You are in: eMedicine Specialties > Orthopedic Surgery > HIP Osteonecrosis, HipArticle Last Updated: Oct 18, 2006AUTHOR AND EDITOR INFORMATIONSection 1 of 12
  Author: Michael Levine, MD, Clinical Instructor of Orthopedic Surgery, University of Pittsburgh School of Medicine, Chief of Orthopedic surgery, West Penn Hospital, Chair, Section of Orthopedic Surgery, Forbes Regional Hospital Michael Levine is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Association of Hip and Knee Surgeons, American Medical Association, Orthopaedic Research Society, Pennsylvania Medical Society, Pennsylvania Orthopaedic Society, and Phi Beta Kappa Coauthor(s): Amar Rajadhyaksha, MD, Resident, Department of Orthopedic Surgery, New York Medical College; Michael Mont, MD, Associate Professor, Department of Orthopaedic Surgery, Johns Hopkins Medical Institution Editors: B Sonny Bal, MD, Associate Professor, Department of Orthopedic Surgery, University of Missouri School of Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; James J McCarthy, MD, FAAOS, FAAP, Associate Professor, Consulting Orthopedic Surgeon, Department of Orthopedics and Rehabilitation, University of Wisconsin School of Medicine and Public Health;; Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital; Carlos J Lavernia, MD, FAAOS, Adjunct Clinical Professor, Department of Orthopedic Surgery, University of Miami School of Medicine; Medical Director, Orthopedic Institute at Mercy Hospital Author and Editor Disclosure Synonyms and related keywords: aseptic necrosis, avascular necrosis, osteonecrosis of the femoral head, ischemic necrosis INTRODUCTIONSection 2 of 12
  Osteonecrosis of the femoral head involves the hip joint. Osteocytes of the femoral head die along with the bone marrow; resorption of the dead tissue by new but weaker osseous tissue can lead to subchondral fracture and collapse. Two forms of osteonecrosis exist, traumatic (the most common form) and atraumatic. Other terms to describe this disorder include avascular necrosis and ischemic necrosis to denote vascular etiology. The term aseptic necrosis also has been used to indicate that infection does not play a causative role. Alexander Munro first identified the condition in 1738. In the mid 1800s, Cruveilhier was the first to attribute the disorder to an aberration of circulation in the femoral head. As recognition of the disorder has improved with better technological identification and awareness in the medical community, the frequency of diagnosis has increased. For excellent patient education resources, visit eMedicine's Breaks, Fractures, and Dislocations Center. Also, see eMedicine's patient education article Total Hip Replacement. ProblemOsteonecrosis is now a commonly recognized disorder with significant morbidity. The end stage of the process is severe destruction of the femoral head with resultant degeneration of the hip joint. In many patients, even early identification and intervention do not alter the result. Unfortunately, patients who are affected with osteonecrosis are young, usually in the third to sixth decades of life. Traumatic and atraumatic osteonecrosis are essentially 2 distinct problems. The traumatic form has a definitive causal event and is isolated to the particular injured bone. The atraumatic form has multiple etiologies and can involve multiple bones. The main focus of this article is atraumatic osteonecrosis. FrequencyApproximately 10,000-20,000 new cases are identified each year in the United States. The traumatic form occurs in 10% of undisplaced femoral neck fractures, 15-30% of displaced femoral neck fractures, and 10% of hip dislocations. Corticosteroid use contributes to the atraumatic form in 5-25% of patients. Male-to-female ratio is about 4:1. At least 50% of patients with atraumatic hip osteonecrosis are thought to have bilateral involvement. Other bones often are involved in the atraumatic form, including the shoulder, knee, and talus. EtiologyAs the name implies, traumatic osteonecrosis is secondary to direct injury to the femoral head with resultant damage of the blood supply. Fracture of the femoral head or neck and hip dislocation are the primary mechanisms of injury. Atraumatic osteonecrosis has many risk factors. The two most commonly associated problems are corticosteroid use and alcohol abuse. The third most common source is idiopathic. Other factors include sickle-cell anemia, Gaucher disease, lupus, coagulopathies, hyperlipidemia, organ transplantation, caisson