: Background and objectives: High mortality and healthcare costs area associated with ventilator-associated pneumonia (VAP) due to Acinetobacter baumannii (A.baumannii). The data concerning the link between multidrug-resistance of A.baumannii strains and outcomes remains controversial. Therefore, we aimed to identify the relation of risk factors for ventilator-associated pneumonia (VAP) and mortality with the drug resistance profiles of Acinetobacter baumannii (A.baumannii) and independent predictors of in-hospital mortality. Methods: A retrospective ongoing cohort study of 60 patients that were treated for VAP due to drug-resistant A.baumannii in medical-surgical intensive care units (ICU) over a two-year period was conducted. Results: The proportions of multidrug-resistant (MDR), extensively drug-resistant (XDR), and potentially pandrug-resistant (pPDR) A.baumannii were 13.3%, 68.3%, and 18.3%, respectively. The SAPS II scores on ICU admission were 42.6, 48.7, and 49 (p = 0.048); hospital length of stay (LOS) prior to ICU was 0, one, and two days (p = 0.036), prior to mechanical ventilation (MV)—0, 0, and three days (p = 0.013), and carbapenem use prior to VAP—50%, 29.3%, and 18.2% (p = 0.036), respectively. The overall in-hospital mortality rate was 63.3%. In MDR, XDR, and pPDR A.baumannii VAP groups, it was 62.5%, 61.3%, and 72.7% (p = 0.772), respectively. Binary logistic regression analysis showed that female gender (95% OR 5.26; CI: 1.21–22.83), SOFA score on ICU admission (95% OR 1.28; CI: 1.06–1.53), and RBC transfusion (95% OR 5.98; CI: 1.41–25.27) were all independent predictors of in-hospital mortality. Conclusions: The VAP risk factors: higher SAPS II score, increased hospital LOS prior to ICU, and MV were related to the higher resistance profile of A.baumannii. Carbapenem use was found to be associated with the risk of MDR A.baumannii VAP. Mortality due to drug-resistant A.baumannii VAP was high, but it was not associated with the A.baumannii resistance profile. Female gender, SOFA score, and RBC transfusion were found to be independent predictors of in-hospital mortality.

The aim of our study was to determine the prevalence of Pseudomonas aeruginosa bacteremia, risk factors, and outcome of patients treated at the Hospital of Kaunas University of Medicine.Material and methods. All hospitalized patients with blood culture positive for Pseudomonas aeruginosa during the 5-year period were included. A retrospective data analysis was performed to evaluate patients' risk factors and mortality caused by P. aeruginosa bacteremia.Results. A total of 47 (58.8%) bacteremia episodes occurred in an intensive care unit (ICU). A primary source of bacteremia was identified in 50 (62.5%) episodes. Overall mortality rate was 58.8%. Univariate risk factors analysis showed the factors, which significantly increased the risk of death: mechanical ventilation (13.67 times, P<0.001), patient hospitalization in the ICU (8.51 times, P<0.001), acute respiratory failure (8.44 times, P<0.001), infection site in the respiratory tract (4.93 times, P=0.003), and central vein catheter (4.44 times, P=0.002). Timely and appropriate treatment and surgery were significant protective factors for 30-day mortality (11.1 and 5.26 times, respectively; P=0.001). Meropenem-resistant Pseudomonas aeruginosa strains caused bacteremia more frequently in patients older than 65 years than meropenem-sensitive strains (57.9%, n=11). All 19 patients with meropenem-resistant Pseudomonas aeruginosa bacteremia received inappropriate empirical antibiotic therapy.Conclusions. Treatment at the intensive care unit, mechanical ventilation, acute respiratory failure, source of infection in respiratory tract, and central vein catheter are the major risk factors associated with an increased mortality rate in patients with Pseudomonas aeruginosa bacteremia.The patients older than 65 years are at increased risk for bacteremia caused by carbapenemresistant Pseudomonas aeruginosa strains.Carbapenems are not antibiotics of the choice of treatment for Pseudomonas aeruginosa bacteremia at Raktažodžiai: Pseudomonas aeruginosa, bakteriemija, rizikos veiksniai.Santrauka. Tyrimo tikslas. Nustatyti pacientų, gydytų Kauno medicinos universiteto klinikose, Pseudomonas aeruginosa sukeltos bakteriemijos dažnį, šių pacientų rizikos veiksnius ir mirštamumą.Tyrimo metodai. Į tyrimą įtraukti visi pacientai, kuriems penkerių metų laikotarpiu iš kraujo buvo išaugintos Pseudomonas aeruginosa padermės. Atlikta retrospektyvioji šių pacientų duomenų analizė, siekiant nustatyti rizikos veiksnius ir su bakteriemija susijusį mirštamumą.Rezultatai. 47 (58,8 proc.) bakteriemijos epizodai buvo nustatyti intensyviosios terapijos skyriuose gydytiems pacientams. Pirminis bakteriemijos židinys buvo nustatytas 50 (62,5 proc.) pacientų. Pacientų mirštamumas -58,8 proc. Mirštamumo riziką statistiškai patikimai didino: dirbtinė plaučių ventiliacija -13,67 karto (p<0,001), pacientų būklė, kai būtinas gydymas intensyviosios terapijos skyriuje -8,51 karto (p<0,001), ūminis kvėpavimo nepakankamumas -8,44 karto (p<0,001), infekcijos židinys kvėpavimo takuose -4,93 karto (p=0,003) ir centr...

