Search

Meniscal injury is a common cause for presentation to the emergency department or primary care physician's office. Meniscal injuries can be the result of a forceful, twisting event in a young athlete's knee or it can insidiously present in the older patient. Many patients with meniscal pathology appropriately undergo conservative management with a primary care physician while some may need referral to an orthopedist for operative intervention. Arthroscopic surgery to address the menisci is the most frequently performed procedure on the knee and one of the most regularly performed surgeries in orthopedic surgery.1 The purpose of this paper is to help elucidate the diagnosis and management of meniscal pathology resulting in knee pain. [Full article available at http://rimed.org/rimedicaljournal-2016-10.asp].

Key Points: The mechanism of therapeutic efficacy of flecainide for catecholaminergic polymorphic ventricular tachycardia (CPVT) is unclear. Model predictions suggest that Na(+) channel effects are insufficient to explain flecainide efficacy in CPVT. This study represents a first step toward predicting therapeutic mechanisms of drug efficacy in the setting of CPVT and then using these mechanisms to guide modelling and simulation to predict alternative drug therapies. Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited arrhythmia syndrome characterized by fatal ventricular arrhythmias in structurally normal hearts during β-adrenergic stimulation. Current treatment strategies include β-blockade, flecainide and ICD implementation--none of which is fully effective and each comes with associated risk. Recently, flecainide has gained considerable interest in CPVT treatment, but its mechanism of action for therapeutic efficacy is unclear. In this study, we performed in silico mutagenesis to construct a CPVT model and then used a computational modelling and simulation approach to make predictions of drug mechanisms and efficacy in the setting of CPVT. Experiments were carried out to validate model results. Our simulations revealed that Na(+) channel effects are insufficient to explain flecainide efficacy in CPVT. The pure Na(+) channel blocker lidocaine and the antianginal ranolazine were additionally tested and also found to be ineffective. When we tested lower dose combination therapy with flecainide, β-blockade and CaMKII inhibition, our model predicted superior therapeutic efficacy than with flecainide monotherapy. Simulations indicate a polytherapeutic approach may mitigate side-effects and proarrhythmic potential plaguing CPVT pharmacological management today. Importantly, our prediction of a novel polytherapy for CPVT was confirmed experimentally. Our simulations suggest that flecainide therapeutic efficacy in CPVT is unlikely to derive from primary interactions with the Na(+) channel, and benefit may be gained from an alternative multi-drug regimen., (© 2015 The Authors. The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.)

Posterior sternoclavicular dislocations are rare but serious injuries. The proximity of the medial clavicle to the vital structures of the mediastinum warrants caution with management of the injury. Radiographs are the initial imaging test, though computed tomography and magnetic resonance imaging are essential for diagnosis and preoperative planning. This paper presents an efficient diagnostic approach and effective technique of closed reduction of posterior sternoclavicular dislocations with a brief review of open and closed reduction procedures.

Context: Stress fractures are common injuries in athletes, often difficult to diagnose. A stress fracture is a fatigue-induced fracture of bone caused by repeated applications of stress over time., Evidence Acquisition: PubMed articles published from 1974 to January 2012., Results: Intrinsic and extrinsic factors may predict the risk of stress fractures in athletes, including bone health, training, nutrition, and biomechanical factors. Based on their location, stress fractures may be categorized as low- or high-risk, depending on the likelihood of the injury developing into a complete fracture. Treatment for these injuries varies substantially and must account for the risk level of the fractured bone, the stage of fracture development, and the needs of the patient. High-risk fractures include the anterior tibia, lateral femoral neck, patella, medial malleolus, and femoral head. Low-risk fractures include the posteromedial tibia, fibula, medial femoral shaft, and pelvis. Magnetic resonance is the imaging test of choice for diagnosis., Conclusions: These injuries can lead to substantial lost time from participation. Treatment will vary by fracture location, but most stress fractures will heal with rest and modified weightbearing. Some may require more aggressive intervention, such as prolonged nonweightbearing movement or surgery. Contributing factors should also be addressed prior to return to sports.

Cardiac rhythms arise from electrical activity generated by precisely timed opening and closing of ion channels in individual cardiac myocytes. These impulses spread throughout the cardiac muscle to manifest as electrical waves in the whole heart. Regularity of electrical waves is critically important since they signal the heart muscle to contract, driving the primary function of the heart to act as a pump and deliver blood to the brain and vital organs. When electrical activity goes awry during a cardiac arrhythmia, the pump does not function, the brain does not receive oxygenated blood, and death ensues. For more than 50 years, mathematically based models of cardiac electrical activity have been used to improve understanding of basic mechanisms of normal and abnormal cardiac electrical function. Computer-based modeling approaches to understand cardiac activity are uniquely helpful because they allow for distillation of complex emergent behaviors into the key contributing components underlying them. Here we review the latest advances and novel concepts in the field as they relate to understanding the complex interplay between electrical, mechanical, structural, and genetic mechanisms during arrhythmia development at the level of ion channels, cells, and tissues. We also discuss the latest computational approaches to guiding arrhythmia therapy.