27 research outputs found

    Medial peritalar fracture dislocation of the talar body

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    Peritalar fracture dislocations typically involve the talar neck and are classified according to Hawkins. To our knowledge, peritalar fracture dislocation involving the talar body has not been formally reported. In this article, we describe a case of peritalar fracture dislocation of the talar body. Keywords: Peritalar dislocation, Talus fracture, Talar body fracture dislocation, Medial subtalar dislocatio

    Concomitant posterior hip dislocation, ipsilateral intertrochanteric- and proximal tibial- fractures with popliteal artery injury: a challenging trauma mélange

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    Constellation of ipsilateral posterior hip dislocation, intertrochanteric- and proximal tibial fracture with popliteal artery injury is rare. Management of this presentation is challenging. A motor vehicle accident victim presented with these injuries, but without any initial signs of vascular compromise. Popliteal artery injury was diagnosed intra-operatively and repaired. This was followed by external fixation of tibial fracture, open reduction of dislocated hip and internal fixation of intertrochanteric fracture. Patient regained bilateral complete weight bearing and returned to pre-accident activity level. Apt surgical management including early repair of vascular injury in such a trauma mélange allows for a positive postoperative outcome

    Medial epicondylitis: Current diagnosis and treatment options

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    Introduction: While commonly referred to as “golfer's elbow,” medial epicondylitis (ME) is a syndrome that more frequently presents in overhead throwing athletes and manual laborers. Repeated eccentric loading of the common flexor tendon attachment to the medial epicondyle leads to a spectrum of inflammation, microtrauma, and degeneration. Ulnar neuritis may be present in up to 60% of patients with ME, and its identification is imperative as up to 63% of these patients will experience persistent neurological symptoms. This review sought to provide a comprehensive reference for the current management of ME. Treatment and outcomes: Conservative management remains the mainstay for ME, with up to 85–95% of patients responding to initial treatment. Possible combinations for conservative treatment include trials of topical and/or oral NSAIDs, physical therapy, reduced activity levels, corticosteroid injections, electrical stimulation, and iontophoresis. Despite initial response to therapy, many patients experience symptom recurrence and progress to surgical intervention. Operative interventions include a variety of open, percutaneous, and arthroscopic approaches, with technique selection depending on patient presentation as well as physician experience and preference. Novel interventions for refractory ME treatment include injections of neutrophil-reduced platelet-rich plasma, and transcatheter arterial embolization. Bone marrow aspirate injections have also demonstrated some success in patients with lateral epicondylitis, but this modality has not yet been studied in ME to date. Conclusions: While less frequently encountered when compared to other upper extremity pathologies, ME remains a clinically important topic due to the prevalence of refractory cases and the constantly evolving treatment possibilities for the condition

    Lumbar Ligamentum Flavum Hypertrophy Is Due to Accumulation of Inflammation-Related Scar Tissue

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    Study Design. A histologic, biologic, and immunohistochemical assessment using human samples of the lumbar ligamentum flavum. Objective. To prove our hypothesis that hypertrophy of the ligamentum flavum is caused by accumulation of inflammation-related scar tissue. Summary of Background Data. Lumbar spinal canal stenosis is 1 of the most common spinal disorders in elderly patients. Canal narrowing, in part, results from hypertrophy of the ligamentum flavum. The hypertrophy mechanism remains unclear. Based on our preliminary analyses, we have previously proposed that the hypertrophy may be due to accumulation of scar tissue in the ligament. Scar tissue is reported to develop after inflammation; however, there is no report, including our previous study, on inflammation in the ligamentum flavum. There is a need for an in-depth investigation of any relationship between inflammation and scar formation in the ligamentum flavum. If inflammation is related to hypertrophy, we may control/delay the hypertrophy by inhibiting the inflammation. Methods. Twenty-one ligamentum flavum samples were obtained for the histologic study. Trichrome and Verhoeff-van Gieson stains were used to assess the degree of fibrosis (scarring) and content of elastic fibers, respectively. Two ligamentum flavum samples, hypertrophied and thin control ligaments, were used for a global genetic assessment by oligonucleotide gene array technology with gene chips. Messenger ribonucleic acid expression of cyclooxygenase (COX)-2 was quantitatively measured from 16 ligamentum flavum samples using real-time reverse transcriptase polymerase chain reaction. Immunohistochemistry evaluated the cellular location of COX-2 in ligamentum flavum. Results. In the hypertrophied ligament, severe fibrosis (scarring) was observed in the entire area of the ligamentum flavum, and the severity of scarring showed a significant (r = 0.79; P \u3c 0.0001) and positive linear correlation with ligamentum flavum thickness. Gene array results showed in both thin/control and hypertrophied ligaments expression of inflammation-related genes such as COX-2, tumor necrosis factor-α, and interleukin-1, 6, 8, and 15. Real-time polymerase chain reaction showed COX-2 messenger ribonucleic acid expression in all ligamentum flavum samples. Its expression showed weak positive linear correlation with the thickness of ligament. COX-2 was released from vascular endothelial cells in ligamentum flavum as per the immunohistochemical analysis. Conclusions. Accumulation of fibrosis (scarring) causes hypertrophy of the ligamentum flavum. Inflammation-related gene expression is found in the ligamentum flavum. It might be possible to prevent the hypertrophy of ligamentum flavum with antiinflammatory drugs
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