Short-term exposure to ambient fine particulate pollution aggravates ventilator-associated pneumonia in pediatric intensive care patients undergoing cardiovascular surgeries.

BACKGROUND: Ambient air pollutants can be hazardous to human health, especially for vulnerable children. The impact of ambient air pollutant exposure before and during intensive care unit (ICU) stays on the development of ventilator-associated pneumonia (VAP) in critically ill children has not been established. We aimed to determine the correlations between short-term exposures to ambient fine particulate matter (PM2.5) and VAP in pediatric cardiac surgery patients in the ICU, and explore the effect of delayed exposure. METHODS: The medical record of 1755 child patients requiring artificial ventilation in the ICU between December 2013 to December 2020, were analyzed. The daily average concentrations of particulate matters (PM2.5 and PM10), sulfur dioxide (SO2), and ozone (O3) were calculated from public data. Interactions between these pollutants and VAP were simulated with the distributed lag non-linear model. RESULTS: Three hundred forty-eight cases (19.829%) of VAP were identified in this study, while the average concentrations of PM2.5, PM10, O3 and SO2 were 58, 118, 98 and 26 µg/m3, respectively. Exposure to increased levels of PM2.5 two days prior (lag 2-day) to VAP diagnosis is significantly correlated with an enhanced risk for VAP development. Even a slight increase of 10 µg/m3 in PM2.5 can translate to a 5.4% increase in VAP incidence (95% CI: 1.4%-9.5%) while the VAP incidence increased to 11.1% (95%CI: 4.5-19.5%) when PM2.5 concentration is well below the National Ambient Air Quality standard (NAAQS) of 50 µg/m3. The association was more pronounced in those aged below 3-months, with low body mass index or suffered from pulmonary arterial hypertension. CONCLUSION: Short-term PM2.5 exposure is a significant risk for development of VAP in pediatric patients. This risk is present even with PM2.5 levels below the NAAQS. Ambient PM2.5 may represent a previously unrecognized risk factor for pneumonia and the current environmental pollution standards need to be reevaluated to consider susceptible populations. TRIAL REGISTRATION: The trial was registered with the National Clinical Trial Center: The correlation between ambient air pollution and the complications in ICU underwent cardiac surgery. TRIAL REGISTRATION NUMBER: ChiCTR2000030507. Date of registration: March 5, 2020. URL of trial registry record: http://www.chictr.org.cn/index.aspx .

Aerosolized antibiotics in the treatment of hospital-acquired pneumonia/ventilator-associated pneumonia.

Aerosolized antibiotics are being increasingly used to treat respiratory infections, especially those caused by drug-resistant pathogens. Their use in the treatment of hospital-acquired pneumonia and ventilator-associated pneumonia in critically ill patients is especially significant. They are also used as an efficient alternative to overcome the issues caused by systemic administration of antibiotics, including the occurrence of drug-resistant strains, drug toxicity, and insufficient drug concentration at the target site. However, the rationale for the use of aerosolized antibiotics is limited owing to their insufficient efficacy and the potential for underestimated risks of developing side effects. Despite the lack of availability of high-quality evidence, the use of aerosolized antibiotics is considered as an attractive alternative treatment approach, especially in patients with multidrug-resistant pathogens. In this review, we have discussed the effectiveness and side effects of aerosolized antibiotics as well as the latest advancements in this field and usage in the Republic of Korea.

Understanding the Concept of Health Care-Associated Pneumonia in Lung Transplant Recipients.

