Effect of patient and nurse ethnicity on emergency department analgesia for children with appendicitis in israeli government hospitals.

BACKGROUND: Ethnicity is a risk factor for disparate Emergency Department (ED) analgesia. We aimed to explore ethnic variations in the administration of ED analgesia to children with acute appendicitis in Israeli government hospitals. METHODS: Children discharged with an International Classification of Disease-Ninth Revision diagnosis of acute appendicitis between 2010 and 2015 were included. The association between patient ethnicity (Jewish, Arab) and analgesia administration (any, opioid) was assessed. Age, gender, triage category, pain score and time of arrival were tested as possible confounders. The effect of patient-nurse ethnic discordance (PNED) was examined. RESULTS: Overall, 4714 children with acute appendicitis, 3520 Jewish and 1194 Arab, were cared for in the EDs; 1516 (32.2%) received any analgesia and 368 (7.8%) opioid analgesia. Stratified by pain score, no statistical differences were found in the administration of any or opioid analgesia between Jewish and Arab patients with either severe pain or moderate pain. In multivariate modelling adjusted for pain score and triage category, the rates of any analgesia for Arab and Jewish patients were 31.8% (95% CI, 30.9-32.6) and 36.5% (95% CI, 36.0-36.9), adjusted OR (aOR) = 1.16 (95% CI, 0.98-1.38), respectively. The rates of opioid analgesia for Arab and Jewish patients were 8.5% (95% CI, 8.2-8.9) and 7.9% (95% CI, 7.3-8.7), aOR = 0.77; (95% CI, 0.59-1.22), respectively. Jewish and Arab nurses treated proportionally fewer patients from the opposite ethnicity with any analgesia (p < 0.01). CONCLUSION: Emergency Department analgesia was markedly low, and not associated with patient ethnicity. PNED was associated with decreased rates of analgesia. SIGNIFICANCE: Emergency Department analgesia for children with acute appendicitis in Israeli government hospitals is markedly low. Patient-provider ethnic discordance may negatively influence the provision of analgesia. Significant efforts should be undertaken in order to increase analgesia provision rates and reduce social inequality.

Characterization of Enterococcus faecium isolates and first report of vanB phenotype-vanA genotype incongruence in the Middle East.

We aimed to characterize the vancomycin genotype/phenotype, carriage of putative virulence genes, and genetic relatedness of Enterococcus faecium isolates in Saudi Arabia. E. faecium isolated from inpatients at our medical center were studied. Sensitivity to ampicillin, linezolid, teicoplanin, quinupristin/dalfopristin, tetracycline, and ciprofloxacin was determined. The presence of van genes and virulence genes for aggregation substance (Asa-1), enterococcal surface proteins (esp), cytolysin (cylA, cylL, cylM), gelatinase (gelE), E. faecium endocarditis antigen (EfaA( fm )), hyaluronidase (hyl), and collagen adhesion (Ace) was assessed. Genetic relatedness was determined by pulsed-field gel electrophoresis (PFGE). Twenty-nine E. faecium isolates were obtained and the majority of isolates (n/N = 22/29) were from stool specimens. PFGE analysis identified eight pulsotypes (A-H) based on 80 % similarities. Isolates were represented in five major pulsotypes: type A (n = 5), type B (n = 3), type D (n = 6), type E (n = 5), and type F (n = 7). All isolates were vanA gene-positive. Thirteen isolates had vanA(+)/vanB(+) genotype. Of these, ten exhibited a vanB phenotype and three had a vanA phenotype. Eight isolates with vanA(+)/vanB(-) genotype exhibited vanB phenotype. Six of these eight isolates belonged to the same pulsotype. All isolates were positive for gelE, esp, and EfaA( fm ) genes. Five were CylA-positive and 24 had the hyl genes. Of the eight isolates harboring a combination of gelE, esp, EfaA( fm ), and hyl genes, five showed vanB phenotype-vanA genotype incongruence. This is the first report of vanB phenotype-vanA genotype incongruent E. faecium in the Middle East region. Molecular typing indicates clonal spread and high occurrence of virulence genes, especially esp genes, associated with epidemic clones.