: 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.
Coping with cardiovascular diseases (CVD), which are of the main causes of death worldwide, has influenced investigation of high sensitivity CRP (hsCRP) and its role in pathogenesis, prognosis and prevention of CVD. hsCRP can be synthesized in vascular endothelium, atherosclerotic plaques, and theory of inflammatory origin of atherosclerosis is being more widely debated, raising questions, whether higher hsCRP plasma concentration might be the cause or the consequence. Summing up controversial data from multiple studies, guidelines recommend hsCRP testing for both, primary (stratifying CVD risk groups, selecting patients for statin therapy) and secondary CVD prevention (prognosis of CVD and its treatment complications, evaluation of treatment efficacy in moderate CVD risk group). hsCRP testing also has role in heart failure, atrial fibrillation, arterial hypertension, valve pathology and prognosis of coronary stent thrombosis or restenosis. Medications (the well-known and the new specific - CRP binding) affecting its concentration are being investigated as well.
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...
Multidrug-resistant A. baumannii (MDRAB) VAP has high morbidity and mortality, and the rates are constantly increasing globally. Mono- and polybacterial MDRAB VAP might differ, including outcomes. We conducted a single-center, retrospective (January 2014–December 2016) study in the four ICUs (12–18–24 beds each) of a reference Lithuanian university hospital, aiming to compare the clinical features and the 30-day mortality of monobacterial and polybacterial MDRAB VAP episodes. A total of 156 MDRAB VAP episodes were analyzed: 105 (67.5%) were monomicrobial. The 30-day mortality was higher (p < 0.05) in monobacterial episodes: overall (57.1 vs. 37.3%), subgroup with appropriate antibiotic therapy (50.7 vs. 23.5%), and subgroup of XDR A. baumannii (57.3 vs. 36.4%). Monobacterial MDRAB VAP was associated (p < 0.05) with Charlson comorbidity index ≥3 (67.6 vs. 47.1%), respiratory comorbidities (19.0 vs. 5.9%), obesity (27.6 vs. 9.8%), prior hospitalization (58.1 vs. 31.4%), prior antibiotic therapy (99.0 vs. 92.2%), sepsis (88.6 vs. 76.5%), septic shock (51.9 vs. 34.6%), severe hypoxemia (23.8 vs. 7.8%), higher leukocyte count on VAP onset (median [IQR] 11.6 [8.4–16.6] vs. 10.9 [7.3–13.4]), and RRT need during ICU stay (37.1 vs. 17.6%). Patients with polybacterial VAP had a higher frequency of decreased level of consciousness (p < 0.05) on ICU admission (29.4 vs. 14.3%) and on VAP onset (29.4 vs. 11.4%). We concluded that monobacterial MDRAB VAP had different demographic/clinical characteristics compared to polybacterial and carried worse outcomes. These important findings need to be validated in a larger, prospective study, and the management implications to be further investigated.
VAP due to multidrug-resistant (MDR) bacteria is a frequent infection among patients in ICUs. Patient characteristics and mortality in mono- and polybacterial cases of VAP may differ. A single-centre, retrospective 3-year study was conducted in the four ICUs of a Lithuanian referral university hospital, aiming to compare both the clinical features and the 60-day ICU all-cause mortality of monobacterial and polybacterial MDR Klebsiella spp. VAP episodes. Of the 86 MDR Klebsiella spp. VAP episodes analyzed, 50 (58.1%) were polybacterial. The 60-day mortality was higher (p < 0.05) in polybacterial episodes: overall (50.0 vs. 27.8%), in the sub-group with less-severe disease (SOFA < 8) at VAP onset (45.5 vs. 15.0%), even with appropriate treatment (41.7 vs. 12.5%), and the sub-group of extended drug-resistant (XDR) Klebsiella spp. (46.4 vs. 17.6%). The ICU mortality (44.0 vs. 22.5%) was also higher in the polybacterial episodes. The monobacterial MDR Klebsiella spp. VAP was associated (p < 0.05) with prior hospitalization (61.1 vs. 40.0%), diabetes mellitus (30.6 vs. 5.8%), obesity (30.6 vs. 4.7%), prior antibiotic therapy (77.8 vs. 52.0%), prior treatment with cephalosporins (66.7 vs. 36.0%), and SOFA cardiovascular ≥ 3 (44.4 vs. 10.0%) at VAP onset. Patients with polybacterial VAP were more likely (p < 0.05) to be comatose (22.2 vs. 52.0%) and had a higher SAPS II score (median [IQR] 45.0 [35.25–51.1] vs. 50.0 [40.5–60.75]) at VAP onset. Polybacterial MDR Klebsiella spp. VAP had distinct demographic and clinical characteristics compared to monobacterial, and was associated with poorer outcomes.
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