Adult Reconstruction, 1st Edition

Section 1 - HIP

Part B - Evaluation and Treatment of Hip Disorders

4

Osteonecrosis of the Femoral Head

Frank A. Petrigliano

Jay R. Lieberman

Osteonecrosis (ON) of the femoral head is a progressive disease that if left untreated often results in subchondral fracture, collapse of the femoral head, and debilitating arthrosis. The precise pathophysiology of ON remains unclear; however, it appears to be the final common pathway of either traumatic or atraumatic factors that compromise the tenuous circulation of the femoral head. The disease typically affects young patients, thereby significantly impacting both work and leisure activity. Accordingly, early diagnosis and treatment are crucial to limit the progression of ON and the subsequent need for total hip arthroplasty. In many cases, however, diagnosis is made in later stages of the disease, when femoral head–preserving treatments are no longer effective. This chapter discusses the natural history of ON, the current diagnostic and treatment options for both early and late stages of the disease, and the limitations of these existing therapies.

Pathogenesis

Epidemiology

Osteonecrosis is observed in 10% to 25% of hip dislocations, with increased risk associated with prolonged duration of dislocation. ¹,² The incidence of traumatic ON of the femoral head following nondisplaced femoral neck fractures is approximately 10%, whereas the incidence following displaced fractures ranges from 15% to 50% and generally correlates with the degree of displacement, time until reduction, and accuracy of reduction. ³,⁴ The true incidence of atraumatic ON is unknown; however, some studies in Western populations show that about 10% of all total hip arthroplasties are performed for ON, leading to estimates that there are at least 20,000 to 30,000 new cases per year in the United States. ⁵ The disease affects men four times more frequently than women and generally presents in the third to fifth decades of life. Atraumatic ON is bilateral in 30% to 70% of patients at the initial time of presentation; however, the stage of disease typically presents asymmetrically. ⁶

Etiology

A number of traumatic and atraumatic factors are associated with the development of ON of the femoral head. Mechanical interruption of the blood supply to the femoral head has been identified as the causative factor of ON following femoral neck fracture or hip dislocation. ⁷Conversely, the precise genesis of atraumatic ON is unclear, but it has been associated with numerous risk factors and underlying clinical conditions (Table 4-1). It is hypothesized that these etiologic factors either result in a compromise of the blood supply of the subchondral region of the femoral head or have direct toxic effect on cells, resulting in cellular necrosis and impaired remodeling potential of the subchondral bone with eventual collapse of the compromised region.

Corticosteroid and alcohol use, thrombophilias, gout, hyperlipidemia, renal osteodystrophy, sickle cell anemia, caisson disease, and other systemic disorders have all been associated with ON of the femoral head. Of these recognized risk factors, corticosteroid use and alcohol abuse are the most commonly implicated, representing 90% of new cases of ON. ⁸ High-dose oral steroid regimens have a stronger association with ON as compared with low-dose therapy. ⁷,⁹ However, in a study of liver transplant patients receiving immunosuppressive corticosteroids, no association was noted between steroid dose and the development of ON. ¹⁰ It appears that transplant patients who develop ON demonstrate an idiosyncratic response to the drug secondary to an underlying hypercoagulability or hypofibrinolysis. With some diseases such as liver and renal failure, it is difficult to separate the effects of corticosteroids on bone from those of the underlying disease. Defining the quantity of alcohol intake that increases the risk of ON has been problematic. One prospective study suggested that patients who consume over 400 mL of alcohol per week were 9.8 times likely to develop ON versus nondrinkers. ¹¹ Additionally, an increasing number of reports document a relationship between human immunodeficiency virus (HIV) infection and ON of the hip. ¹² The causal relationship is difficult to establish because many of these patients have numerous concomitant risk factors; however, there is some evidence implicating antiviral therapy as a causative agent.¹³

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Although each of the etiologic possibilities must be considered, it is important to recognize that the vast majority of patients with the aforementioned risk factors do not develop ON, and in other patients, no risk factor is identified, underscoring the multifactorial genesis of this disease.

Pathophysiology

The exact mechanisms underlying the pathophysiology of atraumatic ON of the femoral head are not clearly defined; however, several theories have implicated both intravascular and extravascular factors that may contribute to this pathologic process. Each of these phenomena shares the final outcome of ischemia, cellular necrosis, and failure of remodeling of the subchondral bone. Osteocyte death has been attributed to alterations in blood flow that may be the result of local or systemic factors. Following fracture or dislocation, disruption of the lateral retinacular arteries may compromise the primary blood supply of the femoral head. This precarious arterial blood supply may also be altered by intravascular microemboli that are generated by systemic diseases including the thrombophilias, sickle cell disease, fat emboli resulting from hyperlipidemia, or air embolization secondary to dysbaric phenomena. ⁷,⁸,¹² Local hyperlipidemia and intravascular lipid deposits have also been noted in patients with corticosteroid and alcohol use, suggesting a causal role for these agents.

