Early clinical outcomes following navigation-assisted baseplate fixation in reverse total shoulder arthroplasty: a matched cohort study.

BACKGROUND: Accurate placement of the glenoid baseplate is an important technical goal of reverse total shoulder arthroplasty (RSA). The use of computer navigated instrumentation has been shown to improve the accuracy and precision of intraoperative execution of preoperative planning. The purpose of this study was to compare early clinical outcomes of patients undergoing navigated RSA vs. a non-navigated matched cohort. METHODS: A retrospective review of a prospectively collected shoulder arthroplasty database was used to identify 113 patients from a single institution who underwent navigated primary RSA with a minimum 2-year follow-up. A matched cohort of 113 non-navigated RSAs was created based on sex, age, follow-up, and preoperative diagnosis. Preoperative and postoperative range of motion, functional outcome scores, and complications were reported. RESULTS: A total of 226 shoulders with a mean age of 71 years were evaluated after navigated (113) or non-navigated (113) RSAs. The mean follow-up was 32.8 months (range: 21-54 months). At the final postoperative follow-up, the navigated group had better active forward elevation (135° vs. 129°, P = .023), active external rotation (39° vs. 32°, P = .003), and Constant scores (71.1 vs. 65.5, P = .003). However, when comparing improvements from the preoperative state, there was no statistically significant difference in range of motion or functional outcome scores between the groups. Complications occurred in 1.8% (2) of patients undergoing navigated RSA compared with 5.3% (6) in the non-navigated group (P = .28). Scapular notching (3.1% vs. 8.0%, P = .21) and revision surgery (0.9% vs. 3.5%, P = .37) were more common in non-navigated shoulders. CONCLUSION: At early follow-up, navigated and non-navigated RSAs yielded similar rates of improvement in range of motion and functional outcome scores. Notching and reoperation was more common in non-navigated shoulders, but did not reach statistical significance. Longer follow-up and larger cohort size are needed to determine if intraoperative navigation lengthens the durability of RSA results and reduces the incidence of postoperative complications.

Traumatic Brain Injury and Secondary Neurodegenerative Disease.

Traumatic brain injury (TBI) is a devastating event with severe long-term complications. TBI and its sequelae are one of the leading causes of death and disability in those under 50 years old. The full extent of secondary brain injury is still being intensely investigated; however, it is now clear that neurotrauma can incite chronic neurodegenerative processes. Chronic traumatic encephalopathy, Parkinson's disease, and many other neurodegenerative syndromes have all been associated with a history of traumatic brain injury. The complex nature of these pathologies can make clinical assessment, diagnosis, and treatment challenging. The goal of this review is to provide a concise appraisal of the literature with focus on emerging strategies to improve clinical outcomes. First, we review the pathways involved in the pathogenesis of neurotrauma-related neurodegeneration and discuss the clinical implications of this rapidly evolving field. Next, because clinical evaluation and neuroimaging are essential to the diagnosis and management of neurodegenerative diseases, we analyze the clinical investigations that are transforming these areas of research. Finally, we briefly review some of the preclinical therapies that have shown the most promise in improving outcomes after neurotrauma.

Thoracic outlet syndrome: a review.

Thoracic outlet syndrome (TOS) is a rare condition (1-3 per 100,000) caused by neurovascular compression at the thoracic outlet and presents with arm pain and swelling, arm fatigue, paresthesias, weakness, and discoloration of the hand. TOS can be classified as neurogenic, arterial, or venous based on the compressed structure(s). Patients develop TOS secondary to congenital abnormalities such as cervical ribs or fibrous bands originating from a cervical rib leading to an objectively verifiable form of TOS. However, the diagnosis of TOS is often made in the presence of symptoms with physical examination findings (disputed TOS). TOS is not a diagnosis of exclusion, and there should be evidence for a physical anomaly that can be corrected. In patients with an identifiable narrowing of the thoracic outlet and/or symptoms with a high probability of thoracic outlet neurovascular compression, diagnosis of TOS can be established through history, a physical examination maneuvers, and imaging. Neck trauma or repeated work stress can cause scalene muscle scaring or dislodging of a congenital cervical rib that can compress the brachial plexus. Nonsurgical treatment includes anti-inflammatory medication, weight loss, physical therapy/strengthening exercises, and botulinum toxin injections. The most common surgical treatments include brachial plexus decompression, neurolysis, and scalenotomy with or without first rib resection. Patients undergoing surgical treatment for TOS should be seen postoperatively to begin passive/assisted mobilization of the shoulder. By 8 weeks postoperatively, patients can begin resistance strength training. Surgical treatment complications include injury to the subclavian vessels potentially leading to exsanguination and death, brachial plexus injury, hemothorax, and pneumothorax. In this review, we outline the diagnostic tests and treatment options for TOS to better guide clinicians in recognizing and treating vascular TOS and objectively verifiable forms of neurogenic TOS.

Subarachnoid hemorrhage: management considerations for COVID-19.

