ABSTRACT
Osteonecrosis of the femoral head (ONFH) is a common and refractory disease in orthopaedic clinics. The number of patients with ONFH is increasing worldwide every year. There are an estimated 8.12 million patients with nontraumatic osteonecrosis in China alone. Treatment of nontraumatic osteonecrosis has always been a clinical challenge for orthopaedic surgeons. To further standardize diagnosis and treatment of ONFH, these guidelines provide not only basic diagnosis, treatment, and evaluation systems for ONFH but also expert advice and standards in many aspects, including epidemiology, aetiology, diagnostic criteria, pathological staging, prevention and treatment options, and postoperative rehabilitation. The aetiological factors of ONFH can currently be divided into two major categories: traumatic and nontraumatic; however, the specific pathological mechanism of ONFH is not completely clear. Currently, the staging system of ONFH formulated by the Association Research Circulation Osseous is widely used in clinical practice. Based on the changes in the intraosseous blood supply at different stages, the corresponding nonsurgical and surgical treatments are recommended, and when there are risk factors for possible ONFH, certain preventive measures to avoid the occurrence of osteonecrosis are recommended. These guidelines provide brief classification criteria and treatment regimen for osteonecrosis. Specification of the aetiology, treatment plan based on comprehensive consideration of the different stages of osteonecrosis, hip function, age, and occupation of the patients are important steps in diagnosis and developing treatment strategies. TRANSLATIONAL POTENTIAL OF THIS ARTICLE: New advances in the epidemiology, etiology, pathophysiology, imaging, diagnosis and treatment of ONFH have been renewed in this revision. This guideline can be used for reference by orthopedic professionals and researchers, and for standardized diagnosis and treatment management under the clinical guidance, which is conducive to the prevention, treatment and further research of ONFH, improving the diagnosis and treatment level, making patients' symptoms under good control, and improving their quality of life.
ABSTRACT
OBJECT: Because of the controversy regarding the benefits of 24-hour administration of methylprednisolone in patients with spinal cord injury (SCI), it is important to investigate its mechanism of action and side effects. This study was conducted to determine if high-dose methylprednisolone modulates neural and vertebral blood flow in an awake large-sized animal model without SCI. METHODS: From a group of 18 immature female domestic pigs born to nine different litters, nine animals were randomly allocated to receive methylprednisolone treatment, whereas their nine female siblings served as controls. Drug or placebo was applied in a blinded fashion by a third person not involved in the study. The following treatment for SCI, as suggested by the North American Spinal Cord Injury Study, was administered to the awake pig: methylprednisolone (30 mg/kg of body weight) was infused into the jugular vein during a 15-minute period, followed by a 45-minute pause, and the infusion was maintained over a 23-hour period at a dose of 5.4 mg/kg body weight/hour. By means of the radioactive tracer microsphere technique, spinal cord blood flow (SCBF) was measured in the awake standing pig in the cerebrum, and in spinal gray and white matter, nerve roots, endplates, cancellous bone, cortical shell, and T12-L2 discs. Blood flow was measured before, 1 hour after initiation of infusion, and 24 hours postinfusion. Examination of blood flow in the neural and vertebral tissue samples, as well as of central hemodynamics, revealed no significant difference between the experimental and control groups, and this parity was maintained throughout the experimental phases. CONCLUSIONS: In the awake pig model, 24-hour methylprednisolone treatment does not modulate cerebral or SCBF, nor does it increase the risk for vertebral osteonecrosis by producing vertebral ischemia.
