Objective This study sought to validate alternative pain management strategies that can reduce reliance on opioids for postoperative pain management in otology. Study Design Prospective cohort study. Setting Single tertiary‐care facility. Methods Adult patients who underwent outpatient otologic surgery from September 2021 to July 2022 were randomized into treatment cohorts. The opioid monotherapy cohort received a standard opioid prescription. The multimodal analgesia cohort received the same opioid prescription, prescriptions for acetaminophen and naproxen, and additional pain management education with a flyer on discharge. All patients completed a questionnaire 1 week after surgery to evaluate opioid usage and pain scores. Results Eighty‐six patients completed the study. The opioid monotherapy cohort (n = 42) and multimodal analgesia cohort (n = 44) were prescribed an average of 42.1 ± 20.4 morphine milligram equivalents (MME) and 38.4 ± 5.7 MME, respectively (p = 0.373). Four patients (9.52%) in the opioid monotherapy cohort required opioid refills compared to 1 patient (2.27%) in the multimodal analgesia cohort (p = 0.156). Multivariate analysis demonstrated that the multimodal analgesia cohort consumed significantly fewer opioids on average than the opioid monotherapy cohort (11.9 ± 15.9 MME vs 22.8 ± 28.0 MME, respectively). There were no significant differences in postoperative rehospitalizations (p = 0.317) or Emergency Department visits (p = 0.150). Pain scores on the day of surgery, postoperative day (POD) 1, POD3, and POD7 were not significantly different between cohorts (p = 0.395, 0.896, 0.844, 0.765, respectively). Conclusion The addition of patient education, acetaminophen, and naproxen to postoperative opioid prescriptions significantly reduced opioid consumption without affecting pain scores, refill rates, or complication rates after otologic surgery.
Background: The Receptor for Advanced Glycation End Products (RAGE), when activated, induces irreversible vascular tissue injury by promoting pro-oxidative and pro-inflammatory signaling pathways. RAGE signal transduction requires the engagement of RAGE cytoplasmic domain with the formin Diaphanous 1 (mDia1) and results in the release of soluble RAGE in the circulation. We have previously demonstrated that the RAGE/sRAGE axis is involved in the development and progression of thoracic aortic aneurysm (TAA) in humans and mice. Elevated levels of sRAGE are found in aneurysmal patients and in mouse models of TAA. In addition, RAGE inhibition counteracts aortic dilatation and the release of sRAGE in the circulation. We hypothesize that RAGE induced vascular remodeling in TAA is mediated by mDia1. Methods: AngII infusion (1000 ng/Kg/min) was performed in C57BL6 male mice, fed with hypercolesterolaemic diet. Mice were treated for 4 weeks with losartan or with a RAGE antagonist (RAP). Ascending aortas of treated animals were harvested at day 28 post-infusion. Aortic dilatation and degeneration were assessed by echocardiography and histology. Immunofluorescence and Real Time PCR were performed to evaluate the expression of RAGE, mDia1, extracellular matrix proteins (ECM) and pro-inflammatory genes. Results: AngII infusion induces ascending aorta dilatation and medial thickening characterized by a substantial ECM deposition. RAGE and mDia1 expression is significantly increased in the aneurysmal aorta of mice chronically infused with AngII together with up-regulation of pro-inflammatory molecules (IL-6, MCP-1, IL1beta, TLR4, CCR2) and markers of extracellular matrix remodeling (Col1, Col3, MMP-2 and MMP12). Inhibition of RAGE dampens mDia1 expression and significantly reduces medial pro-inflammatory and pro-fibrotic signals while counteracting aneurysm formation. Conclusion: Formin mDia1 is involved in RAGE mediated TAA formation. Strategies that block RAGE-mDia1 interaction may unveil novel therapeutic approaches for the treatment of TAA.
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