Rate Of Hospital-acquired Pneumonia Research Articles

Evaluating causative agents, mortality factors, and laboratory data of hospital-acquired pneumonia patients.

In the recent years, the increase in death rates from nosocomial pneumonia draws attention. The aim of this study was to examine the causative agents and mortality factors of patients with pneumonia who were followed up in the chest diseases intensive care unit. Data of 1070 patients with pneumonia were screened for this study. A total of 160 patients with hospital-acquired pneumonia included in this study. The relationship between factors such as patients' comorbidities, length of stay in the intensive care unit, history of hospitalization or respiratory support therapy, infection markers such as C-reactive protein, white blood cell, nutritional markers such as albumin and protein, renal and liver function tests, culture growing microorganisms, and clinical pulmonary infection scores was evaluated and mortality rates were examined. Among 1070 patients, the rate of hospital-acquired pneumonia was 14.9%, and the mortality rate of pneumonia was 16.9%. Mortality was significantly increased in patients who stayed in the intensive care unit for more than 10 days, in patients with a clinical pulmonary infection score of ≥6 and with a history of hospitalization in the past one month, and received invasive mechanical ventilation therapy. Mortality increased in patients with hypoalbuminemia, hypoproteinemia, and high C-reactive protein values. The most commonly grown microorganism was Acinetobacter baumannii, which was also found significantly in patients who underwent invasive mechanical ventilation. In the clinical approach to hospital-acquired pneumonia, in order to prevent mortalities, it is important to reveal whether the newly emerging symptoms and signs are related to pneumonia, to identify the causative pathogen, and to determine the severity of the disease.

Decreased duration of intravenous cephalosporins in intensive care unit patients with selective digestive decontamination: a retrospective before-and-after study.

Selective digestive decontamination (SDD) reduces the rate of infection and improves the outcomes of patients admitted to an intensive care unit (ICU). A risk associated with its use is the development of multi-drug-resistant organisms. We hypothesized that a 1-day reduction in systemic antimicrobial exposure in the SDD regimen would not affect the outcomes of our patients. In this before-and-after study design, 199 patients and 248 patients were included in a 3-day SDD group and a 2-day SDD group, respectively. The rates of hospital-acquired pneumonia and ICU infections were similar in both groups. The rates of bloodstream infection and bacteriuria were significantly lower in the 2-day SDD group than in the 3-day SDD group. Compared with the patients in the 3-day group, the patients in the 2-day SDD group received fewer antibiotics and less exposure to mechanical ventilation, and they used fewer ICU resources. The rates of ICU mortality and 28-day mortality were similar in both groups. The incidence of multi-drug-resistant organisms was similar in both groups. Within the limitations inherent to our study design, reducing the exposure of prophylactic systemic antibiotics in the SDD setting from 3 days to 2 days was not associated with impaired outcomes. Future randomized controlled trials should be conducted to test this hypothesis and investigate the effects on the development of multi-drug resistant organisms.Electronic supplementary materialThe online version of this article (10.1007/s10096-020-03966-w) contains supplementary material, which is available to authorized users.

English

The objective of the study is to evaluate the effect of probiotics to reduce the risk of hospital-acquired pneumonia in Pediatric Intensive Care Unit. The study is a double-blinded randomized placebo-controlled study. Patients were evenly and randomly assigned in two groups. The first group was 50 randomly selected patients who formed the placebo group, while the second group was 70 patients selected randomly to form the intervention group that received the probiotic capsules; Lactobacillus rhamnosus strain GG, once a day. The study site was Pediatric Intensive Care Unit in a university-afi¬liated children’s hospital. Fifteen (30%) patients in the placebo population developed hospital-acquired pneumonia. Of the 15 patients, infections in 22% were caused by Gram-negative organisms. In the intervention group, 10% developed hospital-acquired pneumonia. The causative agents were predominantly Gram-negative organisms (22% Gram-negative vs. 7% Gram-positive; P–value; 0.01). After 72 h of study, significantly higher oral and gastric colonization rates were observed in patients who were given placebo treatment, compared with those given Lactobacilli. The current study is the first to report these higher significant variations. The current study found an influence of probiotic supplementation on the rate of hospital-acquired pneumonia. Key words: Peiatric intensive care unit, probiotics, hospital-acquired, pneumonia.