Subarachnoid hemorrhage (SAH) has deleterious outcomes for patients, and during the hospital stay, patients are susceptible to vasospasm and delayed cerebral ischemia. Coronavirus disease 2019 (COVID-19) has been shown to worsen hypertension through angiotensin-converting enzyme 2 (ACE2) activity, therefore, predisposing to aneurysm rupture. The classic renin-angiotensin pathway activation also predisposes to vasospasm and subsequent delayed cerebral ischemia. Matrix metalloproteinase 9 upregulation can lead to an inflammatory surge, which worsens outcomes for patients. SAH patients with COVID-19 are more susceptible to ventilator-associated pneumonia, reversible cerebral vasoconstriction syndrome, and respiratory distress. Emerging treatments are warranted to target key components of the anti-inflammatory cascade. The aim of this review is to explore how the COVID-19 virus and the intensive care unit (ICU) treatment of severe COVID can contribute to SAH.

Gastrointestinal Microbiome and Neurologic Injury.

Communication between the enteric nervous system (ENS) of the gastrointestinal (GI) tract and the central nervous system (CNS) is vital for maintaining systemic homeostasis. Intrinsic and extrinsic neurological inputs of the gut regulate blood flow, peristalsis, hormone release, and immunological function. The health of the gut microbiome plays a vital role in regulating the overall function and well-being of the individual. Microbes release short-chain fatty acids (SCFAs) that regulate G-protein-coupled receptors to mediate hormone release, neurotransmitter release (i.e., serotonin, dopamine, noradrenaline, γ-aminobutyric acid (GABA), acetylcholine, and histamine), and regulate inflammation and mood. Further gaseous factors (i.e., nitric oxide) are important in regulating inflammation and have a response in injury. Neurologic injuries such as ischemic stroke, spinal cord injury, traumatic brain injury, and hemorrhagic cerebrovascular lesions can all lead to gut dysbiosis. Additionally, unfavorable alterations in the composition of the microbiota may be associated with increased risk for these neurologic injuries due to increased proinflammatory molecules and clotting factors. Interventions such as probiotics, fecal microbiota transplantation, and oral SCFAs have been shown to stabilize and improve the composition of the microbiome. However, the effect this has on neurologic injury prevention and recovery has not been studied extensively. The purpose of this review is to elaborate on the complex relationship between the nervous system and the microbiome and to report how neurologic injury modulates the status of the microbiome. Finally, we will propose various interventions that may be beneficial in the recovery from neurologic injury.

Altered Germinal-Center Metabolism in B Cells in Autoimmunity.

B lymphocytes play an important role in the pathophysiology of many autoimmune disorders by producing autoantibodies, secreting cytokines, and presenting antigens. B cells undergo extreme physiological changes as they develop and differentiate. Aberrant function in tolerogenic checkpoints and the metabolic state of B cells might be the contributing factors to the dysfunctionality of autoimmune B cells. Understanding B-cell metabolism in autoimmunity is important as it can give rise to new treatments. Recent investigations have revealed that alterations in metabolism occur in the activation of B cells. Several reports have suggested that germinal center (GC) B cells of individuals with systemic lupus erythematosus (SLE) have altered metabolic function. GCs are unique microenvironments in which the delicate and complex process of B-cell affinity maturation occurs through somatic hypermutation (SHM) and class switching recombination (CSR) and where Bcl6 tightly regulates B-cell differentiation into memory B-cells or plasma cells. GC B cells rely heavily on glucose, fatty acids, and oxidative phosphorylation (OXPHOS) for their energy requirements. However, the complicated association between GC B cells and their metabolism is still not clearly understood. Here, we review several studies of B-cell metabolism, highlighting the significant transformations that occur in GC progression, and suggest possible approaches that may be investigated to more precisely target aberrant B-cell metabolism in SLE.

Techniques for Decreasing Bacterial Load for Open Shoulder Surgery.

¼: Benzoyl peroxide (BPO) 5% has been shown to reduce Cutibacterium acnes load on the skin. BPO 5% with miconazole nitrate (MN) 2% may be beneficial, whereas BPO 5% with clindamycin cream 1% to 1.2% does not seem to have additive effects when compared with BPO 5% alone. Chlorhexidine gluconate solutions reduce the total bacterial load on the skin, but do not seem to have a significant effect on C. acnes. ¼: ChloraPrep seems to be the best surgical skin preparation to decrease overall positive skin cultures. Preincisional hydrogen peroxide 3% application has been shown to be a cost-effective practice to inhibit growth of C. acnes. Vancomycin powder before deltopectoral interval closure has antimicrobial effects against C. acnes and is a cost-effective practice. Finally, Bactisure surgical lavage is protective against the formation of biofilms. ¼: IV cefazolin has been shown to be more effective for shoulder arthroplasty infection prophylaxis than antibiotic alternatives such as vancomycin. Thus, patients with a questionable history of penicillin allergy should undergo additional testing. ¼: For shoulder surgery infection prophylaxis, we recommend the use of BPO 5% cream for 5 days preoperatively with chlorhexidine wipes the night before and the morning of surgery. IV cefazolin should be administered perioperatively, and patients with a questionable history of penicillin allergy should be tested. Surgeons should consider preincisional application of hydrogen peroxide 3% for 5 minutes, followed by standard ChloraPrep preparation. Normal saline should be used for preclosure lavage. Finally, application of vancomycin powder deep to the deltopectoral interval closure should be considered.