“…Afferents innervating the bone tissue contain neuropeptides commonly associated with nociceptive processing, such as substance P and calcitonin gene-related peptide [ 9 ]. Moreover, bone damage can produce higher levels of prostaglandin E2, a pain-enhancing mediator [ 10 ], compared to soft tissue damage alone [ 11 , 12 ]. This indicates that pain after bone surgery can be severe, and these procedures may carry a higher risk of rescue analgesic use compared to soft tissue surgery.…”
BackgroundPostoperative pain management after upper limb surgery is important for preventing adverse events that can prolong hospital stay and cause readmission. This study aimed to identify the risk factors associated with rescue analgesic use on the first postoperative day after upper limb surgery performed under single-injection brachial plexus block (BPB).FindingsWe retrospectively analyzed records from 930 patients who underwent upper limb surgery under a single-injection BPB. Postoperatively, patients were administered oral loxoprofen regularly and rescue analgesics when analgesia was insufficient. We assessed the association between patient, surgical information, and rescue analgesic use on the first day after surgery (from 7:00 PM on the day of surgery to 7:00 AM on the first postoperative day), using a logistic regression model. Multivariate analysis revealed a significant association between rescue analgesic use and bone surgery, in particular, osteotomy, ligament repair and reconstruction, osteosynthesis, treatment for an amputated digit, and surgical duration.ConclusionBone surgery (osteotomy, ligament repair and reconstruction, osteosynthesis, treatment for an amputated digit) and a longer operative time were risk factors for rescue analgesic use for treating postoperative pain after upper limb surgery performed under single-injection BPB.
“…Afferents innervating the bone tissue contain neuropeptides commonly associated with nociceptive processing, such as substance P and calcitonin gene-related peptide [ 9 ]. Moreover, bone damage can produce higher levels of prostaglandin E2, a pain-enhancing mediator [ 10 ], compared to soft tissue damage alone [ 11 , 12 ]. This indicates that pain after bone surgery can be severe, and these procedures may carry a higher risk of rescue analgesic use compared to soft tissue surgery.…”
BackgroundPostoperative pain management after upper limb surgery is important for preventing adverse events that can prolong hospital stay and cause readmission. This study aimed to identify the risk factors associated with rescue analgesic use on the first postoperative day after upper limb surgery performed under single-injection brachial plexus block (BPB).FindingsWe retrospectively analyzed records from 930 patients who underwent upper limb surgery under a single-injection BPB. Postoperatively, patients were administered oral loxoprofen regularly and rescue analgesics when analgesia was insufficient. We assessed the association between patient, surgical information, and rescue analgesic use on the first day after surgery (from 7:00 PM on the day of surgery to 7:00 AM on the first postoperative day), using a logistic regression model. Multivariate analysis revealed a significant association between rescue analgesic use and bone surgery, in particular, osteotomy, ligament repair and reconstruction, osteosynthesis, treatment for an amputated digit, and surgical duration.ConclusionBone surgery (osteotomy, ligament repair and reconstruction, osteosynthesis, treatment for an amputated digit) and a longer operative time were risk factors for rescue analgesic use for treating postoperative pain after upper limb surgery performed under single-injection BPB.
“…Cartilage, cortical bone, and cancellous bone were incubated first in oxygenated prewarmed (37°C) Tyrode's solution for 30 minutes and then for an additional 30 minutes in Tyrode's solution containing 5 &ml calcium ionophore A23 187. Since in these preliminary experiments, calcium ionophore A23 187 did not show any stimulatory effect on eicosanoid release from cartilage and bone, these tissues were incubated without adding calcium ionophore A23187, for 3 hours as previously described (23,24), for the experiments described below.…”
Objective. To determine the major source of eicosanoid release in arthritic joint tissues and to examine the modulation of this release by indomethacin and diclofenac.
Methods. Release of prostaglandin E2 (PGE2), 6‐keto‐PGF1α, leukotriene B4 (LTB4), and LTC4 was measured in supernatants of synovial tissue, cartilage, and bone incubates from patients with osteoarthritis, active rheumatoid arthritis (RA), inactive RA, and pseudogout. Radioimmunoassay (RIA) was used to determine the levels of the eicosanoids.
Results. Addition of the divalent cation ionophore A23187 resulted in significant release of all eicosanoids measured from synovial tissue, but not from cartilage, cortical bone, or cancellous bone. PG release was significantly inhibited by the addition of indomethacin or diclofenac at either 10–5 moles/liter or 10–7 moles/liter. The amount of LTC4 released from cartilage and bone was only slightly above the detection limit of the RIA, whereas large amounts were released from synovial tissue. Neither indomethacin nor diclofenac had an effect on LTC4 release. LTC4 release from synovial tissue of patients with inactive RA was significantly decreased in comparison with the levels from synovial tissue of patients with the other joint diseases. There was no significant difference in PG release among patients in the various disease groups.
Conclusion. Synovial tissue appears to be the major source of eicosanoids in synovial fluid. Indomethacin and diclofenac inhibit the release of PG, but not LT, from various joint tissues.
“…In the case of fracture, an increased number of prostaglandins of the E-and F-series are released from bone and surrounding muscle tissue [5,41], with the result that both endogenous and exogenous prostaglandins support fracture healing [10,16,24]. At the same time, prostaglandins also promote bone resorption and thus stimulate remodeling [ …”
Section: The Effects Of Nsaids On Bone Metabolismmentioning
confidence: 99%
“…Beim Auftreten einer Fraktur werden Prostaglandine der E-und F-Reihe vermehrt vom Knochen und vom umgebenden Muskelgewebe freigesetzt [5,41], wobei sowohl endogene wie auch exogene Prostaglandine die Frakturheilung unterstützen [10,16,24]. Gleichzeitig wird auch die Resorption von Knochen durch Prostaglandine gefördert und somit das Remodeling angeregt [24,26].…”
Section: Wirkung Von Nsar Auf Den Knochenstoffwechselunclassified
Nonsteroidal anti-inflammatory drugs (NSAIDs) are invaluable in treating a variety of musculoskeletal conditions. As well as their excellent analgesic potency their anti-inflammatory effects are beneficial in treating posttraumatic and postoperative edema. In addition, NSAIDs inhibit heterotopic bone formation after hip arthroplasty. Animal studies, however, have demonstrated that they cause delayed fracture healing. Although clinical studies have not yet supplied unequivocal evidence of this effect in human subjects, the authors recommend that in the presence of other risk factors which may adversely affect fracture healing, such as smoking, diabetes mellitus or peripheral arterial occlusive disease, the indication of NSAID use for analgesia should be strictly limited. Therapeutic alternatives such as centrally acting agents (e. g., weak opioids) should be considered in these patients.
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