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      Fever after bronchoscopy: serum procalcitonin enables early diagnosis of post-interventional bacterial infection

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          Abstract

          Background

          The aim of this study was to differentiate unspecific and self-limiting fever after bronchoscopy from fever due to infection by using serum procalcitonin, C-reactive protein and neutrophil count. Furthermore, frequency of fever after bronchoscopy and procedures as possible risk factors were evaluated.

          Methods

          Three hundred and fourteen consecutive patients were included. All bronchoscopies were performed using jet-ventilation and general anesthesia. Patients were analyzed according to interventions performed during bronchoscopy and laboratory results. Microbiological assessment was done in patients who developed fever to prove or rule out a bacterial infection.

          Results

          Forty-four patients showed fever within 24 h following bronchoscopy (14%). A bacterial infection was proven in 11 patients with fever (3.5%). Procalcitonin, neutrophil count and C-reactive protein were significantly higher in patients with fever after bronchoscopy compared to non-fever patients. To predict bacterial infection in the receiver operating analysis, procalcitonin had the highest area under the curve (0.942; 95% confidence interval [CI], 0.768 to 1.000; p = <0.001), followed by neutrophil count (AUC, 0.804; 95% CI, 0.606 to 0.946; p = 0.005), whereas CRP levels where not statistically significant. Endoscopic airway recanalization was the only intervention that induced fever more frequently than all other interventions (OR 13.629).

          Conclusions

          Fever is frequently seen after bronchoscopy and in some cases caused by bacterial infection. Procalcitonin might be useful to distinguish a bacterial infection from unspecific self-limiting fever. Airway recanalization is a procedure that seems to induce fever significantly more often than other bronchoscopic interventions.

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          Most cited references30

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          Diagnostic value of procalcitonin, interleukin-6, and interleukin-8 in critically ill patients admitted with suspected sepsis.

          To assess the diagnostic value of procalcitonin (PCT), interleukin (IL)-6, IL-8, and standard measurements in identifying critically ill patients with sepsis, we performed prospective measurements in 78 consecutive patients admitted with acute systemic inflammatory response syndrome (SIRS) and suspected infection. We estimated the relevance of the different parameters by using multivariable regression modeling, likelihood-ratio tests, and area under the receiver operating characteristic curves (AUC). The final diagnosis was SIRS in 18 patients, sepsis in 14, severe sepsis in 21, and septic shock in 25. PCT yielded the highest discriminative value, with an AUC of 0.92 (CI, 0.85 to 1.0), followed by IL-6 (0.75; CI, 0.63 to 0.87), and IL-8 (0.71; CI, 0.59 to 0.83; p < 0.001). At a cutoff of 1.1 ng/ml, PCT yielded a sensitivity of 97% and a specificity of 78% to differentiate patients with SIRS from those with sepsis-related conditions. Median PCT concentrations on admission (ng/ ml, range) were 0.6 (0 to 5.3) for SIRS; 3.5 (0.4 to 6.7) for sepsis; 6.2 (2.2 to 85) for severe sepsis; and 21.3 (1.2 to 654) for septic shock (p < 0.001). The addition of PCT to a model based solely on standard indicators improved the predictive power of detecting sepsis (likelihood ratio test; p = 0.001) and increased the AUC value for the routine value-based model from 0.77 (CI, 0.64 to 0.89) to 0.94 (CI, 0.89 to 0.99; p = 0.002). In contrast, no additive effect was seen for IL-6 (p = 0.56) or IL-8 (p = 0.14). Elevated PCT concentrations appear to be a promising indicator of sepsis in newly admitted, critically ill patients capable of complementing clinical signs and routine laboratory parameters suggestive of severe infection.
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            Procalcitonin for diagnosis of infection and guide to antibiotic decisions: past, present and future

