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Introduction: Intrawound application of vancomycin is becoming increasingly controversial for the prevention of surgical site infection (SSI). As children undergoing spinal fusion for secondary scoliosis are at high risk for SSIs, evidence regarding the impact of intraoperative vancomycin installation on SSI rates in these patients is of utmost importance. Methodology: A single surgeon cohort of patients under 18 years of age undergoing surgery for secondary scoliosis in 2017 was analyzed with regard to the development of SSIs requiring surgical revision and adverse events. Use of vancomycin was restricted to cases with higher risk of infection. Patients undergoing distraction surgery for growing devices were excluded. Results: After exclusions, 64 patients remained (vancomycin n = 39, control n = 25). The SSI rates were 12.8% in patients receiving vancomycin (n = 5/39) and 4% in the control group (n = 1/25, p = 0.785). None of the patients suffered from adverse events. Univariable logistic regression revealed younger age (p = 0.03) and meningomyelocele as predictors for SSI (p = 0.006), while the high-risk group receiving vancomycin was not at higher odds for SSI, also after adjustment for possible confounders such as age or MMC (p = 0.031; p = 0.009). Discussion: SSI rates were comparable between groups, suggesting a normalization of SSI risk in the vancomycin-treated patients with a preoperatively increased risk of SSI. Future, larger studies in these rare diseases are needed to confirm these results. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) leads to skeletal changes, including bone loss in the unfractured skeleton, and paradoxically accelerates healing of bone fractures; however, the mechanisms remain unclear. TBI is associated with a hyperadrenergic state characterized by increased norepinephrine release. Here, we identified the β2-adrenergic receptor (ADRB2) as a mediator of skeletal changes in response to increased norepinephrine. In a murine model of femoral osteotomy combined with cortical impact brain injury, TBI was associated with ADRB2-dependent enhanced fracture healing compared with osteotomy alone. In the unfractured 12-week-old mouse skeleton, ADRB2 was required for TBI-induced decrease in bone formation and increased bone resorption. Adult 30-week-old mice had higher bone concentrations of norepinephrine, and ADRB2 expression was associated with decreased bone volume in the unfractured skeleton and better fracture healing in the injured skeleton. Norepinephrine stimulated expression of vascular endothelial growth factor A and calcitonin gene–related peptide-α (αCGRP) in periosteal cells through ADRB2, promoting formation of osteogenic type-H vessels in the fracture callus. Both ADRB2 and αCGRP were required for the beneficial effect of TBI on bone repair. Adult mice deficient in ADRB2 without TBI developed fracture nonunion despite high bone formation in uninjured bone. Blocking ADRB2 with propranolol impaired fracture healing in mice, whereas the ADRB2 agonist formoterol promoted fracture healing by regulating callus neovascularization. A retrospective cohort analysis of 72 patients with long bone fractures indicated improved callus formation in 36 patients treated with intravenous norepinephrine. These findings suggest that ADRB2 is a potential therapeutic target for promoting bone healing. Editor's summary: Fracture healing is enhanced after traumatic brain injury; however, the mechanisms remain unclear. Jahn et al. report that elevated sympathetic nervous system signaling through β2-adrenergic receptors (ADRB2) after traumatic brain injury plays a role in bone maintenance and repair. The authors found that ADRB2 was required for superior fracture repair after traumatic brain injury in mice. ADRB2 signaling increased bone matrix and blood vessel formation in the fracture callus, thereby supporting bone repair in mice. In a retrospective cohort analysis of 72 patients with long bone fractures, those who were administered intravenous norepinephrine, the ligand for ADRB2, showed increased callus formation compared with those who did not receive norepinephrine. These findings suggest that ADRB2 is a potential therapeutic target for promoting bone healing. —Molly Ogle [ABSTRACT FROM AUTHOR]

Traumatic spinal cord injury (TSCI), commonly caused by high energy trauma in young active patients, is frequently accompanied by traumatic brain injury (TBI). Although combined trauma results in inferior clinical outcomes and a higher mortality rate, the understanding of the pathophysiological interaction of co-occurring TSCI and TBI remains limited. This review provides a detailed overview of the local and systemic alterations due to TSCI and TBI, which severely affect the autonomic and sensory nervous system, immune response, the blood–brain and spinal cord barrier, local perfusion, endocrine homeostasis, posttraumatic metabolism, and circadian rhythm. Because currently developed mesenchymal stem cell (MSC)-based therapeutic strategies for TSCI provide only mild benefit, this review raises awareness of the impact of TSCI–TBI interaction on TSCI pathophysiology and MSC treatment. Therefore, we propose that unravelling the underlying pathophysiology of TSCI with concomitant TBI will reveal promising pharmacological targets and therapeutic strategies for regenerative therapies, further improving MSC therapy. [ABSTRACT FROM AUTHOR]

