China
Africa
Explore chapters and articles related to this topic
Paper 2
Published in Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw, The Final FRCR, 2020
Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw
Scurvy is caused by vitamin C deficiency which leads to abnormal collagen and bone development and a bleeding diathesis. Features include ground glass osteoporosis, sclerosis of the margins of the epiphysis (Wimberger sign), metaphyseal spurs, dense metaphyseal lines (lines of Frankel), Trummerfield zone (radiolucent zone on the diaphyseal line of the Frankel line), pencil-point cortical thinning, corner fractures, an exuberant periosteal reaction and haemarthrosis. Coarsened trabeculae are not features of the condition. Cloaca, involucrum and sequestrum are features of osteomyelitis.
The locomotor system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
The following description refers to untreated acute haematogenous osteomyelitis (Figure 13.13). Most cases involve the metaphysis of long bones, in which dilated vascular sinusoids with sluggish blood flow provide an ideal site for the multiplication of bacteria. Bacteria pass into the marrow spaces and provoke an acute inflammatory response. Pus spreads rapidly throughout the medullary cavity and cortex, elevates the periosteum, and forms a subperiosteal abscess. Pus may track into the surrounding soft tissues, ultimately reaching the skin surface to form a sinus. Vascular thrombosis leads to bone necrosis. The piece of dead bone is known as a sequestrum. Meanwhile, cytokines released by the inflammatory cells activate osteoclasts, causing bone destruction. As infection becomes less acute, subperiosteal new bone may form an incomplete shell (involucrum) around the dead bone.
Inflammation and Infection
Published in Manoj Ramachandran, Tom Nunn, Basic Orthopaedic Sciences, 2018
Vikas Khanduja, Sertazniel Singhkang, Manoj Ramachandran
The diagnosis of osteomyelitis is usually made by a combination of clinical findings, radiographs, bone scanning and magnetic resonance imaging (MRI) scans, along with the aspiration of pus from the involved area and positive blood cultures. In chronic osteomyelitis, radiographic signs of necrotic bone (sequestrum) and periosteal new bone formation (involucrum) are evident.
Modern management of diabetic foot osteomyelitis. The when, how and why of conservative approaches
Published in Expert Review of Anti-infective Therapy, 2018
Javier Aragón-Sánchez, Benjamin A Lipsky
The pathophysiology of DFO is different from other types of osteomyelitis, such as infection in large bones secondary to hematogenous spread, infected prostheses, and open fractures. Hematogenous osteomyelitis is rare in adults; when it occurs it most frequently involves vertebral bodies [9]. The pathogenesis of hematogenous osteomyelitis is characterized by initial infection in the bone marrow, with the extension of a sequestrum and necrotic material through the cortical bone via a fistula, which ultimately can break through the soft tissue and skin [9]. Skin rupture and suppuration are the last step, as the infection progresses from ‘inside to outside’ the body. This process is clearly different from cases of DFO, which nearly always progress from ‘outside to inside.’ These infections are mostly associated with skin ulceration (usually related to peripheral neuropathy, and sometimes physical, chemical, or heat trauma), often with associated peripheral arterial disease. Bacteria gain access to the bone by contiguous spread, entering from overlying soft tissue and penetrating the cortex (osteitis) before involving the marrow (medullary infection) [10]. Infection of the bone results in inflammatory destruction, bone necrosis (sequestrum), and ultimately new bone formation (involucrum). This contiguous spread of infection explains why wounds that extend down to bone or joint are at high risk for developing osteomyelitis [3].