Osteomyelitis (OM) is an infection of bone. Symptoms may include pain in a specific bone with overlying redness, fever, and weakness. The long bones of the arms and legs are most commonly involved in children e.g. the femur and humerus, while the feet, spine, and hips are most commonly involved in adults.The cause is usually a bacterial infection, but rarely can be a fungal infection. It may occur by spread from the blood or from surrounding tissue. Risks for developing osteomyelitis include diabetes, intravenous drug use, prior removal of the spleen, and trauma to the area. Diagnosis is typically suspected based on symptoms and basic laboratory tests as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR).This is because plain radiographs are unremarkable in the first few days following acute infection. Diagnosis is further confirmed by blood tests, medical imaging, or bone biopsy.Treatment of bacterial osteomyelitis often involves both antimicrobials and surgery. In people with poor blood flow, amputation may be required. Treatment of the relatively rare fungal osteomyelitis as mycetoma infections entails the use of antifungal medications. In contrast to bacterial osteomyelitis, amputation or large bony resections is more common in neglected fungal osteomyelitis, namely mycetoma, where infections of the foot account for the majority of cases. Treatment outcomes of bacterial osteomyelitis are generally good when the condition has only been present a short time. About 2.4 per 100,000 people are affected each year. The young and old are more commonly affected. Males are more commonly affected than females.
The fact that WPW patients are young and do not have structural heart disease, lead to using catheter ablation of the APs with the elimination of the atrial fibrillation as well as the episodes of re-entrant ventricular tachycardia. This elimination of the atrial fibrillation with ablation implies APs have some pathophysiologic role in the development of a-fib in the WPW patient.Functionally defined re-entry does not require the alternative anatomically defined circuit accessory pathways and it may not reside in just one location. Ventricular fibrillation (VF) following ventricular tachycardia (VT) may be described as a functionally defined re-entry problem caused by multiple mini re-entrant circuits spontaneously created within the ventricular myocardium. The original re-entrant circuit breaks down into multiple mini reentrant circuits. (VF becoming the grand finale of a single prolonged VT larger circus movement, propagating change in the "functional core" of the ventricular myocardium, dissipating mini reentrant circuits, exhibited as ventricular fibrillation.) Ischemia, electrolyte, pH abnormalities, or bradycardia are potential causes of functionally defined re-entry due to changes in the properties of the cardiac tissues functional core. (No accessory pathway required). For reentry to occur, the path length of circuit should be greater than the wave length (ERP × conduction velocity) of impulse. See also
AV reentrant tachycardia
AV nodal reentrant tachycardia

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