Background The influence of in-hospital delay (time between admission and operation) on outcome after appendectomy is controversial. Methods A total of 1,827 adult patients underwent open or laparoscopic appendectomy for suspected appendicitis in eleven Swiss hospitals between 2003 and 2006. Of these, 1,675 patients with confirmed appendicitis were included in the study. Groups were defined according in-hospital delay (B12 vs. [12 h). Results Delay [ 12 h was associated with a significantly higher frequency of perforated appendicitis (29.7 vs. 22.7%; P = 0.010) whereas a delay of 6 or 9 h was not. Size of institution, time of admission, and surgical technique (laparoscopic vs. open) were independent factors influencing in-hospital delay. Admission during regular hours was associated with higher age, higher frequency of co-morbidity, and higher perforation rate compared to admission after hours. The logistic regression identified four independent factors associated with an increased perforation rate: age (B65 years vs. [65 years, odds ratio (OR) 4.5, P \ 0.001); co-morbidity (Charlson index [ 0 vs. Charlson index = 0, OR 2.3, P \ 0.001); time of admission (after hours vs. regular hours, OR 0.8, P = 0.040), in-hospital delay ([12 vs. B12 h, OR 1.5, P = 0.005). Perforation was associated with an increased reintervention rate (13.4 vs. 1.6%; P \ 0.001) and longer length of hospital stay (9.5 vs. 4.4 days; P \ 0.001).Conclusions In-hospital delay negatively influences outcome after appendectomy. In-hospital delay of more than 12 h, age over 65 years, time of admission during regular hours, and the presence of co-morbidity are all independent risk factors for perforation. Perforation was associated with a higher reintervention rate and increased length of hospital stay.

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BackgroundLeukocytes infiltrating inflamed tissue produce and release opioid peptides such as β-endorphin, which activate opioid receptors on peripheral terminals of sensory nerves resulting in analgesia. Gene therapy is an attractive strategy to enhance continuous production of endogenous opioids. However, classical viral and plasmid vectors for gene delivery are hampered by immunogenicity, recombination, oncogene activation, anti-bacterial antibody production or changes in physiological gene expression. Non-viral, non-plasmid minimalistic, immunologically defined gene expression (MIDGE) vectors may overcome these problems as they carry only elements needed for gene transfer. Here, we investigated the effects of a nuclear localization sequence (NLS)-coupled MIDGE encoding the β-endorphin precursor proopiomelanocortin (POMC) on complete Freund's adjuvant-induced inflammatory pain in rats.ResultsPOMC-MIDGE-NLS injected into inflamed paws appeared to be taken up by leukocytes resulting in higher concentrations of β-endorphin in these cells. POMC-MIDGE-NLS treatment reversed enhanced mechanical sensitivity compared with control MIDGE-NLS. However, both effects were moderate, not always statistically significant or directly correlated with each other. Also, the anti-hyperalgesic actions could not be increased by enhancing β-endorphin secretion or by modifying POMC-MIDGE-NLS to code for multiple copies of β-endorphin.ConclusionAlthough MIDGE vectors circumvent side-effects associated with classical viral and plasmid vectors, the current POMC-MIDGE-NLS did not result in reliable analgesic effectiveness in our pain model. This was possibly associated with insufficient and variable efficacy in transfection and/or β-endorphin production. Our data point at the importance of the reproducibility of gene therapy strategies for the control of chronic pain.