The local osseous architecture of the femoral head may predispose the region to extravascular compression and local ischemia. The cancellous bone within the subchondral region of the femoral head is enclosed within rigid cortical bone. This system is particularly susceptible to increases in pressure, and the venous outflow can be exquisitely sensitive to compression. Disorders in fat metabolism, generated by corticosteroid or alcohol use, may cause both adipocytes and osteocytes to hypertrophy, resulting in local microvascular compression. ⁷,⁸,¹² In Gaucher disease, macrophages enlarge as they accumulate sphingolipids, resulting in a similar compressive phenomenon. The direct cytotoxic effects of alcohol and corticosteroids have also been implicated in osteocyte necrosis and may inhibit osteogenic differentiation of mesenchymal stromal cells. ¹⁴,¹⁵

Diagnosis

Physical Examination and History

Clinical Features

A prompt diagnosis of ON allows for earlier treatment, which may result in a more favorable outcome. A thorough history focused on determining associated risk factors should be undertaken. Patients may not have any specific complaints during the early stages of the disease; however, with progression, patients will complain of deep groin pain with ambulation or pain referred to the knee. The onset of pain may be insidious or acute in nature and is typically described as throbbing; night pain and morning stiffness are not uncommon. The findings on physical examination are variable. Some patients have a complete, pain-free, range of motion of the hip and walk without a limp. Others have a limp and discomfort with active and passive range of motion. Collapse of the femoral head is associated with painful internal rotation and a limited range of motion. Individuals with chronic symptoms may have a flexion contracture. It is of utmost importance that the contralateral hip be examined, as bilateral disease is common. Because some patients may develop ON without the existence of any risk factors, an index of suspicion must be developed for young patients with persistent groin pain that is unresponsive to rest and activity modification.

Radiographic Features

Plain Radiographs.

The primary diagnostic workup should include plain anteroposterior and frog-leg lateral radiographs to determine the status of the femoral head. The early stages of the disease may not be visible on plain radiographs, but over time, a predictable pattern of radiographic change becomes evident. This sequence begins with radiolucencies and sclerosis in the femoral head, resulting from bone resorption and new bone formation. Progressive microfractures may result in a pathognomonic crescent sign, most readily visible on frog-leg lateral views (Fig. 4-1A). This represents precollapse of the weakened necrotic subchondral bone. The necrotic angle (measured referencing the center of the femoral head) can be calculated from plain films to stage the size of the necrotic region. This value is the sum of the angle of the necrotic segment as measured on both the anteroposterior and lateral radiographs. Patients with a necrotic angle >200 degrees

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have less favorable results following certain femoral-head sparing procedures. ¹⁶ The end stage of the disease manifests as a complete collapse of the femoral head and subsequent arthritic changes noted on both the femoral head and acetabulum.

Magnetic Resonance Imaging.

Magnetic resonance imaging (MRI) has become the standard in diagnosing ON and should be obtained in all suspected cases in which the plain radiographs are normal. In such cases, examination of both hips should be performed because more than half of all cases are bilateral. The changes noted on T1-weighted images typically include subchondral signal changes located in the anterior superior quadrant of the femoral head with a single-density line demarcating the normal-ischemic bone interface (Fig. 4-1B). The T2-weighted images may demonstrate a high-signal line inside a low-signal region (double-line sign). As lesion size has been associated with prognosis and response to therapy, MRI can be used to determine lesion size or volume. ¹⁷

Radiographic Staging

The most widely recognized radiographic staging system was proposed by Arlet and Ficat in the 1960s and has undergone subsequent modification (Table 4-2). ¹⁸ This classification relies solely on plain radiographs, which are often unrevealing early in the disease. Steinberg et al. have proposed a radiographic classification that incorporates plain x-ray, bone scan, and MRI findings to create a comprehensive and specific description that may be more effective in characterizing the progression of the disease (Table 4-2). ¹⁹ Moreover, this system considers volumetric assessment of femoral head involvement that may have predictive value in the outcomes of specific interventions.

