Computerized tomographic scans of the axial and appendicular skeleton are associated with substantially elevated radiation exposures, but the effective dose declines substantially for anatomic structures that are further away from the torso.

2.

Thoracic outlet syndrome is a well-described disorder caused by thoracic outlet compression of the brachial plexus and/or the subclavian vessels. Neurogenic thoracic outlet syndrome is the most common manifestation, presenting with pain, numbness, tingling, weakness, and vasomotor changes of the upper extremity. Vascular complications of thoracic outlet syndrome are uncommon and include thromboembolic phenomena and swelling. The clinical presentation is highly variable, and no reproducible study exists to confirm the diagnosis; instead, the diagnosis is based on a physician's judgment after a meticulous history and physical examination. Both nonsurgical and surgical treatment methods are available for thoracic outlet syndrome. Whereas nonsurgical management appears to be effective in some persons, surgical treatment has been shown to provide predictable long-term cure rates for carefully selected patients. In addition, physicians who do not regularly treat patients with thoracic outlet syndrome may not have an accurate view of this disorder, its treatment, or the possible success rate of treatment.

Prognostic Level II. See Instructions for Authors for a complete description of levels of evidence.

Background/Aims: In 2003, we reported on a small number of patients in whom acute aortic dissection appeared to be causally related to intense weight lifting. If additional cases could be identified, the phenomenon of weight lifting induced aortic dissection would be further substantiated. We now report a substantially larger number of cases in which aortic dissection is associated with intense physical exertion. Methods: Additional cases of acute aortic dissection occurring at the time of intense physical exertion were accumulated and analyzed. Cases were culled from retrospective review of a large university data base and from reports forwarded to our attention from around the country. We determined type of activity bringing on symptoms, age and sex of the patients, location of the dissection (ascending or descending aorta), aortic size, therapy, and survival. Results: We identified 31 patients in whom acute aortic dissection occurred in the context of severe physical exertion, predominantly weight lifting or similar activities. All patients except one were males. Mean age was 47.3 (range = 19–76). All except four dissections were in the ascending aorta. Only three patients (9.7%) had a family history of aortic disease. Mean aortic diameter on the initial imaging study was 4.63 cm. Twenty-six of the 31 cases were diagnosed ante-mortem and 5 post-mortem. Overall, 10 of the 31 patients (32.2%) died. Of 24 patients reaching surgical therapy, 20 (83.3%) survived. Conclusion: Weight lifting related acute aortic dissection appears to be a real phenomenon, with increasing evidence for the association of extreme exertion with this catastrophic aortic event. Moderate aortic dilatation confers vulnerability to exertion-related aortic dissection. Individuals with known aortic dilatation should be cautioned to refrain from weight lifting or strenuous exertion. Routine echocardiographic screening of individuals engaging in heavy strength training should be considered, in order to prevent this tragic loss of life.

There is a compelling clinical need for bone grafts with initial bone-like mechanical properties that actively remodel for repair of weight-bearing bone defects, such as fractures of the tibial plateau and vertebrae. However, there is a paucity of studies investigating remodeling of weight-bearing bone grafts in preclinical models, and consequently there is limited understanding of the mechanisms by which these grafts remodel in vivo. In this study, we investigated the effects of the rates of new bone formation, matrix resorption, and polymer degradation on healing of settable weight-bearing polyurethane/allograft composites in a rabbit femoral condyle defect model. The grafts induced progressive healing in vivo, as evidenced by an increase in new bone formation, as well as a decrease in residual allograft and polymer from 6 to 12 weeks. However, the mismatch between the rates of autocatalytic polymer degradation and zero-order (independent of time) new bone formation resulted in incomplete healing in the interior of the composite. Augmentation of the grafts with recombinant human bone morphogenetic protein-2 not only increased the rate of new bone formation, but also altered the degradation mechanism of the polymer to approximate a zero-order process. The consequent matching of the rates of new bone formation and polymer degradation resulted in more extensive healing at later time points in all regions of the graft. These observations underscore the importance of balancing the rates of new bone formation and degradation to promote healing of settable weight-bearing bone grafts that maintain bone-like strength, while actively remodeling.

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