acinetobacter baumannii, and/or Stenotrophomonas maltophilia, 135 consecutive episodes of VAP observed in a single ICU over a 25-mo period were prospectively studied. For all patients, VAP was diagnosed based on results of bronchoscopic protected specimen brush (> or = 10(3) cfu/ml) and bronchoalveolar lavage (> or = 10(4) cfu/ml) specimens. Seventy-seven episodes were caused by "potentially resistant" bacteria and 58 episodes were caused by "other" organisms. According to logistic regression analysis, three variables among potential factors remained significant: duration of mechanical ventilation (MV) > or = 7 d (odds ratio [OR] = 6.0), prior antibiotic use (OR = 13.5), and prior use of broad-spectrum drugs (third-generation cephalosporin, fluoroquinolone, and/or imipenem) (OR = 4.1). Distribution of the 245 causative bacteria was analyzed according to four groups defined by prior duration of MV ( or = 7 d) and prior use or lack of use (within 15 d) of antibiotics. Although 22 episodes of early-onset VAP in patients receiving no prior antibiotics were caused by antibiotic-susceptible bacteria, 84 episodes of late-onset VAP in patients receiving prior antibiotics were mainly caused by potentially resistant bacteria. Differences in the potential efficacies (ranging from 100% to 11%) against microorganisms of 15 antimicrobial regimens were studied according to classification into these four groups. These findings may provide a more rational basis for selecting the initial therapy of patients suspected of having VAP.
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                Author and article information

                Contributors
                miferrer@clinic.ub.es
                difrancescoleonardo@yahoo.it
                mliapikou@yahoo.com
                marianorinaudo@gmail.com
                marco.carbonara@gmail.com
                glibassi@clinic.ub.es
                gabarrus@clinic.ub.es
                +34 93 227 55 49 , ATORRES@clinic.ub.es
                Journal
                Crit Care
                Critical Care
                BioMed Central (London )
                1364-8535
                1466-609X
                23 December 2015
                23 December 2015
                2015
                : 19
                : 450
                Affiliations
                [ ]Department of Pneumology, Thorax Institute, Hospital Clinic, Villarroel 170, 08036 Barcelona, Spain
                [ ]Institut d’Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), Barcelona, Spain
                [ ]Centro de Investigación Biomédica en Red-Enfermedades Respiratorias (CibeRes CB06/06/0028)-Instituto de Salud Carlos III (ISCiii), Madrid, Spain
                [ ]Department of Internal Medicine, Ospedale Sant’Andrea, “Sapienza” University, Via di Grottarossa 1035-1039, Rome, Italy
                [ ]Sotiria Chest Diseases Hospital, 6rd Respiratory Department, Mesogion 152, Athens, Greece
                [ ]Department of Anesthesia, Università degli Studi di Milano, IRCCS Fondazione Ospedale Maggiore Policlinico Cà Granda Milano, Milan, Italy
                Article
                1165
                10.1186/s13054-015-1165-5
                4699341
                26703094
                4cdcfa1d-8662-4b57-b53d-275e746778fc
                © Ferrer et al. 2015

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 23 October 2015
                : 10 December 2015
                Funding
                Funded by: Generalitat Catalunya
                Award ID: 2009-SGR-911
                Funded by: ICREA
                Award ID: ICREA academia 2013
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100004587, Instituto de Salud Carlos III;
                Award ID: Juan de la Cierva 2012 (JCI-2012-14801)
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100006123, Instituto Nacional de Ciência e Tecnologia para o Controle das Intoxicações por Plantas (BR);
                Award ID: (SAF2012-33744)
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100008593, European Respiratory Society ;
                Award ID: ERS Fellowship
                Award Recipient :
                Funded by: CibeRes
                Award ID: CB06/06/0028
                Funded by: IDIBAPS
                Categories
                Research
                Custom metadata
                © The Author(s) 2015

                Emergency medicine & Trauma
                hospital-acquired pneumonia,icu-acquired pneumonia,ventilator-acquired pneumonia,polymicrobial pneumonia

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