Critical Care 2017, 21(Suppl 1):P349 Introduction Imbalance in cellular energetics has been suggested to be an important mechanism for organ failure in sepsis and septic shock. We hypothesized that such energy imbalance would either be caused by metabolic changes leading to decreased energy production or by increased energy consumption. Thus, we set out to investigate if mitochondrial dysfunction or decreased energy consumption alters cellular metabolism in muscle tissue in experimental sepsis. Methods We submitted anesthetized piglets to sepsis (n = 12) or placebo (n = 4) and monitored them for 3 hours. Plasma lactate and markers of organ failure were measured hourly, as was muscle metabolism by microdialysis. Energy consumption was intervened locally by infusing ouabain through one microdialysis catheter to block major energy expenditure of the cells, by inhibiting the major energy consuming enzyme, N+/K + -ATPase. Similarly, energy production was blocked infusing sodium cyanide (NaCN), in a different region, to block the cytochrome oxidase in muscle tissue mitochondria. Results All animals submitted to sepsis fulfilled sepsis criteria as defined in Sepsis-3, whereas no animals in the placebo group did. Muscle glucose decreased during sepsis independently of N+/K + -ATPase or cytochrome oxidase blockade. Muscle lactate did not increase during sepsis in naïve metabolism. However, during cytochrome oxidase blockade, there was an increase in muscle lactate that was further accentuated during sepsis. Muscle pyruvate did not decrease during sepsis in naïve metabolism. During cytochrome oxidase blockade, there was a decrease in muscle pyruvate, independently of sepsis. Lactate to pyruvate ratio increased during sepsis and was further accentuated during cytochrome oxidase blockade. Muscle glycerol increased during sepsis and decreased slightly without sepsis regardless of N+/K + -ATPase or cytochrome oxidase blocking. There were no significant changes in muscle glutamate or urea during sepsis in absence/presence of N+/K + -ATPase or cytochrome oxidase blockade. ConclusionsThese results indicate increased metabolism of energy substrates in muscle tissue in experimental sepsis. Our results do not indicate presence of energy depletion or mitochondrial dysfunction in muscle and should similar physiologic situation be present in other tissues, other mechanisms of organ failure must be considered. , and long-term follow up has shown increased fracture risk [2]. It is unclear if these changes are a consequence of acute critical illness, or reduced activity afterwards. Bone health assessment during critical illness is challenging, and direct bone strength measurement is not possible. We used a rodent sepsis model to test the hypothesis that critical illness causes early reduction in bone strength and changes in bone architecture. Methods 20 Sprague-Dawley rats (350 ± 15.8g) were anesthetised and randomised to receive cecal ligation and puncture (CLP) (50% cecum length, 18G needle single pass through anterior and posterior wa...

Intensive care unit stay before infection and source of infection in the respiratory tract were independently associated with patient mortality. Resistance to carbapenems had no impact on mortality rates. Carbapenem-resistant Acinetobacter spp. isolates had high resistance rates to other antimicrobial drugs.

The aim of this study was to determine the characteristics of carbapenem-resistant Pseudomonas aeruginosa (P. aeruginosa) strains and 5-year changes in resistance in a tertiary university hospital. Material and Methods. The study included 90 and 101 randomly selected P. aeruginosa strains serotyped in 2003 and 2008, respectively. The standardized disk diffusion test and E-test were used to determine resistance to antibiotics. P. aeruginosa strains were considered to have high-level resistance if a minimum inhibitory concentration (MIC) for imipenem or meropenem was >32 μg/mL. To identify serogroups, sera containing specific antibodies against O group antigens of P. aeruginosa were used. P. aeruginosa isolates resistant to imipenem or/and meropenem were screened for metallo-β-lactamase (MBL) production by using the MBL E-test. Results. Comparison of the changes in resistance of P. aeruginosa strains to carbapenems within the 5-year period revealed that the level of resistance to imipenem increased. In 2003, 53.3% of P. aeruginosa strains were found to be highly resistant to imipenem, while in 2008, this percentage increased to 87.8% (P=0.01). The prevalence of MBL-producing strains increased from 15.8% in 2003 to 61.9% in 2008 (P<0.001). In 2003 and 2008, carbapenem-resistant P. aeruginosa strains were more often resistant to ciprofloxacin and gentamicin than carbapenem-sensitive strains. In 2008, carbapenem- resistant strains additionally were more often resistant to ceftazidime, cefepime, aztreonam, piperacillin, and amikacin than carbapenem-sensitive strains. MBL-producing P. aeruginosa strains belonged more often to the O:11 serogroup than MBL-non-producing strains (51.7% vs. 34.3%, P<0.05). A greater percentage of non-MBL-producing strains had low MICs against ciprofloxacin and amikacin as compared with MBL-producing strains. Conclusions. The results of our study emphasize the need to restrict the spread of O:11 serogroup P. aeruginosa strains and usage of carbapenems to treat infections with P. aeruginosa in the intensive care units of our hospital