INTRODUCTION:Imipenem‐resistant Pseudomonas aeruginosa resulting from metallo‐β‐lactamases has been reported to be an important cause of nosocomial infection and is a critical therapeutic problem worldwide, especially in the case of bacteremia.OBJECTIVES:To determine the frequency of metallo‐β‐lactamases among imipenem‐resistant Pseudomonas aeruginosa isolates and to compare methods of phenotypic and molecular detection.METHODS:During 2006, 69 imipenem‐resistant Pseudomonas aeruginosa samples were isolated from blood and tested for metallo‐β‐lactamase production using phenotypic methods. Minimal Inhibitory Concentratrions (MIC) (µg/mL) was determined with commercial microdilution panels. Pulsed Field Gel Electrophoresis (PFGE) was performed among metallo‐β‐lactamase producers.RESULTS:Of all the blood isolates, 34.5% were found to be imipenem‐resistant Pseudomonas aeruginosa. Positive phenotypic tests for metallo‐β‐lactamases ranged from 28%‐77%, and Polymerase Chain Reaction (PCR) were positive in 30% (of note, 81% of those samples were blaSPM‐1 and 19% were blaVIM‐2). Ethylenediamine tetracetic acid (EDTA) combinations for the detected enzymes had low kappa values; thus, care should be taken when use it as a phenotypic indicator of MBL. Despite a very resistant antibiogram, four isolates demonstrated the worrisome finding of a colistin MIC in the resistant range. PFGE showed a clonal pattern.CONCLUSION:Metallo‐β‐lactamases among imipenem‐resistant Pseudomonas aeruginosa were detected in 30.4% of imipenem‐resistant Pseudomonas aeruginosa isolates. This number might have been higher if other genes were included. SPM‐1 was the predominant enzyme found. Phenotypic tests with low kappa values could be misleading when testing for metallo‐β‐lactamases. Polymerase Chain Reaction detection remains the gold standard.
Background: We hypothesized that one single episode of acute kidney injury (AKI) reduces long-term survival compared with no acute kidney injury (No AKI) following recovery from critical illness. Materials and methods: A prospective cohort of 2,010 patients admitted to the ICU between 2000 and 2009 at a provincial referral hospital was followed to determine whether AKI influences long-term survival. Results: Of the 1,844 eligible patients, 18.4% had AKI stage 1, 12.1% had stage 2, 26.5% had stage 3, and 43.0% had No AKI, using the KDIGO classification. The mean and median follow-up time was 8.1 and 8.7 years. The 28-day, 1-year, 5-year and 10-year survival rates were 59.6%, 44.9%, 37.4%, and 33.4%, in patients with any AKI (stage 1, stage 2, stage 3), which was significantly worse compared with the critically ill patients with no AKI at any time (P < 0.01). The adjusted 10-year mortality risk associated with AKI was 1.44 (95% CI = 1.2 to 1.7) among 28-day survivors. Patients who had mild AKI (stage 1) had significantly worse survival at 28 days, 1 year, 3 years, 5 years and 10 years compared with No AKI (P < 0.01) (Figure 1A). Patients with sepsis and AKI who survived 28 days had significantly poorer 5-year and 10-year survival compared with nonseptic AKI (P < 0.01) (Figure 1B). Conclusions: Patients with one episode of mild (stage 1) AKI have significantly lower survival rates over 10 years than critically ill patients without AKI. The causes and mechanisms of this association warrant further careful study. Close medical follow-up of these patients may be warranted and mechanistic research required understanding how AKI influences distant events.
Background
Appropriate use of antimicrobials is essential to improve outcomes in sepsis. The aim of this study was to determine whether the use of a rapid molecular blood test—Septi
Fast
(SF) reduces the antibiotic consumption through early de-escalation in patients with nosocomial sepsis compared with conventional blood cultures (BCs).
Methods
This was a prospective, randomized, superiority, controlled trial conducted at Sao Paulo Heart Institute in the period October 2012–May 2016. Adult patients admitted to the hospital for at least 48 h with a diagnosis of nosocomial sepsis underwent microorganism identification by both SF test and BCs. Patients randomized into the intervention group received antibiotic therapy adjustment according to the results of SF. Patients randomized into the control group received standard antibiotic adjustment according to the results of BCs. The primary endpoint was antimicrobial consumption during the first 14 days after randomization.
Results
A total of 200 patients were included (100 in each group). The intention to treat analysis found no significant differences in median antibiotic consumption. In the subgroup of patients with positive SF and blood cultures (19 and 25 respectively), we found a statistically significant reduction in the median antimicrobial consumption which was 1429 (1071–2000) days of therapy (DOT)/1000 patients-day in the intervention group and 1889 (1357–2563) DOT/1000 patients-day in the control group (
p
= 0.017), in the median time of antimicrobial de-escalation (8 versus 54 h—
p
< 0.001), in the duration of antimicrobial therapy (
p
= 0.039) and in anti-gram-positive antimicrobial costs (
p
= 0.002). Microorganism identification was possible in 24.5% of patients (45/184) by SF and 21.2% (39/184) by BC (
p
= 0.45).
Conclusion
This randomized clinical trial showed that the use of a rapid molecular-based pathogen identification test does not reduce the median antibiotic consumption in nosocomial sepsis. However, in patients with positive microbiological tests, the use of Septi
Fast
reduced antimicrobial consumption through early de-escalation compared to conventional blood cultures. These results were driven by a reduction in the consumption of antimicrobials used for Gram-positive bacteria.
Trial registration
The trial was registered at ClinicalTrials.gov (
NCT 01450358
) on 12th October 2011
Electronic supplementary material
The online version of this article (10.1186/s40560-019-0391-3) contains supplementary material, which is available to authorized users.
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