disease, and thyroid disorders. Hip osteonecrosis resulting from corticosteroid use and alcohol abuse often is associated with the worst prognosis. Frequently, steroid-induced osteonecrosis often involves multiple bones and, in the case of the hip, results in nearly 100% bilateral involvement. The exact dose required to induce osteonecrosis remains an enigma, but most studies indicate that higher doses, even over a short duration, present the highest risk. Often, patients on steroids have other associated risk factors. Osteonecrosis associated with alcohol abuse usually occurs in those in those who drink more than 400 mL of alcohol per week. It is more common in those with a long-term history of heavy consumption. PathophysiologyTraumatic osteonecrosis is a direct result of disruption of blood supply to the femoral head. Death of bone marrow occurs within 6-12 hours after vascular insult. Death of the bone becomes apparent several days later. The pathophysiology in atraumatic osteonecrosis remains controversial. Fat cell hypertrophy with resultant pressure increase within the femoral head, leading to vascular collapse and then necrosis, has been proposed as a mechanism for steroid-induced osteonecrosis. A fat embolism phenomenon with resultant vascular occlusion is another proposed mechanism. A hyperlipidemic state seems to be related to causation, but the exact cause is unknown. Similarly, the lipid hypothesis also has been applied to cases associated with alcohol abuse. In caisson disease, circulating nitrogen bubbles occlude blood vessels in response to reduction in ambient pressure during decompression. Sickle-cell anemia results in bone death secondary to the sickling process and subsequent vascular occlusion. Increased intraosseous pressure contributes directly to the propagation of necrosis, regardless of etiology. As bone death occurs, a repair process takes place as dead bone is removed and replaced by new bone. During this phase, the bone underlying the joint surface is weakened. In most patients, subchondral fracture alters the articular surface resulting in abnormal mechanics and arthritic alterations to the joint. ClinicalPatients with osteonecrosis usually are men in sixth decade of life who experience pain primarily in the groin but occasionally the buttocks. Pain usually is deep and throbbing and is worse with ambulation, but it also is significant at night. Onset often can be described as acute. Patients frequently describe a catching or popping sensation with motion. A history of prior trauma, steroid use, alcohol abuse, and other risk factors should be entertained. Physical examination reveals pain with range of motion and ambulation. Limitation of internal rotation in both flexion and extension are prevalent, with passive internal rotation in extension being particularly painful. A Trendelenburg gait often is present. Plain x-ray findings frequently are normal. Therefore, a high index of suspicion should arise based on the history and physical. INDICATIONSSection 3 of 12
History and physical examinations are paramount to diagnosis. Treatment is indicated after diagnosis is confirmed with radiographic studies. Most studies indicate that the risk for disease progression is greater with nonsurgical treatment than with surgical intervention. RELEVANT ANATOMYSection 4 of 12
Blood is supplied to the femoral head primarily from branches of the medial and lateral circumflex vessels, which arise from the femoral artery. The retinacular branches deep to the posterior capsule are the most important. Blood also is supplied from the obturator artery. CONTRAINDICATIONSSection 5 of 12
There are few contraindications to surgical treatment of osteonecrosis. Obvious disorders aside (eg, severe systemic disease, systemic sepsis), those afflicted often are young and have few surgical contraindications. WORKUPSection 6 of 12
Lab Studies
Imaging Studies
Diagnostic Procedures
Histologic FindingsThe first histologic findings are marrow and adipocyte necrosis. Next, liquefaction necrosis and interstitial edema occur. Pyknotic nuclei with empty lacunae are identified as the osteocyte necrosis occurs. Eventually, the zone of necrosis is surrounded by repair tissue as revascularization is occurring. During this phase, the subchondral plate is weakened as resorption occurs faster than reformation, leading to subchondral collapse and eventual cartilage damage. StagingSeveral radiographic staging systems are currently used.
