SummaryThe International Working Group on the Diabetic Foot appointed an expert panel to provide evidence-based guidance on the management of osteomyelitis in the diabetic foot. Initially, the panel formulated a consensus scheme for the diagnosis of diabetic foot osteomyelitis (DFO) for research purposes, and undertook a systematic review of the evidence relating to treatment. The consensus diagnostic scheme was based on expert opinion; the systematic review was based on a search for reports of the effectiveness of treatment for DFO published prior to December 2006.The panel reached consensus on a proposed scheme that assesses the probability of DFO, based on clinical findings and the results of imaging and laboratory investigations.The literature review identified 1168 papers, 19 of which fulfilled criteria for detailed data extraction. No significant differences in outcome were associated with any particular treatment strategy. There was no evidence that surgical debridement of the infected bone is routinely necessary. Culture and sensitivity of isolates from bone biopsy may assist in selecting properly targeted antibiotic regimens, but empirical regimens should include agents active against staphylococci, administered either intravenously or orally (with a highly bioavailable agent). There are no data to support the superiority of any particular route of delivery of systemic antibiotics or to inform the optimal duration of antibiotic therapy. No available evidence supports the use of any adjunctive therapies, such as hyperbaric oxygen, granulocyte-colony stimulating factor or larvae.We have proposed a scheme for diagnosing DFO for research purposes. Data to inform treatment choices in DFO are limited, and further research is urgently needed.
Although there is correlation between the histological and radiological features of intraosseous lipomas in general, some discrepancies occur in the radiological appearances of lipomas in different sites. The evidence that these lesions are true benign tumours of fat is controversial. Several aetiological factors have been implicated in their development. The constant location of os calcis lesions at the critical angle suggests an aetiology that may be related to biomechanical lines of stress. In other instances it is possible that involution of pre-existing lesions may lead to the development of lipomas.
From a retrospective, cohort study of 205 patients diagnosed with full-thickness tears of the rotator cuff, we determined, using ultrasound, the prevalence of such tears in their 129 siblings. Using 150 spouses as controls, the relative risk of full-thickness tears in siblings versus controls was 2.42 (95% CI 1.77 to 3.31). The relative risk of symptomatic fullthickness tears in siblings versus controls was 4.65 (95% CI 2.42 to 8.63).The significantly increased risk for tears in siblings implies that genetic factors play a major role in the development of full-thickness tears of the rotator cuff.In the UK the shoulder is the third commonest site of musculoskeletal disease (16%) after the spine and knee (23% and 19%, respectively) 1 as well as being the third most common reason for orthopaedic referral in the USA (7.9%) after the knee and spine (14.9% and 8.2%, respectively). 2 Full-thickness tears of the rotator cuff are among the most frequently encountered causes of pain and dysfunction in the shoulder. 3 Estimates for the prevalence of full-thickness tears vary widely. Most cadaver studies give a prevalence of 20%, 4 but estimates of 5% to 30% 5,6 have been published. In asymptomatic individuals estimates of prevalence of 15% to 23.4% have been described after investigation by MRI 7 and ultrasound. 8 All studies agree that the prevalence increases with age and that its associated morbidity, in terms of pain and loss of function, can be severely debilitating. Pain in the shoulder is a common cause of absenteeism from work and is a burden on medical resources. 9 Reported estimates for the mean cost of repair of a rotator cuff vary from US$ 9444 10 to US$ 25 870 11 with a mean time off work of seven months.Theories regarding the causes of full-thickness tears are varied. Historically, mechanical compression of the tendons of the cuff was thought to be the initiating factor. Acromial morphology and the presence of spurs, the morphology of the coracohumeral ligament and the presence of osteophytes at the acromioclavicular joint were all considered to be relevant, although, as early as 1934, Codman 12 favoured an intrinsic theory of degeneration of the tendons of the cuff. Current opinion favours a combination of repetitive microtrauma in association with age-related degenerative changes within the tendons. There is a lack of understanding as to what causes pain in a full-thickness tear and why symptoms are so variable.Increasingly, such tears are being regarded as a normal consequence of the ageing process. 8,13 No studies to date have addressed a possible genetic basis for their pathogenesis and symptomatology. We therefore describe the results of a prospective, cross-sectional study of patients with full-thickness tears. Our aim was to establish the relative risk of their development as well as the risk of occurrence of symptomatic tears in siblings of patients with tears which had been diagnosed by ultrasound. Patients and MethodsComputerised hospital records were used to identify all patients who had been diag...
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