Background: Current structural bone graft options used for glenoid augmentation in glenohumeral instability have known drawbacks. The scapular spine may be a possible alternative graft choice, but its dimensions and anatomy are not fully reported. Hypothesis: The scapular spine’s harvestable graft dimensions will be similar to harvestable dimensions of the coracoid and iliac crest. Study Design: Descriptive laboratory study. Methods: The scapular spine, coracoid, and iliac crest dimensions were recorded and compared bilaterally in 50 patients with 3-dimensional computed tomography imaging. The portion of the scapular spine with the largest harvestable dimensions was quantified and its location defined. Measurements were independently taken by 2 investigators and averaged for the final result. Results: The scapular spine has 81.5 mm of harvestable length and a “flare” located approximately 49.6 mm lateral to the medial scapular border, where the widest harvestable cross section is located (mean harvestable dimensions: 10.9-mm height, 11.5-mm width). Mean coracoid dimensions were 24-mm length, 14.2-mm height, and 10.6-mm width. Mean iliac crest width was 14.7 mm. In sum, 96% of scapular spines, 85% of coracoids, and 100% of iliac crests exceeded minimum dimensions of 8 mm × 8 mm × 20 mm. The coronal radius of curvature of the glenoid was significantly different from the corresponding plane of all measured structures. Conclusion/Clinical Relevance: The scapular spine has dimensions similar to the coracoid and iliac crest in the majority of patients and is therefore appropriate for further investigation as a potential graft choice in glenohumeral instability. A harvest location 49.6 mm lateral to the medial scapular border will provide the largest cross-sectional graft while avoiding the acromial base.

Retrospective cohort study, Level III.

The objective of this review was to evaluate the potential of tauroursodeoxycholic acid (TUDCA) for neuroprotection in traumatic brain injury (TBI) patients in the neurocritical care setting. Specifically, we surveyed preclinical studies describing the neuroprotective and systemic effects of TUDCA, and the potential therapeutic application of TUDCA. Preclinical studies have provided promising data supporting its use in neurological disease characterized by apoptosis-induced neuronal loss. TUDCA inhibits multiple proteins involved in apoptosis and upregulates cell survival pathways. In addition, TUDCA exhibits anti-inflammatory effects in models of neuroinflammation and attenuates neuronal loss in chronic neurodegenerative diseases. This may be applicable to TBI, which also triggers inflammatory and apoptotic processes. Additionally, preliminary data support the use of pharmacological therapies that reduce apoptosis and inflammation associated with TBI. The anti-apoptotic and anti-inflammatory mechanisms of TUDCA could prove promising in the treatment of TBI. Currently, there are no published data supporting improvement in clinical outcomes of TBI by treatment with TUDCA, but future studies should be considered.

No abstract