Assessment of knowledge and implementation practices of the ventilator acquired pneumonia (VAP) bundle in the intensive care unit of a private hospital
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ABSTRACT: Supplementary Information
The online version contains supplementary material available at 10.1186/s13756-021-01027-1.
SUBMITTER: Abad C
PROVIDER: S-EPMC8587499 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:OBJECTIVES:To study the incidence, etiology and risk factors associated with ventilator associated pneumonia (VAP) in children. METHODS:This prospective cohort study was conducted on patients admitted to the Pediatric Intensive Care Unit (PICU) of a tertiary care institute of North India, from June 2012 through March 2014, who received mechanical ventilation for more than 24 h. All enrolled children were assessed daily for development of ventilator associated pneumonia (VAP) using the case definition given by Centers for Disease Control and Prevention (CDC). Chest radiograph and microbiologic samplings were performed in children suspected to have VAP. Risk factors associated with VAP were calculated by doing bivariate and multivariate analysis. RESULTS:A total of 128 patients were screened and 86 were enrolled (median age 30 mo 95% CI 4.0-84.0; 72% boys). The most common admitting diagnosis was sepsis (16%) followed by acyanotic congenital heart disease with pneumonia (14%) and the most common indication for ventilation was respiratory failure (45.3%). The incidence of VAP according to CDC criteria was 38.4%, while the incidence of microbiologically confirmed VAP was 24.4%. The incidence of ventilator associated tracheobronchitis (VAT) was found to be 11.6%. Acinetobacter was the most frequently isolated organism (47%) followed by Pseudomonas (28%), Klebsiella (15%), E. coli (5%) and Enterobacter (5%). Risk factors for VAP on bivariate analysis were use of proton pump inhibitor (PPI) (p?=?0.027, OR 5.2, 95% CI 1.1-24.3), enteral feeding (p?<?0.001, OR 6.5, 95% CI 2.1-19.4) and re-intubation (p?=?0.024, OR 3.3 and 95% CI 1.1-9.6). On multivariate analysis, use of PPI (p?=?0.03, OR 8.47, 95% CI 1.19-60.33) and enteral feeding (p?<?0.001, OR 12.2, 95% CI 2.58-57.78) were identified as independent risk factors for VAP. CONCLUSIONS:Ventilator associated pneumonia is an important complication in children receiving mechanical ventilation in PICU and Gram negative bacilli (Acinetobacter and Pseudomonas) being the important causative agents. Ventilator associated tracheobronchitis is an emerging entity; recognition and treatment of same might prevent the development of VAP.
| S-EPMC7101689 | biostudies-literature
Project description:Among hospital-acquired infections (HAIs) in children, ventilator-associated pneumonia (VAP) is the most common after blood stream infection (BSI). VAP can prolong length of ventilation and hospitalization, increase mortality rate, and directly change a patient's outcome in Pediatric Intensive Care Units (PICU).The research on VAP in children is limited, especially in Iran; therefore, the identification of VAP incidence and mortality rate will be important for both clinical and epidemiological implications.Mechanically ventilated pediatric patients were assessed for development of VAP during hospital course on the basis of clinical, laboratory and imaging criteria. We matched VAP group with control group for assessment of VAP related mortality in the critically ill ventilated children.VAP developed in 22.9% of critically ill children undergoing mechanical ventilation. Early VAP and late VAP were found in 19.3% and 8.4% of VAP cases, respectively. Among the known VAP risk factors that were investigated, immunodeficiency was significantly greater in the VAP group (p = 0.014). No significant differences were found between the two groups regarding use of corticosteroids, antibiotics, PH (potential of hydrogen) modifying agents (such as ranitidine or pantoprazole), presence of nasogastric tube and total or partial parenteral nutrition administration. A substantial number of patients in the VAP group had more than four risk factors for development of VAP, compared to those without VAP (p = 0.087). Mortality rate was not statistically different between the VAP and control groups (p = 0.477).VAP is still one of the major causes of mortality in PICUs. It is found that altered immune status is a significant risk factor for acquiring VAP. Also, occurrence of VAP was high in the first week after admission in PICU.
