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BACKGROUND Proximal junctional kyphosis (PJK) is a common radiographic complication of adult spinal deformity (ASD) corrective surgery. Although previous literature has reported a 5 to 61% incidence of PJK, these studies are limited by small sample sizes and short-term follow-up. OBJECTIVE To assess the incidence of PJK utilizing a high-powered ASD database. METHODS Retrospective review of a prospective multicenter ASD database. Operative ASD patients > 18 yr old from 2009 to 2017 were included. PJK was defined as ≥ 10° for the sagittal Cobb angle between the inferior upper instrumented vertebra (UIV) endplate and the superior endplate of the UIV + 2. Chi-square analysis and post hoc testing assessed annual and overall incidence of acute (6-wk follow-up [f/u]), progressive (increase in degree of PJK from 6 wk to 1 yr), and delayed (1-yr, 2-yr, and 3-yr f/u) PJK development. RESULTS A total of 1005 patients were included (age: 59.3; 73.5% F; body mass index: 27.99). Overall PJK incidence was 69.4%. Overall incidence of acute PJK was 48.0%. Annual incidence of acute PJK has decreased from 53.7% in 2012 to 31.6% in 2017 (P = .038). Overall incidence of progressive PJK was 35.0%, with stable rates observed from 2009 to 2016 (P = .297). Overall incidence of 1-yr-delayed PJK was 9.3%. Annual incidence of 1-yr-delayed PJK has decreased from 9.2% in 2009 to 3.2% in 2016 (P < .001). Overall incidence of 2-yr-delayed PJK development was 4.3%. Annual incidence of 2-yr-delayed PJK has decreased from 7.3% in 2009 to 0.9% in 2015 (P < .05). Overall incidence of 3-yr-delayed PJK was 1.8%, with stable rates observed from 2009 to 2014 (P = .594). CONCLUSION Although progressive PJK has remained a challenge for physicians over time, significantly lower incidences of acute and delayed PJK in recent years may indicate improving operative decision-making and management strategies.

BackgroundPeri-articular injury may result in functional deficits and pain. In particular, post-traumatic elbow stiffness is a debilitating condition, precluding patients from performing activities of daily living. As such, clinicians and basic scientists alike, aim to develop novel therapeutic interventions to prevent and treat elbow stiffness; thereby reducing patient morbidity. Yet, there is a paucity of pre-clinical models of peri-articular stiffness, especially of the upper extremity, necessary to develop and test the efficacy of therapeutics. We set out to develop a pre-clinical murine model of elbow stiffness, resulting from soft tissue injury, with features characteristic of pathology observed in these patients.MethodsA soft tissue peri-elbow injury was inflicted in mice using cardiotoxin. Pathologic tissue repair was induced by creating an investigator-imposed deficiency of plasminogen, a protease essential for musculoskeletal tissue repair. Functional testing was conducted through analysis of grip strength and gait. Radiography, microcomputed tomography, and histological analyses were employed to quantify development of heterotopic ossification.ResultsAnimals with peri-elbow soft tissues injury in conjunction with an investigator-imposed plasminogen deficiency, developed a significant loss of elbow function measured by grip strength (2.387 ± 0.136 N vs 1.921 ± 0.157 N, ****, p < 0.0001) and gait analysis (35.05 ± 2.775 mm vs 29.87 ± 2.075 mm, ***, p < 0.0002). Additionally, plasminogen deficient animals developed capsule thickening, delayed skeletal muscle repair, fibrosis, chronic inflammation, and heterotopic ossification; all features characteristic of pathology observed in patients with trauma-induced elbow stiffness.ConclusionA soft tissue injury to the peri-elbow soft tissue with a concomitant deficiency in plasminogen, instigates elbow stiffness and pathologic features similar to those observed in humans. This pre-clinical model is valuable for translational studies designed to investigate the contributions of pathologic features to elbow stiffness or as a high-throughput model for testing therapeutic strategies designed to prevent and treat trauma-induced elbow stiffness.Electronic supplementary materialThe online version of this article (10.1186/s40634-018-0155-3) contains supplementary material, which is available to authorized users.

Introduction: This study assessed the incidence and risk factors for pseudarthrosis among primary spine fusion patients. Methods: Retrospective review of ACS-NSQIP (2005-2013. Differences in comorbidities between spine fusion patients with and without pseudarthrosis (Pseud, N-Pseud) were assessed using chi-squared tests and Independent Samples t-tests. Binary logistic regression assessed patient-related and procedure-related predictors for pseudarthrosis. Results: 52,402 patients (57yrs, 53%F, 0.4% w/pseudarthrosis). Alcohol consumption (OR:2.6[1.2-5.7]) and prior history of surgical revision (OR:1.6[1.4-1.8]) were risk factors for pseudarthrosis operation. Pseud patients at higher risk for deep incisional SSI (at 30-days:OR:6.6[2.0-21.8]). Pseud patients had more perioperative complications (avg:0.24 ± 0.43v0.18 ± 0.39,p=0.026). Conclusions: Alcoholism and surgical revision are major risk factors for pseudarthrosis in patients undergoing spine fusion.