            There are a number of limitations to using conventional diagnostic markers for patients with clinical suspicion of infection. As a consequence, unnecessary and prolonged exposure to antimicrobial agents adversely affect patient outcomes, while inappropriate antibiotic therapy increases antibiotic resistance. A growing body of evidence supports the use of procalcitonin (PCT) to improve diagnosis of bacterial infections and to guide antibiotic therapy. For patients with upper and lower respiratory tract infection, post-operative infections and for severe sepsis patients in the intensive care unit, randomized-controlled trials have shown a benefit of using PCT algorithms to guide decisions about initiation and/or discontinuation of antibiotic therapy. For some other types of infections, observational studies have shown promising first results, but further intervention studies are needed before use of PCT in clinical routine can be recommended. The aim of this review is to summarize the current evidence for PCT in different infections and clinical settings, and discuss the reliability of this marker when used with validated diagnostic algorithms.
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              Expression and secretion of procalcitonin and calcitonin gene-related peptide by adherent monocytes and by macrophage-activated adipocytes.

              To explore the roles of peripheral blood mononuclear cells (PBMCs) and PBMC-derived macrophages in sepsis-related increased procalcitonin and calcitonin gene-related peptide (CGRP) I production. Prospective, in vitro primary human cell culture study and human tissue samples gene expression analysis. University hospital research laboratories. Cells from healthy donors and septic patients. PBMCs were obtained from healthy donors. Isolation of pure monocyte cultures was performed by magnetic depletion of nonmonocyte cells from PBMCs. Adipose tissue biopsies and circulating leukocytes were collected from septic patients. Expressions of calcitonin messenger RNA and CGRP I messenger RNA were analyzed using reverse transcriptase-polymerase chain reaction and quantitative real-time polymerase chain reaction. Supernatant procalcitonin and CGRP protein content were determined by ultrasensitive chemiluminometric and radioimmunoassays, respectively. PBMCs expressed and secreted procalcitonin and CGRP within 3-5 hrs after adherence to endothelial cells or plastic surfaces. This induction was transient, as it was not detectable after 18 hrs. No calcitonin or CGRP I messenger RNA was observed in leukocytes obtained from septic patients with markedly increased serum procalcitonin concentrations. Stimulation with cytokines, endotoxin, or Escherichia coli did not induce expression of calcitonin and CGRP I messenger RNA in PBMC-derived macrophages. However, inflammatory factors released from activated macrophages induced a marked expression of procalcitonin and CGRP in co-cultured human adipocytes. The adhesion-induced, transient expression and secretion of procalcitonin and CGRP in vitro may play an important role during monocyte adhesion and migration in vivo. PBMC-derived macrophages may contribute to the marked increase in circulating procalcitonin by recruiting parenchymal cells within the infected tissue, as exemplified with adipocytes.
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                Author and article information

                Contributors
                klaus.hackner@krems.lknoe.at
                waltraud.riegler@krems.lknoe.at
                sabin.handzhiev@krems.lknoe.at
                rosemarie.bauer@krems.lknoe.at
                jan.veres@krems.lknoe.at
                manuela.speiser@krems.lknoe.at
                karin.meisinger@krems.lknoe.at
                peter.errhalt@krems.lknoe.at
                Journal
                BMC Pulm Med
                BMC Pulm Med
                BMC Pulmonary Medicine
                BioMed Central (London )
                1471-2466
                28 November 2017
                28 November 2017
                2017
                : 17
                : 156
                Affiliations
                [1 ]Department of Pneumonology, Krems University Hospital, Mitterweg 10, Krems, Austria
                [2 ]Karl Landsteiner University of Health Science, Krems, Austria
                Author information
                http://orcid.org/0000-0002-6378-5840
                Article
                508
                10.1186/s12890-017-0508-1
                5704393
                29179755
                7a5b5b78-3012-4097-aa40-f8b03f4bbfe4
                © The Author(s). 2017

                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
                : 6 August 2017
                : 17 November 2017
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2017

                Respiratory medicine
                Respiratory medicine

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