Vol. 13 Issue 11
Clinical Case Report
A Case of Nontraumatic Avascular Necrosis of the Hip
A 42-year-old African American woman presented to the orthopedic department for follow-up with a new onset of occasional right inguinal hip pain, which was greatest with full weight-bearing. The patient denied fever, chills, night pain, weight loss or a history of trauma. Laboratory data obtained in the emergency room showed normal values for rheumatoid factor (RF), HLAb27, thyroid function tests (TFTs), uric acid and complete blood count; however, the erythrocyte sedimentation rate (ESR) was 34 mm/hour.
A right hip X-ray demonstrated an ill-defined translucency at the lateral aspect of the right femoral head with mild periosteal elevation (Figures 1 and 2).
An MRI was ordered and an orthopedic consultation was submitted. Approximately one week later, the patient was evaluated in the department of orthopedics, and she was much improved, with only mild discomfort in her right hip area during ambulation.
Further review of her medical records found that the patient had been evaluated for right knee pain approximately six months previously. Her complaint on that visit was atraumatic right knee pain and swelling. Normal laboratory data obtained on that visit were antinuclear antibody and uric acid; however, her ESR was 38 mm/hour. Her knee X-rays demonstrated a slight mottled appearance to the distal femur and proximal tibia, with widening of the femoral metaphysis and a questionable thickened medial cortex. Her physical exam was without effusion with full range of motion and mild patella femoral crepitus. No ligamentous laxity was found. She was diagnosed with multiple-joint pain with a suspect of systemic arthropathy.
A repeat of laboratory tests was ordered, including ESR, RF, HLAb27 and TFTs, which again were all within normal limits except the ESR, at 34 mm/hour. Also, a right knee MRI was ordered, and the patient was advised to follow-up on completion of these tests. The knee MRI was not performed, and the patient had not returned for her follow-up exam until the emergency room visit approximately eight months later.
On obtaining the patient's medical history, she was found to have chronic severe reactive airway disease, which she had been treating with oral and inhaled steroid treatment over the last 17 years. The patient volunteered information that while she lived in Panama from 1997 until 1999, she was treated by a civilian physician with high-dose oral prednisone, as high as 1,200 mg per day. She also had a history of tobacco abuse, which consisted of one pack of cigarettes per day over the last 17 years.
The remaining medical history was benign. During her orthopedic physical exam, she was found to have full range of motion to both right knee and hip without crepitus or discomfort. She experienced mild discomfort with direct pressure over the right greater trochanter area and mild discomfort on internal rotation. No leg length discrepancy was present. Neurovascular status was intact, as was the skin, without erythema or rashes.
On review of her hip MRI, she was found to have bilateral femoral head crescent sign, with the right greater than the left (Figures 3 and 4). The patient was placed on crutches and non-weight-bearing and scheduled for right core decompression. However, on her preoperative history and physical visit, she arrived in the orthopedic clinic ambulating without crutches. Therefore, repeat radiologic studies were obtained and demonstrated right-sided femoral head collapse. It was decided to perform left-sided femoral head core decompression and anticipate right-sided hemiarthroplasty at a later date.
Avascular necrosis of the femoral head may be primary or idiopathic, with no clear etiologic factor established. One text describes osteonecrosis as a condition of the hip, not a disease of bone.1 Various secondary causative factors include alcohol abuse, gout, caisson disease, Gaucher's disease, renal osteodystrophy, sickle cell anemia and systemic steroid use.2 The widespread use of corticosteroids is probably the principal reason for the high number of nontraumatic cases of osteonecrosis seen over the last three decades.1
The major blood supply to the femoral head in adults are the branches of the medial and lateral circumflex arteries, which enter the capsule at its distal attachment and pass with the reflected capsule proximally along the posterior surface of the femoral neck. At the level of the femoral head base, the blood supply to the head is derived peripherally from minute arterioles, primarily situated posteriorly and centrally from the endosteal vessels of the femoral neck. A small blood supply enters the fovea by way of the ligamentum teres, which diminishes with advancing age.3
Avascular necrosis of the femoral head develops when the blood supply is interrupted by traumatic or nontraumatic factors as outlined in the accompanying table.1,3,4
North American and European studies have demonstrated that persons who regularly consume greater than 400 mL per week of alcohol were at 13 times greater risk of developing osteonecrosis than those who never consume alcohol.2 With idiopathic avascular necrosis of the femoral head, men most commonly are affected, with a ratio of 4:1, typically in the 40s and 50s, and is bilateral in 40% to 80% of patients.2 When the diagnosis is made during the 20s and 30s, it has been described as osteochondritis dissecans.
Warner and colleagues reported five years of experience with core decompression for treatment of avascular necrosis of the femoral head that was predominantly steroid-induced. Fifty percent of patients who continued the use of steroids demonstrated a disease progression, compared with 22% when steroids were discontinued.5
Generally, the patient may present with low-grade pain about the hip but that at first may be referred to the thigh or knee. The patient may present with or without an antalgic gait.4 In the past, plain radiographs, whole bone scans and computed tomography were important tools in assisting in the diagnosis of osteonecrosis, and they still play an important role on initial evaluation.
With the initial suspicion of osteonecrosis, two specialized anteroposterior radiographs may be helpful. The first is centered over the hip with the thigh flexed approximately 40 degrees, which allows visualization of the anteriorly localized necrotic sectors. The second view is with the thigh fully extended and the X-ray beam tilted 30 degrees, angled from superior proximal to inferior distal region. This second view helps capture the posterior portion of the femoral head.