| S-EPMC5532548 | biostudies-other
Project description:IntroductionThe efficacy and safety of telavancin versus vancomycin in microbiologically evaluable patients with hospital-acquired or ventilator-associated pneumonia (HAP/VAP) caused by Staphylococcus aureus with vancomycin minimum inhibitory concentration (MIC) ≥ 1.0 µg/mL was analyzed using data derived from previously reported Assessment of Telavancin for Treatment of Hospital-Acquired Pneumonia (ATTAIN) trials.MethodsThis post hoc subgroup analysis of two randomized, double-blind, comparator-controlled, parallel-group phase 3 trials conducted at 274 sites in 38 countries included 194 microbiologically evaluable patients with HAP/VAP caused by monomicrobial S. aureus with vancomycin MIC ≥ 1.0 µg/mL. Patients received intravenous telavancin (10 mg/kg every 24 h) or intravenous vancomycin (1 g every 12 h with site-specific modifications) for 7-21 days. Efficacy was assessed by clinical cure, defined as improvement or non-progression of radiographic findings at end of treatment and resolution of pneumonia signs and symptoms at follow-up/test-of-cure visits, and survival 28 days post-randomization. Safety was assessed from categorical shifts in creatinine clearance during therapy and adverse events (AEs).ResultsClinical cure rates were numerically greater following telavancin versus vancomycin treatment overall (85.4% vs. 74.3%; treatment difference [95% confidence interval (CI)], 11.1% [- 0.002%, 22.2%]) and in patients aged ≥ 65 years (81.6% vs. 66.2%; treatment difference [95% CI], 15.5% [- 0.9%, 30.2%]) patients with VAP (92.3% vs. 47.6%; treatment difference [95% CI], 44.7% [18.1%, 64.9%]), and patients with baseline Acute Physiology And Chronic Health Evaluation II score ≥ 20 (71.4% vs. 55.6%; treatment difference [95% CI], 15.9% [- 11.7%, 40.5%]). Renal function declined in 7 (7.9%) patients receiving telavancin and 6 (5.7%) patients receiving vancomycin. Survival proportion was numerically higher (85.2% vs. 80.2%; treatment difference [95% CI], 5.0% [- 5.8%, 15.8%]) and AEs were comparable in patients treated with telavancin versus vancomycin.ConclusionTelavancin is an alternative to vancomycin for HAP/VAP caused by S. aureus with vancomycin MIC ≥ 1 µg/mL.FundingTheravance Biopharma R&D, Inc., South San Francisco, CA, USA.
| S-EPMC6702499 | biostudies-literature
Project description:BackgroundVentilator associated pneumonia (VAP) caused by more than one microorganisms is not uncommon and may be potentially challenging, but the relevant data is scarce in ventilated neonates. We aimed to investigate the clinical characteristics and outcomes of polymicrobial VAP in the neonatal intensive care unit (NICU).MethodsAll neonates with definite diagnosis of VAP from a tertiary level neonatal intensive care unit (NICU) in Taiwan between October 2017 and September 2020 were prospectively observed and enrolled for analyses. All clinical features, therapeutic interventions and outcomes were compared between the polymicrobial VAP and monomicrobial VAP episodes. Multivariate regression analyses were used to find the independent risk factors for treatment failure.ResultsAmong 236 episodes of neonatal VAP, 60 (25.4%) were caused by more than one microorganisms. Polymicrobial VAP episodes were more likely to be associated with multidrug-resistant pathogens (53.3% versus 34.7%, P = 0.014), more often occurred in later days of life and in neonates with prolonged intubation and underlying bronchopulmonary dysplasia. Otherwise most clinical characteristics of polymicrobial VAP were similar to those of monomicrobial VAP. The therapeutic responses and treatment outcomes were also comparable between these two groups, although modification of therapeutic antibiotics were significantly more common in polymicrobial VAP episodes than monomicrobial VAP episodes (63.3% versus 46.2%; P < 0.001). None of any specific pathogens was significantly associated with worse outcomes. Instead, it is the severity of illness, including presence of concurrent bacteremia, septic shock, and requirement of high-frequency oscillatory ventilator and underlying neurological sequelae that are independently associated with treatment failure.ConclusionsPolymicrobial VAP accounted for 25.4% of all neonatal VAP in the NICU, and frequently occurred in neonates with prolonged intubation and underlying bronchopulmonary dysplasia. In our cohort, most clinical features, therapeutic responses and final outcomes of neonates with monomicrobial and polymicrobial VAP did not differ significantly.
