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Button Sequestrum
Published in Michael E. Mulligan, Classic Radiologic Signs, 2020
United States Army Colonel Paul Wells’ wrote about the button sequestrum in 1956. He described four patients with eosinophilic granulomas affecting their skulls who were seen at Letterman Army Hospital in San Francisco. In each case, a central sequestrum resembling a button was evident on the plain-film radiographs (Figure 1). Among the many articles which describe this lesion, however, only one has specifically called attention to the rather characteristic sequestrum produced in some of these cases. This sequestrum appears as a ‘button’ of intact bone in the center of a circular area of destruction.’1 He referred to a 1946 paper by four other Army officers, also from Letterman Army Hospital, that discussed nine cases of eosinophilic granuloma2. One of the cases in the earlier article had sequestra found at operation but they could not be seen on the preoperative roentgenogram and there was no discussion of sequestra in that report.
Head and neck cancer
Published in Peter Hoskin, Peter Ostler, Clinical Oncology, 2020
Difficulty in mastication, swallowing, dysarthria and dysphonia result from surgical resection of structures involved in these processes. Poor healing is a particular problem following extensive surgery when the vascularity of the tissue has been compromised, especially if the tissues have been previously irradiated. Osteomyelitis can complicate surgery when there has been a resection of bone (e.g. mandibulectomy), which has become secondarily infected. Treatment is with high doses of the appropriate antibiotic and further surgery might be required to remove the sequestrum.
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.
Recent advances in the local antibiotics delivery systems for management of osteomyelitis
Published in Drug Delivery, 2021
Reem Khaled Wassif, Maha Elkayal, Rehab Nabil Shamma, Seham A. Elkheshen
The three categories of osteomyelitis can occur in acute or chronic phases. Acute osteomyelitis develops over several days or weeks in contrast to the chronic one, which is known to evolve over a span of months or even years. The mechanism of acute infection involves the entry of the microorganisms, which release proteolytic enzymes and toxic free radicals causing inflammation and destruction of the surrounding tissues. This leads to unreachable blood flow to the area of infection, which causes poor vascularized area. The poor vascularization enhances the chance of forming sequestrum that results from the destruction of bone and hence boosts the impediment of penetration of the antimicrobial agents, which accounts later for the chronicity of the infection. Chronic osteomyelitis has different stages demonstrating the progression of the disease as well as the degree of deterioration of bones. Surgery is usually needed to remove the infection focus for the complete resolution of infection.
Primary Calvarial Tuberculosis: a report of three cases
Published in British Journal of Neurosurgery, 2019
Subramanya G. S. Datta, Vidhu Bhatnagar, Somnath Pan, Ritu Mehta, Chandraprakash Sharma
Treatment for Calvarial tuberculosis usually includes surgery and ATT therapy. Neurosurgical intervention is required for cases with large extradural collections/granulation tissue, necrotic bone or large scalp swellings (with or without sinus formation). Surgery is also indicated in some cases to establish the diagnosis. The procedure usually described is an incision in normal skin with proper care in raising the flap, evacuation of pus, debridement of necrotic tissue, excision of involved bone and the sinus tract if any. Dura should be left untouched. Surgery is not indicated for small lesions, even in the presence of a sequestrum, provided there is a favorable response to chemotherapy. Although there are some reports in the literature favoring antituberculous therapy alone, recent studies indicate that combination treatment is better, as areas of diseased bone may harbor tuberculous bacilli.15,19–21
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].