Abstract WP317: Reducing Hospital-acquired Pneumonia Rate in Stroke Patients

Objective: To reduce the hospital-acquired pneumonia rate in stroke patients. Background: The hospital-acquired pneumonia rate for stroke patients at our institution was 6.2% in 2014. This is the 39th percentile for the Joint Commission Comprehensive Stroke Centers in the University HealthSystem Consortium. Our goal was to achieve top decile performance by reducing our hospital-acquired pneumonia rate for stroke patients to 3.0%. Methods: A multidisciplinary team was assembled with representation from administration, coding, nursing, resident physicians, and attending physicians from stroke, neurocritical care and infectious disease. The team analyzed benchmarking data and decided to use chart review to validate the data. The team decided to use the CDC’s definition and clinical criteria for hospital-acquired pneumonia. Further chart review was performed to find information on swallow evaluations, incentive spirometer use, oral care, and head of bed elevation. A coding manager reviewed the documentation and the coding decision for each patient. After results were presented, the team decided on a course of action. Results: Review of stroke patients with hospital-acquired pneumonia showed 44% of the patients coded with pneumonia did not meet the clinical definition on physician review. When reviewed by a coding manager, all coding was found to be correct based on the documentation in the chart. To solve this documentation problem, attending physicians discharging stroke patients were informed of these results about unclear pneumonia documentation and were asked to clarify documentation if the diagnosis was not appropriate. After this change, the hospital acquired pneumonia rate in stroke patients fell from 6.2% prior to the changes from April 2014 to March 2015 to 1.9% after the changes were implemented from April to June 2015. Conclusion: Our facility was able to reduce the rate of hospital-acquired pneumonia in stroke patients from 6.2% to 1.2% through a multidisciplinary approach to achieve more accurate documentation and coding. The widespread over-documentation showed it is clinically difficult to make a diagnosis of pneumonia in this population. Therefore, the rate of hospital-acquired pneumonia is not a valid measure of quality of care.

Etomidate increases susceptibility to pneumonia in trauma patients

To investigate the impact of etomidate on the rate of hospital-acquired pneumonia (HAP) in trauma patients and the effects of hydrocortisone in etomidate-treated patients. This was a sub-study of the HYPOLYTE multi-centre, randomized, double-blind, placebo-controlled trial of hydrocortisone in trauma patients (NCT00563303). Inclusion criterion was trauma patient with mechanical ventilation (MV) of ≥48 h. The use of etomidate was prospectively collected. Endpoints were the results of the cosyntropin test and rate of HAP on day 28 of follow-up. Of the 149 patients enrolled in the study, 95 (64 %) received etomidate within 36 h prior to inclusion. 79 (83 %) of 95 patients receiving etomidate and 34 of the 54 (63 %) not receiving etomidate had corticosteroid insufficiency (p = 0.006). The administration of etomidate did not alter basal cortisolemia (p = 0.73), but it did decrease the delta of cortisolemia at 60 min (p = 0.007). There was a correlation between time from etomidate injection to inclusion in the study and sensitivity to corticotropin (R (2) = 0.19; p = 0.001). Forty-nine (51.6 %) patients with etomidate and 16 (29.6 %) patients without etomidate developed HAP by day 28 (p = 0.009). Etomidate was associated with HAP on day 28 in the multivariate analysis (hazard ratio 2.48; 95 % confidence interval 1.19-5.18; p = 0.016). Duration of MV with or without etomidate was not significantly different (p = 0.278). Among etomidate-exposed patients, 18 (40 %) treated with hydrocortisone developed HAP compared with 31 (62 %) treated with placebo (p = 0.032). Etomidate-exposed patients treated with hydrocortisone had fewer ventilator days (p < 0.001). Among the patients enrolled in the study, etomidate did not alter basal cortisolemia, but it did decrease reactivity to corticotropin. We suggest that in trauma patients, etomidate is an independent risk factor for HAP and that the administration of hydrocortisone should be considered after etomidate use.

