Current management options for osteonecrosis of the femoral head: part 1, diagnosis and nonoperative management.

Osteonecrosis of the femoral head is a multifactorial disease that can result in significant clinical morbidity and affects patients of any age, including young and active patients. Late sequelae of femoral head osteonecrosis include femoral head collapse and subsequent degeneration of the hip joint. A high index of suspicion and improved radiographic evaluation allow orthopedic surgeons to identify this disease at an earlier stage. Current management options for hip osteonecrosis have results that vary according to patient population and disease stage. Modifications of older techniques, as well as emerging technologies, have led to the development of management strategies that may be able to alter the course of femoral head osteonecrosis.

Relative risk factors for requirement of blood transfusion after total hip arthroplasty.

One thousand thirty-five total hip arthroplasty (THA) cases were retrospectively reviewed, and the number and type (autologous and allogenic) of postoperative units of blood transfused were analyzed with respect to pre-, intra-, and postoperative variables. The most significant and consistent predictors of a blood transfusion after THA were advanced age and the use of low-molecular-weight heparin for deep venous thrombosis prophylaxis. Our recommendations for predonation are 1 unit for THA patients younger than 75 years if hemoglobin is 130 g/dL or greater and 2 units or a combination of 1 unit of predonated blood and 1 unit of directed or banked blood for THA patients older than 75 years.

Disease-modifying therapies for osteoarthritis : current status.

Osteoarthritis, the most common form of arthritis, is a debilitating progressive disease principally affecting the elderly. Osteoarthritis therapy has evolved in the past few decades from symptomatic treatment to possible disease-modifying solutions. In this paper, the pathophysiology of osteoarthritis is first reviewed, including an examination of the mechanisms underlying osteoarthritis and discussions of the roles of cartilage, synovial fluid and subchondral bone. The remainder of the paper discusses therapeutic approaches in current use and those in development, with special attention given to pharmacological treatments. Current approaches to treating osteoarthritis--i.e. medications; nonpharmacological modalities, such as physical therapy, exercise, weight management and orthotics; and (as a last resort) surgery--focus on reducing pain and improving (or at least maintaining) mobility. Drugs currently used to treat osteoarthritis fall into several categories: analgesics, NSAIDs, cyclo-oxygenase-2 (COX-2) inhibitors, corticosteroids, viscosupplementation, and symptomatic slow-acting drugs ('nutraceuticals'). The analgesics (paracetamol [acetaminophen] and opiates) have demonstrated less symptomatic efficacy than NSAIDs, while the latter have displayed mixed results in terms of joint space narrowing. COX-2 inhibitors have been demonstrated to be equal to or superior to NSAIDs in effectiveness. However, once considered a safer alternative, COX-2 inhibitors have become the subject of intense scrutiny since recent clinical evidence has cast suspicion on their cardiovascular safety profile. Injectable therapies, such as corticosteroids and viscosupplementation have elicited favorable short-term response but no long-term structural modification. On the other hand, the slow-acting drugs, especially chondroitin and glucosamine sulfate, have shown promising results. Also reviewed are other established and experimental therapies that seek to modify and/or even reverse the course of osteoarthritis. These include such medications as colchicine, bisphosphonates and hormones; dietary therapeutics, such as ginger extract and green tea; and such truly experimental treatments as matrix metalloproteinase inhibitors, cytokines, nitric oxide, growth factors and gene therapy. Osteoarthritis continues to be a difficult disorder to treat, as there is no cure as such and current treatments focus mainly on relieving pain and maintaining joint function. The search nevertheless continues for management regimens that can slow, alter or reverse the degenerative processes of osteoarthritis.

Stiffness after total knee arthroplasty.

Postoperative stiffness is a debilitating complication of total knee arthroplasty. Preoperative risk factors include limited range of motion, underlying diagnosis, and history of prior surgery. Intraoperative factors include improper flexion-extension gap balancing, oversizing or malpositioning of components, inadequate femoral or tibial resection, excessive joint line elevation, creation of an anterior tibial slope, and inadequate resection of posterior osteophytes. Postoperative factors include poor patient motivation, arthrofibrosis, infection, complex regional pain syndrome, and heterotopic ossification. The first steps in treating stiffness are mobilizing the patient and instituting physical therapy. If these interventions fail, options include manipulation, lysis of adhesions, and revision arthroplasty. Closed manipulation is most successful within the first 3 months after total knee arthroplasty. Arthroscopic or modified open lysis of adhesions can be considered after 3 months. Revision arthroplasty is preferred for stiffness from malpositioned or oversized components. Patients who initially achieve adequate range of motion (>90 degrees of flexion) but subsequently develop stiffness more than 3 months after surgery should be assessed for intrinsic as well as extrinsic causes.

Risks associated with blood transfusion after total knee arthroplasty.

A retrospective study of 1,402 patients who underwent primary total knee arthroplasty (TKA) (1,194 unilateral, 208 bilateral) was performed. The strongest predictors for allogenic transfusion after surgery were advancing age (P<.001), low preoperative hemoglobin (P<.001), and the use of low-molecular-weight heparin postoperatively (P<.01). Pre-donation of 1 unit of autologous blood before TKA decreased the allogenic transfusion rate from a baseline of 38% to 11%, whereas pre-donating 2 units lowered the rate of breakthrough transfusion of allogenic blood to 7%. A patient with a preoperative hemoglobin >150 g/L or who is younger than age 65 with a preoperative hemoglobin >130 g/L may not benefit from pre-donation, and a high rate of wastage may result.