Study Design: Retrospective review of a prospective cohort study., Objective: To identify the association between Oswestry Disability Index (ODI) subsections and overall improvement 2 years after lumbar surgery for degenerative lumbar spondylolisthesis (DLS)., Background: DLS often necessitates lumbar surgery. The ODI is a trusted measure for patient-reported outcomes (PROMs) in assessing spinal disorder outcomes. Surgeons utilize the ODI for baseline functional assessment and post-surgery progress tracking. However, it remains uncertain if and how each subsection influences overall ODI improvement., Methods: This retrospective cohort study analyzed patients who underwent lumbar surgery for DLS between 2016 and 2018. Preoperative and 2-year postoperative ODI assessments were conducted. The study analyzed postoperative subsection scores and defined ODI improvement as ODIpreop-ODIpostop >0. Univariate linear regression was applied, and receiver operating characteristic (ROC) analysis determined cut-offs for subsection changes and postoperative target values to achieve overall ODI improvement., Results: 265 patients (60% female, mean age 67±8 y) with a baseline ODI of 50±6 and a postoperative ODI of 20±7 were included. ODI improvement was noted in 91% (242 patients). Achieving a postoperative target score of ≤2 in subsections correlated with overall ODI improvement. Walking had the highest predictive value for overall ODI improvement (AUC 0.91, sensitivity 79%, specificity 91%). Pain intensity (AUC 0.90, sensitivity 86%, specificity 83%) and changing degree of pain (AUC 0.87, sensitivity 86%, specificity 74%) were also highly predictive. Sleeping had the lowest predictability (AUC 0.79, sensitivity 84%, specificity 65%). Except for sleeping, all subsections had a Youden-index >50%., Conclusion: These findings demonstrate how the different ODI subsections associate with overall improvement post-lumbar surgery for DLS. This understanding is crucial for refining preoperative education, addressing particular disabilities, and evaluating surgical efficacy. Additionally, it shows that surgical treatment does not affect all subsections equally., Competing Interests: Declaration of conflicting interest: The Authors declare that there is no conflict of interest concerning materials or methods used in this study or the findings specified in this paper., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Study Design: Retrospective cohort study., Objective: To analyze the relationship of abdominal aortic calcification (AAC) and a reduction in the cross-sectional area (CSA) and the fatty infiltration (FI) of the paravertebral muscles in patients undergoing lumbar fusion surgery., Background: Both AAC and paraspinal muscle degeneration have been shown to be associated with poorer outcomes after surgical treatment of degenerative diseases of the lumbar spine. However, there is a lack of data on the association between AAC and paraspinal muscle changes in patients undergoing spine surgery., Methods: We retrospectively analyzed patients undergoing lumbar fusion for degenerative spinal pathologies. Muscular and spinal degeneration were measured on magnetic resonance imaging (MRI). AAC was classified on lateral lumbar radiographs. The association of AAC and paraspinal muscle composition was assessed by a multivariate regression analysis adjusted for age, sex, body mass index (BMI), comorbidities, and lumbar degeneration., Results: A total of 301 patients was included. Patients with AAC showed significantly higher degrees of intervertebral disc and facet joint degeneration as well as higher total endplate scores at the L3/4 level. The univariable regression analysis showed a significant positive correlation between the degree of AAC and the FI of the erector spinae (b=0.530, P<0.001) and multifidus (b=0.730, P<0.001). The multivariable regression analysis showed a significant positive correlation between the degree of AAC and the FI of the erector spinae (b=0.270, P=0.006) and a significant negative correlation between the degree of AAC and the CSA of the psoas muscle (b=-0.260, P=0.003)., Conclusion: This study demonstrates a significant and independent association between AAC and degeneration of the erector spinae and the psoas muscles in patients undergoing lumbar fusion. As both AAC and degeneration of paraspinal muscles impact postoperative outcomes negatively, preoperative assessment of AAC may aid in identifying patients at higher risk after lumbar surgery., Competing Interests: Declaration of Conflicting Interest: The Authors declare that there is no conflict of interest concerning materials or methods used in this study or the findings specified in this paper., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)