BACKGROUND: Limited data are available regarding the etiologic impact of health care-associated pneumonia (HCAP) in lung transplant recipients. Therefore, our aim was to evaluate the microbiologic differences between HCAP and hospital-acquired pneumonia (HAP)/ventilator-associated pneumonia (VAP) in lung transplant recipients with a radiographically confirmed diagnosis of pneumonia. METHODS: We performed a retrospective cohort study of lung transplant recipients with pneumonia at one transplant center over a 7-year period. Eligible patients included lung transplant recipients who developed a first episode of radiographically confirmed pneumonia ≥ 48 h following transplantation. HCAP, HAP, and VAP were classified according to the American Thoracic Society/Infectious Diseases Society of America 2005 guidelines. χ² and Student t tests were used to compare categorical and continuous variables, respectively. RESULTS: Sixty-eight lung transplant recipients developed at least one episode of pneumonia. HCAP (n = 42; 62%) was most common, followed by HAP/VAP (n = 26; 38%) stratified in HAP (n = 20; 77%) and VAP (n = 6; 23%). Pseudomonas aeruginosa was the predominantly isolated organism (n = 22; 32%), whereas invasive aspergillosis was uncommon (< 10%). Multiple-drug resistant (MDR) pathogens were less frequently isolated in patients with HCAP compared with HAP/VAP (5% vs 27%; P = .009). Opportunistic pathogens were less frequently identified in lung transplant recipients with HCAP than in those with HAP/VAP (7% vs 27%; P = .02). Lung transplant recipients with HCAP had a similar mortality at 90 days (n = 9 [21%] vs n = 4 [15%]; P = .3) compared with patients with HAP/VAP. CONCLUSIONS: HCAP was the most frequent infection in lung transplant recipients. MDR pathogens and opportunistic pathogens were more frequently isolated in HAP/VAP. There were no differences in 30- and 90-day mortality between lung transplant recipients with HCAP and those with HAP/VAP.

Ventilator-associated pneumonia, liver disease and oral chlorhexldine.

As part of the ventilator care bundle, the Department of Health (DH) in the U.K. recommends the use of chlorhexidine (CHX) for oral care to prevent the occurrence of ventilator-associated pneumonia (VAP) in all mechanically ventilated patients. Due to the heterogenous nature of this population, however, it is important to consider whether such recommendations are also relevant to specific critical care patient population groups. This article reviews the available scientific evidence on the use of CHX in the prevention of VAP, with a focus on critically ill mechanically ventilated patients who have liver dysfunction. Findings will be discussed with reference to the wider research literature in order to make recommendations for future practice.

Relationship between inhaled ß2-agonists and ventilator-associated pneumonia: a cohort study.

OBJECTIVE: To determine the impact of aerosolized bronchodilators on ventilator-associated pneumonia. DESIGN: Prospective cohort study. SETTING: A 30-bed medical and surgical intensive care unit. METHODS: All intubated patients requiring mechanical ventilation for >48 hrs were eligible during a 13-month period. Nebulized ß2-agonists were administered at the intensive care unit physician's discretion. Ventilator-associated pneumonia definition included clinical and quantitative microbiological criteria. Only first ventilator-associated pneumonia episodes were analyzed. Risk factors for ventilator-associated pneumonia were determined using univariate and multivariate analyses. The influence of inhaled ß2-agonists on ventilator-associated pneumonia occurrence was also adjusted for confounding factors using Cox's proportional-hazards model. RESULTS: Ventilator-associated pneumonia was diagnosed in 137 (31%) of the 439 enrolled patients. Ventilator-associated pneumonia was early-onset in 14 (10%) patients. The incidence rate of ventilator-associated pneumonia was 20 per 1,000 ventilator days. Ventilator-associated pneumonia was polymicrobial in 16 (11%) patients, and related to multidrug-resistant bacteria in 42 (28%) patients. Most cases of ventilator-associated pneumonia were caused by Gram-negative bacteria. Inhaled ß2-agonists were significantly more frequently used in patients with ventilator-associated pneumonia compared with those without ventilator-associated pneumonia (49% vs. 34%, odds ratio [95% confidence interval] = 1.9 [1.2-2.8], p = .003). Multivariate analysis identified aerosolized ß2-agonists (odds ratio [95% confidence interval] = 1.7 [1.1-2.6], p = .012), Simplified Acute Physiology Score II at intensive care unit admission (odds ratio [95% confidence interval] = 1.01 [1.001-1.02] per point, p = .031), and red blood cell transfusion (odds ratio [95% confidence interval] = 2 [1.3-3.1], p = .001) as independent risk factors for ventilator-associated pneumonia. Cox's proportional-hazards model also identified inhaled ß2-agonists as a risk factor for ventilator-associated pneumonia (odds ratio [95% confidence interval] = 1.52 [1.06-2.19], p = .021). CONCLUSION: Use of aerosolized bronchodilators in intensive care unit mechanically ventilated patients is an independent risk factor for ventilator-associated pneumonia.