TREATMENTSection 7 of 12
Medical therapyNonsurgical treatment of osteonecrosis is limited. Observation and protected weightbearing are options. Certain cases of early stage disease (eg, Ficat stage 1) can be treated successfully with this option. However, most studies indicate that the risk for disease progression is greater with nonsurgical treatment than with surgical intervention. Nonsteroidal anti-inflammatory drugs can be used to reduce pain and inflammation in patients who cannot have surgery for medical or other reasons or for patients who are undergoing surgical treatment. Physical therapy can be helpful to restore motion and improve gait. Electrical stimulation has been used in several centers and in some studies has been helpful in treatment prior to femoral head collapse. Controversy exists regarding the benefit of surgical treatment options versus observation in certain cases. Further study is required at this time. Pharmacotherapy that attacks the pathophysiology of the disease has had mixed results. Examples include Lopid for hyperlipidemias and nifedipine for vascular disorders. Short-term follow-up (about 24 months) of patients in alendronate studies have demonstrated delayed femoral head collapse (Lai, 2005). Surgical therapyThe mainstay of treatment for osteonecrosis is surgical. Numerous procedures are available, indicating that no single procedure is distinctly advantageous. Preoperative staging, particularly with collapse of the femoral head, and acetabular involvement are the determining factors for choosing a particular operation. Preoperative detailsThe decision for each procedure is based on preoperative staging. Core decompression and cancellous and cortical bone grafting procedures usually are indicated in Ficat stage IIa or earlier stages. The trapdoor procedure and allograft procedures are indicated for stage IIb or III lesions. Osteotomies are used for stage II and III disease. Arthrodesis and arthroplasty are utilized primarily for stages III and IV but occasionally are used for stages I and II. Intraoperative detailsThe objective in core decompression is to stimulate revascularization and decrease pressure within the femoral head. The patient is placed supine on a fracture table. Using image intensification through a lateral incision above the trochanteric ridge, a 10-mm core of bone is removed from the femoral necrotic lesion. Bone grafting has several techniques.
Several different techniques are available for osteotomy, but the concept is to rotate the area of the femoral head away from the weightbearing surface.
Arthrodesis is fusion of the hip joint. The joint is denuded of articular cartilage, and the femoral head and acetabulum are fixed to create a solid interface. In arthroplasty, conventional techniques are used, with either surgical approach using cemented or cementless implants.
The trapdoor procedure involves open excision of the necrotic bone by elevation of the cartilage and cancellous grafting. Limited femoral resurfacing for young patients with intact acetabular cartilage with a collapsed femoral head is a valuable alternative to total hip replacement. Total hip replacement, with a femoral and acetabular component, currently is the end result of the disease. Postoperative details
Follow-up
COMPLICATIONSSection 8 of 12
OUTCOME AND PROGNOSISSection 9 of 12
The success rate in patients not treated by arthroplasty in stage 0 or I approaches 90% in some series. Once femoral head collapse occurs, these treatments offer limited benefit. Procedures such as the trapdoor procedure potentially may improve results in stage II and III, but presently, total hip replacement remains the treatment of choice once collapse has occurred. If not treated, 80% of femoral heads collapse within 4 years of diagnosis. FUTURE AND CONTROVERSIESSection 10 of 12
The natural history of atraumatic osteonecrosis is still not well understood. Different etiologies of the disease often have different clinical courses. Steroid-induced disease has the worst prognosis, and most cases progress to collapse of the femoral head. Future studies hopefully will focus on the natural history of the disease and identify surgical procedures of limited morbidity to prevent collapse in the early stages, along with development of procedures for use following collapse but before development of arthritis, short of total hip replacement. Future prostheses with novel bearing surfaces (ie, metal on metal, ceramic on ceramic) are being tried to increase the success rate for total hip replacements in patients with osteonecrosis. MULTIMEDIASection 11 of 12
REFERENCESSection 12 of 12
Article Last Updated: Oct 18, 2006 | |||||||||||||||||||||||||||||||||||