| S-EPMC8446475 | biostudies-literature
Project description:Data on the relationship between antimicrobial resistance and mortality remain scarce, and this relationship needs to be investigated in intensive care units (ICUs). The aim of this study was to compare the ICU mortality rates between patients with ICU-acquired pneumonia due to highly antimicrobial-resistant (HAMR) bacteria and those with ICU-acquired pneumonia due to non-HAMR bacteria. We conducted a multicenter, retrospective cohort study using the French National Surveillance Network for Healthcare Associated Infection in ICUs ("REA-Raisin") database, gathering data from 200 ICUs from January 2007 to December 2016. We assessed all adult patients who were hospitalized for at least 48 h and presented with ICU-acquired pneumonia caused by S. aureus, Enterobacteriaceae, P. aeruginosa, or A. baumannii. The association between pneumonia caused by HAMR bacteria and ICU mortality was analyzed using the whole sample and using a 1:2 matched sample. Among the 18,497 patients with at least one documented case of ICU-acquired pneumonia caused by S. aureus, Enterobacteriaceae, P. aeruginosa, or A. baumannii, 3081 (16.4%) had HAMR bacteria. The HAMR group was associated with increased ICU mortality (40.3% vs. 30%, odds ratio (OR) 95%, CI 1.57 [1.45-1.70], P < 0.001). This association was confirmed in the matched sample (3006 HAMR and 5640 non-HAMR, OR 95%, CI 1.39 [1.27-1.52], P < 0.001) and after adjusting for confounding factors (OR ranged from 1.34 to 1.39, all P < 0.001). Our findings suggest that ICU-acquired pneumonia due to HAMR bacteria is associated with an increased ICU mortality rate, ICU length of stay, and mechanical ventilation duration.
| S-EPMC8363636 | biostudies-literature
Project description:Ventilator associated pneumonia (VAP) is the 2nd most common hospital acquired infection associated with high morbidity, mortality and increased hospitalization. Current practice of diagnosis is based on clinical symptoms and bronchoalvolar lavage (BAL) culture. The procedures of BAL collections are invasive whereas, endotracheal aspirate (ETA), a matrix of upper airway collection is minimally invasive and underexplored in VAP diagnosis. The study describes first in detail characterization of proteome of longitudinal ETA collections from 16 intubated patients including 11 VAP patients and explores potential utility of ETA in VAP diagnosis.
2020-07-27 | PXD010715 | Pride
Project description:Alarm fatigue is a well-recognized patient safety concern in intensive care settings. Decreased nurse responsiveness and slow response times to alarms are the potentially dangerous consequences of alarm fatigue. The aim of this study was to determine the factors that modulate nurse responsiveness to critical patient monitor and ventilator alarms in the context of a private room neonatal intensive care setting.The study design comprised of both a questionnaire and video monitoring of nurse-responsiveness to critical alarms. The Likert scale questionnaire, comprising of 50 questions across thematic clusters (critical alarms, yellow alarms, perception, design, nursing action, and context) was administered to 56 nurses (90% response rate). Nearly 6000 critical alarms were recorded from 10 infants in approximately 2400 hours of video monitoring. Logistic regression was used to identify patient and alarm-level factors that modulate nurse-responsiveness to critical alarms, with a response being defined as a nurse entering the patient's room within the 90s of the alarm being generated.Based on the questionnaire, the majority of nurses found critical alarms to be clinically relevant even though the alarms did not always mandate clinical action. Based on video observations, for a median of 34% (IQR, 20-52) of critical alarms, the nurse was already present in the room. For the remaining alarms, the response rate within 90s was 26%. The median response time was 55s (IQR, 37-70s). Desaturation alarms were the most prevalent and accounted for more than 50% of all alarms. The odds of responding to bradycardia alarms, compared to desaturation alarms, were 1.47 (95% CI = 1.21-1.78; <0.001) while that of responding to a ventilator alarm was lower at 0.35 (95% CI = 0.27-0.46; p <0.001). For every 20s increase in the duration of an alarm, the odds of responding to the alarm (within 90s) increased to 1.15 (95% CI = 1.1-1.2; p <0.001). The random effect per infant improved the fit of the model to the data with the response times being slower for infants suffering from chronic illnesses while being faster for infants who were clinically unstable.Even though nurses respond to only a fraction of all critical alarms, they consider the vast majority of critical and yellow alarms as useful and relevant. When notified of a critical alarm, they seek waveform information and employ heuristics in determining whether or not to respond to the alarm.Amongst other factors, the category and duration of critical alarms along with the clinical status of the patient determine nurse-responsiveness to alarms.