The factors affecting noninvasive mechanical ventilation failure in COPD exacerbations

To evaluate causes of noninvasive mechanical ventilation (NIMV) failure. The rate of NIMV failure in respiratory failure due to chronic obstructive pulmonary disease (COPD) exacerbations was reported as 5%-40%. Materials and methods: The necessity of endotracheal intubation was accepted as NIMV failure. The causes of NIMV failure were assessed in 54 patients (45 males; mean age: 67.7 ± 11.0 years) treated with NIMV because of COPD exacerbations and respiratory failure in an intensive care unit (ICU). Results: There was NIMV failure in 20 patients (37.0%). The rates of hospital-acquired pneumonia and in-hospital mortality were higher (P = 0.003 and P = 0.002, respectively) and the duration of ICU stay was longer (P < 0.0001) in patients with NIMV failure. On admission, arterial pH, serum albumin, and Glasgow Coma Scale levels were lower (P = 0.032, P = 0.024, and P = 0.013, respectively) in the NIMV failure group. Arterial pH was lower (P = 0.039) and respiratory rate was higher (P = 0.010) after 1 h, and the PaO2/FiO2 rate was lower (P = 0.017) and respiratory and heart rates were higher (P = 0.002 and P = 0.020, respectively) after 3 h in the NIMV failure group. Conclusion: The present data strongly suggest that baseline and follow-up clinical and arterial blood gas evaluations can give important clues about NIMV failure in COPD exacerbations.

Steroids After Severe Injury

N THIS ISSUE OF JAMA ,R OQUILLY AND COLLEAGUES 1 report the results of the HYPOLYTE (Hydrocortisone Polytraumatise) study, a randomized controlled trial of early hydrocortisone administration to severely injured patients with a primary outcome of hospital-acquired pneumonia within 28 days of injury. All patients were given a short corticotrophin stimulation test, and those meeting their definition of corticosteroid insufficiency continued taking the blinded study treatment, while all other patients had study treatment discontinued. All patients were followed up for the clinical outcomes, and both an intentionto-treat and modified intention-to-treat analysis were conducted. Patients in the hydrocortisone group were found to have significant reduction in pneumonia risk (35.6% vs 51.3%) and a shorter duration of mechanical ventilation (ventilator-free days, 16 days vs 12 days). This study has many strengths including the randomized, placebocontrolled, blinded design, strict definition of the clinical outcome including bronchoalveolar lavage to confirm the diagnosis of pneumonia, and corticotrophin stimulation testing for all patients. Even though the authors demonstrated a significant reduction in the rate of hospital-acquired pneumonia and a reduction in ventilator days, this study, with a sample size of 149 patients, was not adequately powered to assess the effects of steroid on mortality in this patient population. There was no statistical difference in mortality between the 2 treatment groups, although the absolute mortality was higher in the hydrocortisone group (6 deaths, 8.2% vs 4 deaths, 5.3%). Previous studies of steroid administration suggest the need for caution in the interpretation of these results. The prior Corticosteroid Randomization After Significant Head Injury (CRASH) trial, 2 which randomized more than 10000 patients with traumatic brain injury to administration of methylprednisolone for 48 hours early after injury, demonstrated a higher mortality in the steroidtreated group (relative risk, 1.15; 95% confidence interval, 1.07-1.24), but found no difference in the rate of pneumonia between treatment groups. In a trial by Steinberg et al, 3 administration of methylprednisolone to patients with acute respiratory distress syndrome (ARDS) resulted in lower rates of suspected or probable pneumonia in the steroid-treated group but resulted in a significantly higher 60-day mortality for patients given steroids more than 14 days after the onset of ARDS. Although the dosage strategies and timing were different in these studies compared with those in the HYPOLYTE study, the overall evidence suggests that further study with a larger sample size is needed to better define the safety profile and risk of mortality in this patient population. There have been several reports of adrenal insufficiency after severe injury based on corticotrophin stimulation testing; however, comparison between studies is limited by variability in the definition of critical illness–related corticosteroid insufficiency. 4-7 In the HYPOLYTE study, the definition of corticosteroid insufficiency was based on a basal cortisol level of less than 15 µg/dL or a maximal increase of less than 9 µg/dL following a corticotrophin stimulation test. The consensus conference definition of corticosteroid insufficiency is based on patients who are hypotensive and have responded poorly to fluid resuscitation or vasopressor agents, primarily in the setting of sepsis. 8 The recommended threshold for diagnosis in this patient population is a random total cortisol less than 10 µg/dL or maximal increase of less than 9 µg/dL following a corticotrophin stimulation test. 8 The increasing use of etomidate for intubation in critically ill patients also challenges the true incidence of corticosteroid insufficiency because early assessment of adrenal function may be limited by drug-induced adrenal suppression. 5 Roquilly et al 1 acknowledge that further studies are needed to better define the true incidence of corticosteroid insufficiency in severely injured patients. Additional studies also are needed to better define the effectsofearlysteroidadministrationontheinflammatoryresponse of patients following severe injury. Traditional understanding of the immune-inflammatory response after