Introduction: Obesity is associated with acceleration of musculoskeletal degenerative diseases and functional impairment secondary to spinal disorders. Bariatric surgery (BS) is an increasingly common treatment for severe obesity but can affect bone and mineral metabolism. The effect of BS on degenerative spinal disorders is yet to be fully described. The aim of our study was to analyze changes in bariatric patients’ risk for spinal degenerative diseases and spinal surgery. Methods: Retrospective analysis of the prospectively collected New York State Inpatient Database (NYSID) years (2004–2013) using patient linkage codes. The incidence of degenerative spinal diagnoses and spinal surgery was queried using International Classification of Diseases, Ninth Revision (ICD)-9 codes for morbidly obese patients (ICD-9 278.01) with and without a history of BS. The incidence of degenerative spinal diagnoses and spinal surgery was determined using χ2 tests for independence. Logistic testing controlled for age, sex, and comorbidity burden. Results: A total of 18,176 patients were identified in the NYSID database with a history of BS and 146,252 patients were identified as morbidly obese without a history of BS. BS patients have a significantly higher rate of spinal diagnoses than morbidly obese patients without BS (19.3% vs. 8.1%, P<0.001). Bariatric patients were more likely to have spinal diagnoses and procedures than nonbariatric obese patients (P<0.001). This was mostly observed in lumbar spinal stenosis (5.0%), cervical disk herniation (3.3%), lumbar disk degeneration (3.4%), lumbar spondylolisthesis (2.9%), lumbar spondylosis (1.9%), and cervical spondylosis with myelopathy (2.0%). Spine procedure rates are higher for bariatric patients than nonbariatric overall (25.6% vs. 2.3, P<0.001) and for fusions and decompressions (P<0.001). When controlling for age, sex, and comorbidities (and diagnosis rate with regards to procedure rates), these results persist, with BS patients having a higher likelihood of spinal diagnoses and procedures. In addition, bariatric patients had a lower comorbidity burden than morbidly obese patients without a history of BS. Conclusions: Morbidly obese BS patients have a dramatically higher incidence of spinal diagnoses and procedures, relative to morbidly obese patients without BS. Further study is necessary to determine if there is a pathophysiological mechanism underlying this higher risk of spinal disease and intervention in bariatric patients, and the effect of BS on these rates following treatment. Level of Evidence: Level III.

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Background:Klippel–Feil syndrome (KFS) includes craniocervical anomalies, low posterior hairline, and brevicollis, with limited cervical range of motion; however, there remains no consensus on inheritance pattern. This study defines incidence, characterizes concurrent diagnoses, and examines trends in the presentation and management of KFS.Methods:This was a retrospective review of the Kid's Inpatient Database (KID) for KFSpatients aged 0–20 years from 2003 to 2012. Incidence was established using KID-supplied year and hospital-trend weights. Demographics and secondary diagnoses associated with KFS were evaluated. Comorbidities, anomalies, and procedure type trends from 2003 to 2012 were assessed for likelihood to increase among the years studied using ANOVA tests.Results:Eight hundred and fifty-eight KFS diagnoses (age: 9.49 years; 51.1% females) and 475 patients with congenital fusion (CF) (age: 8.33 years; 50.3% females) were analyzed. We identified an incidence rate of 1/21,587 discharges. Only 6.36% of KFS patients were diagnosed with Sprengel's deformity; 1.44% with congenital fusion. About 19.1% of KFS patients presented with another spinal abnormality and 34.0% presented with another neuromuscular anomaly. About 36.51% of KFS patients were diagnosed with a nonspinal or nonmusculoskeletal anomaly, with the most prevalent anomalies being of cardiac origin (12.95%). About 7.34% of KFS patients underwent anterior fusions, whereas 6.64% of KFS patients underwent posterior fusions. The average number of levels operated on was 4.99 with 8.28% receiving decompressions. Interbody devices were used in 2.45% of cases. The rate of fusions with <3 levels (7.46%) was comparable to that of 3 levels or greater (7.81%).Conclusions:KFS patients were more likely to have other spinal abnormalities (19.1%) and nonnervous system abnormalities (13.63%). Compared to congenital fusions, KFS patients were more likely to have congenital abnormalities such as Sprengel's deformity. KFS patients are increasingly being treated with spinal fusion.Level of Evidence:III