Nevertheless, MRI and SPECT provide the greatest ability to detect osteonecrosis at its earliest stages. MRI can be an early detector of the extent of osteonecrosis of femoral head involvement and for assessment of the contralateral hip, because bilateral involvement in nontraumatic cases is approximately 60%. CT can be quite beneficial for spatial localization and may help verify subchondral collapse.1
The typical increased density noted on plain films does not appear before two months have elapsed and may not be easily identified for up to six months. Avascular necrosis of the femoral head must be differentiated from necrotic changes, which follow irradiation and caisson disease (the bends).4
Osteonecrosis staging is described in detail by Enneking and by Ficat, on which our treatment plan was based.6
With clinical suspicion and/or early diagnosis of osteonecrosis, it is very important to prohibit weight-bearing on the affected side. Premature weight-bearing causes the necrotic head to collapse with subsequent degenerative changes.
Radiographic and clinical follow-up are used at six-week intervals. Protective weight-bearing may take a minimum of three to six months before the patient would be able to full weight-bear without a device. However, it should be noted that the success for stage 1 and stage 2 hips has been reported to range from less than 5% to 20% at five-year follow-up.
Core decompression is performed to try to effectively lower intraosseous pressure and to remove a central core of bone from the lesional area. A biopsy may be obtained and can confirm the disease histologically. The procedure is performed under fluoroscopy and typically involves minimal morbidity (Figures 5 and 6).
Postoperatively, patients should remain non-weight-bearing for six weeks to protect the lateral cortical window. Operative treatment routinely has been unsuccessful, especially in patients with Ficat stages 2, 3 and 4. One text shows that core decompression success rates vary from 45% to 95% for stage 1 hips, 30% to 85% for stage 2 hips and 15% to 60% for stage 3 hips.2 Therefore, this procedure is best suited for stage 1 and early stage 2 hips in which pain relief and preservation of the femoral head are predictable (greater than 70%).
Other surgical readings describe a transtrochanteric rotational osteotomy of the femoral head for idiopathic avascular necrosis to prevent progressive collapse of the articulating surface and to improve the congruity of the hip joint with articular collapse followed by femoral head subluxation. The rationale for this procedure is to reposition the necrotic anterior superior part of the femoral head to a non-weight-bearing location.1,2,4
One group of researchers reported a major complication rate of 15%, including subtrochanteric femoral fracture, femoral neck fracture, joint penetration and a broken trephine.2 Hungerford reported intraoperative as well as postoperative care fractures or perforation of the femoral head during core biopsy.2
Avascular necrosis of the femoral head may be primary or idiopathic, with no clear etiologic factor established. The widespread use of corticosteroids is probably the principal reason for the high number of nontraumatic cases of osteonecrosis seen over the last three decades. MRI and SPECT provide the greatest ability to detect osteonecrosis and its earliest stages.
Typically, increased density noted on plain films is not apparent before two months have elapsed and may not be easily identified up to six months. Early clinical suspicion and diagnosis is imperative in preventing premature weight-bearing on the affected side, helping to prevent the necrotic femoral head to collapse with subsequent degenerative changes.
Ficat's and Enneking's stages of osteonecrosis provide important disease staging and treatment regarding the patients symptoms, radiographs and pathology. Core decompression is performed to try and effectively lower intraosseous pressures and to remove a central core of bone from the lesional area.
Postoperatively, the patient should remain non-weight-bearing for six weeks to protect the lateral cortical window area. Core decompression would be best suited for stage 1 and early stage 2 hips in which pain relief and preservation of the femoral head would be more predictable.1
Various authors have documented complications to include subtrochanteric femoral fracture, femoral neck fracture, joint penetration and broken trephine.
David P. Wonchala is a PA in orthopedics at Elmendorf Air Force Base, near Anchorage, Alaska.
1. Callaghan JJ, Dennis DA, Paprosky WG, Rosenberg AG, eds. Orthopaedic Knowledge Update: Hip and Knee Reconstruction. Rosemont, Ill: American Academy of Orthopaedic Surgeons; 1995:87-111.
2. Crenshaw AH. Campbell's Operative Orthopaedics. 8th ed. St Louis, Mo: Mosby-Year Book; 1992:2038-2045.
3. Netter FH. The CIBA Collection of Medical Illustrations. 8th ed. Summit, NJ: Ciba-Geigy Corp; 1999;149.
4. Turek SL. Orthopaedic Principles and Their Application. 3rd ed. Philadelphia, Pa: JB Lippincott Co; 1972:1077-1081.
5. Warner JJ, Philip JH, Brodsky GL, Thornhill TS. Studies of nontraumatic osteonecrosis. The role of core decompression in the treatment of nontraumatic osteonecrosis of the femoral head. Clin Orthop Relat Res. 1987;225:104-127.
6. Miller MD. Review of Orthopaedics. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1996:1-35.
Diagnoses Associated With Osteonecrosis
• Alcoholism sickness
• Diabetes mellitus
• Systemic lupus erythematosus
• Toxic shock
• Anticoagulant deficiencies
• Sickle-cell crisis
• Nephritic syndrome
• Dysbaric phenomena–decompression
• Endotoxin reaction
• Serum sickness
• Inflammatory bowel disease
• Brain/spinal surgery
• Storage diseases–Gaucher's disease
• Vascular disorders–arteriosclerosis
Adapted from: Miller MD. Review of Orthopaedics. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1996:1-35.