Addition of a Second Calcaneal Pin for Spanning Ankle External Fixation.

Spanning ankle external fixation is a commonly used technique for the treatment of fractures of the lower extremity. Traditionally, a single pin is placed in the safe zone of the calcaneus to provide a point of traction for fracture reduction and stabilization. Complications include infection and pin loosening with subsequent loss of fracture reduction. We aim to highlight the benefits and techniques of adding a second calcaneal pin to reduce the likelihood of infection, pin loosening, and possible loss of fracture reduction. Using the standard medial-to-lateral placement technique, two centrally threaded Schanz pins were placed within the safe zone of the calcaneus approximately 2 cm apart and were connected by clamps and a short carbon fiber rod. The remainder of the external fixation apparatus is assembled using a standard technique after obtaining fracture reduction. There is an increased incidence of infection and pin loosening with decreased bone quality and a longer duration within an external fixator. The addition of a second calcaneal pin can be used to reduce the incidence of pin loosening and associated sequela, especially in patients with decreased bone quality, thus improving outcomes for patients undergoing spanning ankle external fixation.

Spondyloarthropathies That Mimic Ankylosing Spondylitis: A Narrative Review.

Ankylosing spondylitis is the most common type of seronegative inflammatory spondyloarthropathy often presenting with low back or neck pain, stiffness, kyphosis and fractures that are initially missed on presentation; however, there are other spondyloarthropathies that may present similarly making it a challenge to establish the correct diagnosis. Here, we will highlight the similarities and unique features of the epidemiology, pathophysiology, presentation, radiographic findings, and management of seronegative inflammatory and metabolic spondyloarthropathies as they affect the axial skeleton and mimic ankylosing spondylitis. Seronegative inflammatory spondyloarthropathies such as psoriatic arthritis, reactive arthritis, noninflammatory spondyloarthropathies such as diffuse idiopathic skeletal hyperostosis, and ochronotic arthritis resulting from alkaptonuria can affect the axial skeleton and present with symptoms similar those of ankylosing spondylitis. These similarities can create a challenge for providers as they attempt to identify a patient's condition. However, there are characteristic radiographic findings and laboratory tests that may help in the differential diagnosis. Axial presentations of seronegative inflammatory, non-inflammatory, and metabolic spondyloarthropathies occur more often than previously thought. Identification of their associated symptoms and radiographic findings are imperative to effectively diagnose and properly manage patients with these diseases.

First-Degree Heart Block: The Guiding Light to Discovering an Aortic Root Abscess.

Minor conduction abnormalities such as first-degree heart blocks are generally overlooked on electrocardiogram (EKG) as their impact on clinical management is usually not substantial. However, they can be an important screening tool for early diagnosis of infective endocarditis (IE) and associated perivalvular complications, especially in patients with surgical valve replacements. This case report describes a 58-year-old male with a past medical history of bicuspid aortic valve status post replacement five years prior to presentation who initially presented with presumed symptoms of a complicated urinary tract infection (UTI) and later developed chest pain and shortness of breath. He showed no initial signs of infection including negative blood and urine cultures. EKG showed new onset prolonged PR interval. He then underwent a transthoracic echocardiogram (TTE) which showed prosthetic valve dysfunction and subsequently underwent transesophageal echocardiogram (TEE) which revealed vegetations on all leaflets and circumferential peri-aortic abscess encompassing both coronary ostia and extending towards the tricuspid and mitral valve leaflets. The patient then underwent redo-sternotomy for dissection of mediastinal adhesions, extraction of the aortic bio-prosthesis, and debridement of the aortic root abscess. The aortic root was replaced with a homograft and the valve cultures were positive for Enterococcus faecium. The patient developed complete heart block afterwards and received a permanent pacemaker; repeat cultures showed no further evidence of infection. This case report is presented to reiterate the importance of early detection of IE-related aortic valve abscess and their rare sequelae. Early screening for conduction abnormalities via EKG and subsequently a TEE can allow prompt identification and management of valvular abnormalities to prevent life-threatening complications and improve patient outcomes.

Biphasic regulation of lysosomal exocytosis by oxidative stress.

Oxidative stress drives cell death in a number of diseases including ischemic stroke and neurodegenerative diseases. A better understanding of how cells recover from oxidative stress is likely to lead to better treatments for stroke and other diseases. The recent evidence obtained in several models ties the process of lysosomal exocytosis to the clearance of protein aggregates and toxic metals. The mechanisms that regulate lysosomal exocytosis, under normal or pathological conditions, are only beginning to emerge. Here we provide evidence for the biphasic effect of oxidative stress on lysosomal exocytosis. Lysosomal exocytosis was measured using the extracellular levels of the lysosomal enzyme beta-hexosaminidase (ß-hex). Low levels or oxidative stress stimulated lysosomal exocytosis, but inhibited it at high levels. Deletion of the lysosomal ion channel TRPML1 eliminated the stimulatory effect of low levels of oxidative stress. The inhibitory effects of oxidative stress appear to target the component of lysosomal exocytosis that is driven by extracellular Ca2+. We propose that while moderate oxidative stress promotes cellular repair by stimulating lysosomal exocytosis, at high levels oxidative stress has a dual pathological effect: it directly causes cell damage and impairs damage repair by inhibiting lysosomal exocytosis. Harnessing these adaptive mechanisms may point to pharmacological interventions for diseases involving oxidative proteotoxicity or metal toxicity.