Introduction: Antibiotic-resistant infections have become increasingly prevalent nowadays. As a result, it is essential to examine the key socioeconomic and political factors which contribute to the rise in the prevalence of antibiotic resistance in developing and developed nations. This study aims to identify the various contributors to the development of antibiotic resistance in each type of nation. Methods: PUBMED was used to identify primary research, systematic reviews, and narrative reviews published before Jan 2017. Search terms included antibiotic resistance, antimicrobial resistance, superbugs, multidrug-resistant organisms, developing countries, developed countries. Publications from different countries were included to ensure generalizability. Publications were excluded if they didn't mention factors causing resistance, focused on the molecular basis of resistance, or if they were case reports. Publicly available reports from national and international health agencies were used. Results: In developing countries, key contributors identified included: (1) Lack of surveillance of resistance development, (2) poor quality of available antibiotics, (3) clinical misuse, and (4) ease of availability of antibiotics. In developed countries, poor hospital-level regulation and excessive antibiotic use in food-producing animals play a major role in leading to antibiotic resistance. Finally, research on novel antibiotics is slow ing down due to the lack of economic incentives for antibiotic research. Conclusion: Overall, multiple factors, which are distinct for developing and developed countries, contribute to the increase in the prevalence of antibiotic resistance globally. The results highlight the need to improve the regulatory framework for antibiotic use and research globally.
Ventilator-associated pneumonia in critically ill patients is associated with substantial morbidity, longer ICU stays, and prolonged mechanical ventilation. Along with systemic therapy, aerosolized aminoglycosides are valuable adjuncts in select patients with minimal risk of antibiotic resistance.
Trauma patients with B-VAP have a similar mortality but greater morbidity than those with VAP alone. The number of PRBC received is the most significant risk factor for developing B-VAP. More than two-thirds of patients with B-VAP have contemporaneous extra-pulmonic infections. Trauma patients with B-VAP may benefit from increased surveillance for additional concomitant infections and from more aggressive empiric antimicrobial coverage.
The response of ICU patients to continuously infused ketamine when it is used for analgesia and/or sedation remains poorly established. OBJECTIVES:To describe continuous infusion (CI) ketamine use in critically ill patients, including indications, dose and duration, adverse effects, patient outcomes, time in goal pain/sedation score range, exposure to analgesics/sedatives, and delirium. DESIGN, SETTING, AND PARTICIPANTS:Multicenter, retrospective, observational study from twenty-five diverse institutions in the United States. Patients receiving CI ketamine between January 2014 and December 2017. MAIN OUTCOMES AND MEASURES:Chart review evaluating institutional and patient demographics, ketamine indication, dose, administration, and adverse effects. Pain/sedation scores, cumulative doses of sedatives and analgesics, and delirium screenings in the 24 hours prior to ketamine were compared with those at 0-24 hours and 25-48 hours after. RESULTS:A total of 390 patients were included (median age, 54.5 yr; interquartile range, 39-65 yr; 61% males). Primary ICU types were medical (35.3%), surgical (23.3%), and trauma (17.7%). Most common indications were analgesia/sedation (n = 357, 91.5%). Starting doses were 0.2 mg/kg/hr (0.1-0.5 mg/kg/hr) and continued for 1.6 days (0.6-2.9 d). Hemodynamics in the first 4 hours after ketamine were variable (hypertension 24.0%, hypotension 23.5%, tachycardia 19.5%, bradycardia 2.3%); other adverse effects were minimal. Compared with 24 hours prior, there was a significant increase in proportion of time spent within goal pain score after ketamine initiation (24 hr prior:
Introduction: Heparin induced thrombocytopenia (HIT) occurs in up to 5% of adults exposed to heparin due to formation of heparin-dependent antibodies to the heparin/platelet factor 4 (PF4) complex. Patients develop thrombocytopenia and are at risk for severe thrombotic complications. Mortality rates can be as high as 20%, but are often much lower with prompt recognition, cessation of heparin, and treatment with alternative anticoagulants. However, these alternative medications are often both labor-intensive drips and expensive, highlighting the need for quick decision making in such challenging cases. The classic workup of HIT involves assessing clinical suspicion (often using the "4T score" on a scale of 0-8), followed by lab testing for detection of the heparin-dependent antibody and then a functional assay to confirm pathogenicity of the antibody. Our institution uses an in-house rapid Particle ImmunoFiltration Assay (PIFA), which is a same-day test and reported as "positive" or "negative." Other testing available includes send-out tests for Enzyme-Linked Immunoassay (ELISA) to IgG, A, and M of the PF4 antibody as well as the C-14 Serotonin Release Assay (SRA) functional assay. The goal of this retrospective review is to analyze the utility of an algorithmic approach to laboratory testing in aiding the rapidity of diagnosis of HIT without missing possible critical cases. Methods: This was a single institutional study at a large urban academic medical center. We reviewed inpatient charts from 2015-2018 of patients who had any lab testing for HIT. As per institutional guidelines, first-line testing is recommended by using the in-house same-day testing PIFA. If positive, a sample is automatically reflexed and sent-out for PF4 ELISA testing and SRA. Furthermore, clinicians are able to directly order ELISA and SRA testing at their medical discretion. Our analysis looked at those patients with at least two different "HIT-related" laboratory tests to best analyze the concordance and discordance rates of the above testing to assess for sensitivity, specificity, and overall accuracy of using a stepwise testing approach. We used a cutoff value of >0.4 optical density (OD) for ELISA testing, and >20% release at low-dose heparin concentration for SRA testing. Results: There were 118 patients who had at least two different HIT-related laboratory tests sent. 91 patients had both PIFA and ELISA testing, with 37/79 (47%) positive concordance rate and 6/12 (50%) negative concordance rate, for a sensitivity of 86% and specificity of 13%. 3 patients with positive PIFA also had positive SRA, and there were 2 patients with negative PIFA with positive SRA testing (see attached Table). When comparing ELISA testing to SRA, 4/41 (10%) had concordant positive testing, while no patient with a negative ELISA test had a positive SRA (28 concordant negative cases). Overall, of 94 SRA tests run, 5 were positive, of which 2/5 had negative PIFA and 0/4 had negative ELISA testing. Conclusions: While PIFA testing had a high sensitivity compared to ELISA, the overall accuracy compared to ELISA was low, while ELISA testing was 100% sensitive in this analysis. Furthermore, there was still a risk of missing cases of HIT using PIFA testing alone. In both cases of positive SRA with a negative PIFA, patients had a high 4T score of >6, consistent with a high clinical suspicion for HIT. We conclude that PIFA testing is not equivalent to ELISA testing, and that use of a laboratory "algorithm only" approach would be inappropriate in the diagnosis of HIT. Our results highlight the importance of using both clinical scoring systems and appropriate lab testing together in the workup and diagnosis of HIT. Disclosures No relevant conflicts of interest to declare.
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