| S-EPMC5628801 | biostudies-literature
Project description:BACKGROUND:There is little descriptive data on Stenotrophomonas maltophilia hospital-acquired pneumonia (HAP) in critically ill patients. The optimal modalities of antimicrobial therapy remain to be determined. Our objective was to describe the epidemiology and prognostic factors associated with S. maltophilia pneumonia, focusing on antimicrobial therapy. METHODS:This nationwide retrospective study included all patients admitted to 25 French mixed intensive care units between 2012 and 2017 with hospital-acquired S. maltophilia HAP during intensive care unit stay. Primary endpoint was time to in-hospital death. Secondary endpoints included microbiologic effectiveness and antimicrobial therapeutic modalities such as delay to appropriate antimicrobial treatment, mono versus combination therapy, and duration of antimicrobial therapy. RESULTS:Of the 282 patients included, 84% were intubated at S. maltophilia HAP diagnosis for duration of 11 [5-18] days. The Simplified Acute Physiology Score II was 47 [36-63], and the in-hospital mortality was 49.7%. Underlying chronic pulmonary comorbidities were present in 14.1% of cases. Empirical antimicrobial therapy was considered effective on S. maltophilia according to susceptibility patterns in only 30% of cases. Delay to appropriate antimicrobial treatment had, however, no significant impact on the primary endpoint. Survival analysis did not show any benefit from combination antimicrobial therapy (HR = 1.27, 95%CI [0.88; 1.83], p = 0.20) or prolonged antimicrobial therapy for more than 7 days (HR = 1.06, 95%CI [0.6; 1.86], p = 0.84). No differences were noted in in-hospital death irrespective of an appropriate and timely empiric antimicrobial therapy between mono- versus polymicrobial S. maltophilia HAP (p = 0.273). The duration of ventilation prior to S. maltophilia HAP diagnosis and ICU length of stay were shorter in patients with monomicrobial S. maltophilia HAP (p = 0.031 and p = 0.034 respectively). CONCLUSIONS:S. maltophilia HAP occurred in severe, long-stay intensive care patients who mainly required prolonged invasive ventilation. Empirical antimicrobial therapy was barely effective while antimicrobial treatment modalities had no significant impact on hospital survival. TRIAL REGISTRATION:clinicaltrials.gov, NCT03506191.
| S-EPMC6873544 | biostudies-literature
Project description:Community-acquired pneumonia (CAP) is a major cause of sepsis. Despite several clinical trials targeting components of the inflammatory response, no specific treatment other than antimicrobial therapy has been approved. This argued for a deeper understanding of sepsis immunopathology, in particular factors that can modulate the host response. Small non-coding RNA, for example, micro (mi)RNA, have been established as important modifiers of cellular phenotypes. Notably, miRNAs are not exclusive to the intracellular milieu but have also been detected extracellular in the circulation with functional consequences. Here, we sought to determine shifts in circulatory small RNA levels of critically ill patients with CAP-associated sepsis and to determine the influence of clinical severity and causal pathogens on small RNA levels. Blood plasma was collected from 13 critically ill patients with sepsis caused by CAP on intensive care unit admission and from 5 non-infectious control participants. Plasma small RNA-sequencing identified significantly altered levels of primarily mature miRNAs in CAP relative to controls. Pathways analysis of high or low abundance miRNA identified various over-represented cellular biological pathways. Analysis of small RNA levels against common clinical severity and inflammatory parameters indices showed direct and indirect correlations. Additionally, variance of plasma small RNA levels in CAP patients may be explained, at least in part, by differences in causal pathogens. Small nuclear RNA levels were specifically altered in CAP due to Influenza infection in contrast to Streptococcus pneumoniae infection. Pathway analysis of plasma miRNA signatures unique to Influenza or Streptococcus pneumoniae infections showed enrichment for specific proteoglycan, cell cycle, and immunometabolic pathways.
| S-EPMC8358855 | biostudies-literature
Project description: Not available
| S-BSST810 | biostudies-other