ACS is an encouraging treatment option for patients with unilateral lumbar radicular compression. The decrease in pain was pronounced, clinically remarkable, and potentially superior to steroid injection.
Treatment with corticosteroids is a risk factor for non-traumatic avascular necrosis of the femoral head, but the pathological mechanism is poorly understood. Short-term treatment with high doses of methylprednisolone is used in severe neurotrauma and after kidney and heart transplantation. We investigated the effect of such treatment on the pattern of perfusion of the femoral head and of bone in general in the pig. We allocated 15 immature pigs to treatment with high-dose methylprednisolone (20 mg/kg per day intramuscularly for three days, followed by 10 mg/kg intramuscularly for a further 11 days) and 15 to a control group. Perfusion of the systematically subdivided femoral head, proximal femur, acetabulum, humerus, and soft tissues was determined by the microsphere technique. Blood flow in bone was severely reduced in the steroid-treated group. The reduction of flow affected all the segments and the entire epiphysis of the femoral head. No changes in flow were found in non-osseous tissue. Short-term treatment with high-dose methylprednisolone causes reduction of osseous blood flow which may be the pathogenetic factor in the early stage of steroid-induced osteonecrosis.
In beagle dogs, the alterations of intraosseous pressure and blood supply in the femoral head that result from the administration of vasoactive substances were examined, and the changes were documented by magnetic resonance imaging (MRI). Vasoactive substance were infused into the medial and lateral circumflex femoral arteries of 12 beagle dogs. All infusions were done under standardised conditions with simultaneous measurements of venous blood flow and intraosseous pressure distribution in the proximal femur. The drugs were infused in three cycles of 30 min each separated by 30 min recovery periods, followed by MRI examination at the end of each experiment. At an intraosseous pressure of 14.3 (+/- 4.2) mmHg in the femoral head epiphysis (I), 11.6 (+/- 2.7) mmHg in the greater trochanter (II) and 9.3 (+/- 3.2) mmHg in the femoral shaft (III), a baseline flow of 96.2 (+/- 18.8, n = 12) ml/min was measured in the femoral vein. After infusing bradykinin at a concentration of 10(-6) moles, which is commonly known to lead to cerebral and subcutaneous oedema formation by vessel dilatation, the intraosseous pressure increased to (I): 49.1 (+/- 6.2) mmHg, (II): 42.5 (+/- 5.8) mmHg and (III): 38.3 (+/- 7.1) mmHg in the three measured femoral areas (n = 3). After the bradykinin injection, femoral vein flow increased to a peak value of 238.4 (+/- 43.4) ml/min and then dropped to 62.3 (+/- 14.2) ml/min after discontinuation of the bradykinin infusion. In a second and third series of tests, hyperosmolar (20% NaCl) and hypo-osmolar (distilled water) solutions were applied, also resulting in increased but lower mean intraosseous pressure values (17.3 +/- 4.1 and 25.7 +/- 5.1 ml/min, respectively) in all regions. When administering bradykinin, MRI scans taken immediately after completion of the experiment showed substantial oedema in the femoral muscular system, but without any changes of osseous signals in T1- or short time inversion recovery (STIR)-weighted images, nor did any changes occur when solutions of 20% NaCl or distilled H2O were injected. The results of our experiments demonstrate that acute increases of intraosseous pressure do not cause MRI signal alterations. We therefore conclude that in addition to the described pressure increase, other intraosseous alterations must occur to lead to the detectable signal changes found among patients with diagnosed femoral head necrosis. Finally, the short time period between the rise in intraosseous pressure and performing a conventional MRI may be one reason for missing the development of an intraosseous oedema. On the other hand, conventional MRI might have additional disadvantages for detecting intraosseous fluid compared with a dynamic imaging modality.
T reatment with corticosteroids is a risk factor for non-traumatic avascular necrosis of the femoral head, but the pathological mechanism is poorly understood. Short-term treatment with high doses of methylprednisolone is used in severe neurotrauma and after kidney and heart transplantation. We investigated the effect of such treatment on the pattern of perfusion of the femoral head and of bone in general in the pig.We allocated 15 immature pigs to treatment with high-dose methylprednisolone (20 mg/kg per day intramuscularly for three days, followed by 10 mg/kg intramuscularly for a further 11 days) and 15 to a control group. Perfusion of the systematically subdivided femoral head, proximal femur, acetabulum, humerus, and soft tissues was determined by the microsphere technique. Blood flow in bone was severely reduced in the steroid-treated group. The reduction of flow affected all the segments and the entire epiphysis of the femoral head. No changes in flow were found in non-osseous tissue. Short-term treatment with high-dose methylprednisolone causes reduction of osseous blood flow which may be the pathogenetic factor in the early stage of steroid-induced osteonecrosis.
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