The local hospital milieu and healthcare-associated vancomycin-resistant enterococcus acquisition.

BACKGROUND: Vancomycin-resistant enterococcus (VRE) causes 4% of all healthcare-associated infections in the USA. The process by which the local hospital milieu contributes to VRE acquisition is not fully understood. AIM: To determine the importance of specific factors within the local hospital environment for healthcare-associated VRE acquisition. METHODS: This retrospective cohort study included patients admitted to six intensive care units at an academic medical centre from January 2012 to December 2016 with negative rectal VRE cultures on admission. VRE acquisition was defined as a positive surveillance swab performed at any time after the initial negative swab during the index hospitalization. The exposures of interest were VRE colonization pressure, VRE importation pressure, and use of vancomycin. Multivariable Cox proportional hazards modelling was performed, with patients followed until VRE acquisition, death, or for up to 30 days. FINDINGS: Of 8485 patients who were initially VRE negative, 161 patients acquired VRE. On univariate analysis, patients with VRE acquisition were more likely to have received vancomycin, to have had a neighbouring patient who received vancomycin, to have high VRE importation pressure, or to have high VRE colonization pressure. On multivariable analysis, only high VRE colonization pressure was an independent predictor of VRE acquisition (adjusted hazard ratio: 1.79; 95% confidence interval: 1.19-2.70). CONCLUSION: VRE colonization pressure was the most important risk factor for healthcare-associated VRE acquisition, regardless of VRE importation pressure. Interventions seeking to reduce VRE acquisition should focus on minimizing transmission between patients with known VRE and the local hospital environment.

Methods for identifying suicide or suicidal ideation in EHRs.

Electronic health records contain important data elements for detection of novel adverse drug reactions, genotype/phenotype identification and psychosocial factor analysis, and the role of each of these as risk factors for suicidality warrants further investigation. Suicide and suicidal ideation are documented in clinical narratives. The specific purpose of this study was to define an algorithm for automated detection of this serious event. We found that ICD-9 E-Codes had the lowest positive predictive value: 0.55 (90% CI: 0.42-0.67), while combining ICD-9 and NLP had the best PPV: 0.97 (90% CI: 0.92-0.99). A qualitative analysis and classification of the types of errors by ICD-9 and NLP automated coding compared to manual review are also discussed.

Accuracy of serum pepsinogens I and II, gastrin-17 and anti-helicobacter pylori antibodies in histological diagnoses of atrophic gastritis.

AIM: Atrophic gastritis is defined as a chronic inflammatory process in gastric mucosa leading to loss of glandular cells. It is considered a precancerous condition, thus its early diagnosis is of importance. Although histo-pathologic studies remain as the gold standard of diagnosis, non-invasive methods suitable for screening purposes are being developed. This includes measurement of serum gastric profile. METHODS: Two hundred and fifty 250 patients who were planned to undergo upper gastrointestinal endoscopy were randomly selected to be included in this study. Serum levels of pepsinogen I and II, gastrin-17 and anti-Helicobacter pylori (Hp) antibody were measured and the results were compared with that of histopathologic assessment of biopsy specimens obtained during endoscopy. RESULTS: IgG anti-Hp, PGII and PGI/PGII ratio showed correlation with age. PGI/PGII ratio showed best sensitivity (96.1%) and negative predictive value (97.7%). PGI has the highest specificity (94.6%), and PGII also had a high negative predictive value (90.7%). IgG anti-Hp showed poor sensitivity and specificity (58.8% and 26.5%, respectively). CONCLUSIONS: Pepsinogen I/II ratio appears to be the most suitable single measurement for screening purposes in atrophic gastritis.