Surgical predictors of acute postoperative pain after hip arthroscopy

BACKGROUND: Pain following hip arthroscopy is highly variable and can be severe. Little published data exists demonstrating reliable predictors of significant pain after hip arthroscopy. The aim of this study was to identify influence of intraoperative factors (arthroscopic fluid infusion pressure, operative type) on the severity of postoperative pain. METHODS: A retrospective review of 131 patients who had received a variety of arthroscopic hip interventions was performed. A standardized anaesthetic technique was used on all patients and postoperative pain was analysed using recovery pain severity outcomes and analgesic use. A multivariate logistic regression analysis was performed on intraoperative factors including patient age, sex and BMI, arthroscopic infusion pressures (40 vs 80 mm Hg), amount of fluid used, length of surgery and types of arthroscopic interventions performed. Thirty six patients were also prospectively examined to determine arthroscopic fluid infusion rates for 40 and 80 mm Hg infusion pressures. RESULTS: Use of a higher infusion pressure of 80 mm Hg was strongly associated with all pain severity endpoints (OR 2.8 – 8.2). Other significant factors included hip arthroscopy that involved femoral chondro-ostectomy (OR 5.8) and labral repair (OR 7.5). Length of surgery and total amount of infusion fluid used were not associated with increased pain. CONCLUSIONS: 80 mm Hg arthroscopic infusion pressures, femoral chondro-osteoectomy and labral repair are strongly associated with significant postoperative pain, whereas intraoperative infusion volumes or surgical duration are not. Identification of these predictors in individual patients may guide clinical practice regarding the choice of more invasive regional analgesia options. The use of 40 mm Hg arthroscopic infusion pressures will assist in reducing postoperative pain

NOD2, RIP2 and IRF5 Play a Critical Role in the Type I Interferon Response to Mycobacterium tuberculosis

While the recognition of microbial infection often occurs at the cell surface via Toll-like receptors, the cytosol of the cell is also under surveillance for microbial products that breach the cell membrane. An important outcome of cytosolic recognition is the induction of IFNα and IFNβ, which are critical mediators of immunity against both bacteria and viruses. Like many intracellular pathogens, a significant fraction of the transcriptional response to Mycobacterium tuberculosis infection depends on these type I interferons, but the recognition pathways responsible remain elusive. In this work, we demonstrate that intraphagosomal M. tuberculosis stimulates the cytosolic Nod2 pathway that responds to bacterial peptidoglycan, and this event requires membrane damage that is actively inflicted by the bacterium. Unexpectedly, this recognition triggers the expression of type I interferons in a Tbk1- and Irf5-dependent manner. This response is only partially impaired by the loss of Irf3 and therefore, differs fundamentally from those stimulated by bacterial DNA, which depend entirely on this transcription factor. This difference appears to result from the unusual peptidoglycan produced by mycobacteria, which we show is a uniquely potent agonist of the Nod2/Rip2/Irf5 pathway. Thus, the Nod2 system is specialized to recognize bacteria that actively perturb host membranes and is remarkably sensitive to mycobacteria, perhaps reflecting the strong evolutionary pressure exerted by these pathogens on the mammalian immune system

The role of the inflammasome in nonmyeloid cells.

Inflammasomes are cytosolic multiprotein complexes that can proteolytically activate caspase-1. Activated caspase-1 is needed for the maturation and secretion of interleukin (IL)-1beta and IL-18. In the past decade, there has been tremendous progress in our knowledge of inflammasome function and IL-1 signaling, mainly in cells of the innate immune system, such as monocytes, macrophages, neutrophils, and dendritic cells. Because nonimmune cells, including keratinocytes, synovial cells, or astrocytes, can form an interface between the body and the environment or a defined compartment (brain, joint), they are important guardians for the detection of danger signals and the consecutive initiation of an inflammatory response. They are present in anatomical compartments that are less accessible to myeloid cells and thus can fulfill tasks usually performed by residential macrophages. This review focuses on recent progress in our understanding of the processing and functional role of IL-1 in epithelial, mesenchymal, and neuronal cells and in conditions such as tissue repair