Effect of histamine-2-receptor antagonists versus sucralfate on stress ulcer prophylaxis in mechanically ventilated patients: a meta-analysis of 10 randomized controlled trials.

INTRODUCTION: We conducted a meta-analysis in order to investigate the effect of histamine-2-receptor antagonists (H2RA) versus sucralfate on stress ulcer prophylaxis in mechanically ventilated patients in the intensive care unit (ICU). METHODS: A systematic literature search of Medline, EMBASE, Cochrane Central Register of Controlled Trials (1966 to January 2010) was conducted using specific search terms. A review of Web of Science and a manual review of references were also performed. Eligible studies were randomized control trials (RCTs) that compared H2RA and sucralfate for the prevention of stress ulcer in mechanically ventilated patients. Main outcome measures were rates of overt bleeding, clinically important gastrointestinal (GI) bleeding, ventilator-associated pneumonia, gastric colonization and ICU mortality. RESULTS: Ten RCTs with 2,092 participants on mechanical ventilation were identified. Meta-analysis showed there was a trend toward decreased overt bleeding when H2RA was compared with sucralfate (OR = 0.87, 95% CI: 0.49 to 1.53). A total of 12 clinically important GI bleeding events occurred among 667 patients (1.8%) in the H2RA group compared with 26 events among 673 patients (3.9%) in the sucralfate groups. Prophylaxis with sucralfate decreased the incidence of gastric colonization (OR = 2.03, 95% CI: 1.29 to 3.19) and ventilator-associated pneumonia (OR = 1.32, 95% CI: 1.07 to 1.64). Subgroup analysis showed H2RA was not superior to sucralfate in reducing early-onset pneumonia (OR = 0.62, 95%CI: 0.36 to 1.07) but had a higher late-onset pneumonia rate (OR = 4.36, 95%CI: 2.09 to 9.09) relative to sucralfate. No statistically significant reduction was observed in mortality of ICU between groups (OR = 1.08, 95% CI: 0.86 to 1.34). CONCLUSIONS: In patients with mechanical ventilation, H2RA resulted in no differential effectiveness in treating overt bleeding, but had higher rates of gastric colonization and ventilator-associated pneumonia. Additional RCTs of stress ulcer prophylaxis with H2RA and sucralfate are needed to establish the net benefit and risks of adverse effect in mechanically ventilated patients.

Nosocomial pneumonia risk and stress ulcer prophylaxis: a comparison of pantoprazole vs ranitidine in cardiothoracic surgery patients.

BACKGROUND: Stress ulcer prophylaxis (SUP) using ranitidine, a histamine H2 receptor antagonist, has been associated with an increased risk of ventilator-associated pneumonia. The proton pump inhibitor (PPI) pantoprazole is also commonly used for SUP. PPI use has been linked to an increased risk of community-acquired pneumonia. The objective of this study was to determine whether SUP with pantoprazole increases pneumonia risk compared with ranitidine in critically ill patients. METHODS: The cardiothoracic surgery database at our institution was used to identify retrospectively all patients who had received SUP with pantoprazole or ranitidine, without crossover between agents. From January 1, 2004, to March 31, 2007, 887 patients were identified, with 53 patients excluded (pantoprazole, 30 patients; ranitidine, 23 patients). Our analysis compared the incidence of nosocomial pneumonia in 377 patients who received pantoprazole with 457 patients who received ranitidine. RESULTS: Nosocomial pneumonia developed in 35 of the 377 patients (9.3%) who received pantoprazole, compared with 7 of the 457 patients (1.5%) who received ranitidine (odds ratio [OR], 6.6; 95% confidence interval [CI], 2.9 to 14.9). Twenty-three covariates were used to estimate the probability of receiving pantoprazole as measured by propensity score (C-index, 0.77). Using this score, pantoprazole and ranitidine patients were stratified according to their probability of receiving pantoprazole. After propensity adjusted, multivariable logistic regression, pantoprazole treatment was found to be an independent risk factor for nosocomial pneumonia (OR, 2.7; 95% CI, 1.1 to 6.7; p = 0.034). CONCLUSION: The use of pantoprazole for SUP was associated with a higher risk of nosocomial pneumonia compared with ranitidine. This relationship warrants further study in a randomized controlled trial.