Diagnostic Workup Algorithm

For young patients presenting with hip pain, a thorough history focused on delineating risk factors for the development of ON should be obtained. However, other causes of hip pain should be considered. An examination of the spine should be performed to rule out lumbar pathology. In cases where infection is suspected, hip aspiration may prove useful. Plain anteroposterior and frog-leg lateral radiographs of both hips should be obtained to evaluate for sclerosis or collapse of the femoral head in ON, but these studies may also reveal other painful conditions including hip dysplasia or neoplasm. When plain radiographs are normal, or sclerosis of the femoral head is noted, MRI examination of the affected and the contralateral hip should be undertaken. In pregnant females or males in the fifth decade of life, it is important to consider transient osteoporosis of the hip (TOH), which, if diagnosed, is self-limited. Unlike the localized changes found in ON, TOH demonstrates diffuse osteopenia on plain radiographs, and the MRI often has a global decrease in T1-weighted signal throughout the femoral head and neck metaphysis (Fig. 4-2) and a global increase in the T2-weighted signal in the same regions. Treatment includes protected weight bearing until the condition resolves, which may take up to 6 months. ⁹ Figure 4-3 presents a diagnostic workup algorithm.

Treatment

Patient age, activity level, and general constitution must be considered in conjunction with radiographic and clinical

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findings to formulate a treatment plan. Young, healthy patients without significant acetabular disease will generally be better served by procedures that attempt to preserve the femoral head. Conversely, arthroplasty may be an excellent option for patients with collapse of the femoral head or acetabular involvement. It is important to recognize that the indications for existing treatment regimens remain controversial and are often dictated by the surgeon's clinical expertise and familiarity with available surgical options.

Nonoperative Management

The role of nonoperative modalities in the treatment of ON of the femoral head remains limited. The prescription of protected weight-bearing regimens in forestalling the progression of disease has proven ineffective in most cases. ⁶,²⁰ This approach may be reserved for those patients who are incapable of tolerating a surgical intervention or are of limited life expectancy. Other nonoperative modalities including electrical stimulation and hyperbaric oxygen have been evaluated in the treatment of ON. These modalities have demonstrated varying success in preventing collapse of the femoral head. ²¹,²² More recently, the results of extracorporeal shock-wave therapy were compared with those of core decompression and bone grafting. The authors concluded that extracorporeal shock-wave treatment appeared to be more effective than core decompression and nonvascularized fibular grafting in patients with early-stage ON of the femoral head. ²³ The role of pharmacologic therapies in the treatment of ON has not been well defined and requires further investigation. Antihyperlipidemic, antihypertensive, and anticoagulant medications all have been proposed as candidate treatment agents. Most recently, the bisphosphonate alendronate has been shown to be effective in delaying the progression of femoral head collapse in a cohort of patients with early-stage disease. ²⁴ Again, long-term evaluation is mandated to determine if this agent truly prevents, rather than merely retards, collapse of the femoral head.

Operative Management

Many femoral head–sparing procedures have been used in attempts to prevent collapse, arthrosis, and the subsequent need for arthroplasty. Currently, core decompression is the most commonly used and most comprehensively studied treatment for early-stage ON of the femoral head. Originally described by Ficat and Arlet as a diagnostic intervention,

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core decompression was found to alleviate pain, presumably by reducing femoral head pressure and restoring physiologic blood flow. ⁷Eventually core decompression was adopted as a treatment modality. The procedure involves creating a decompression tract from the lateral cortex of the femur to the area of necrosis, the diameter of which can range from 9 to 12 mm depending on the diameter of the femoral neck. A biopsy is usually obtained at the time of surgery, and protected weight bearing is advised for a minimum of 6 weeks following the procedure. Although the success rates following the procedure are variable, for small and medium-sized precollapse lesions, the results of core decompression are generally 80% to 90% successful. ²⁵ However, the results are poor in the presence of a crescent sign or definitive collapse of the femoral head. ²⁶,²⁷

More recently, vascularized fibular bone grafting has been advocated for treating early-stage disease. Vascularized fibular grafts have the potential advantage of providing structural support, osteoconductive factors, osteoinductive factors, and a vascular supply to the necrotic region. However, this procedure requires a longer operation and is associated with donor site morbidity, ankle instability, peroneal nerve palsy, heterotopic ossification, and subtrochanteric fracture. ²⁸,²⁹,³⁰ Patients may not bear weight for a minimum of 6 weeks following the procedure and may be only partially weight bearing for an additional 3 to 5 months. The relative benefit of vascularized fibular graft versus nonvascularized graft or core decompression has yet to be conclusively proven. However, reported results are satisfactory in hips that do not have significant head depression. ²⁸,²⁹,³⁰

Bone grafting of the femoral head with demineralized bone matrix is an appealing option because it may enhance healing without significantly altering the anatomy of the femoral neck if arthroplasty is necessary. Biologic adjuvants including growth factors (such as VEGF, BMP) and autologous bone marrow cells may also play a role in treating osteonecrotic lesions and have prompted a great deal of clinical interest. Lieberman et al. demonstrated that allograft bone grafts in combination with BMP prevented radiographic progression of ON in 14 of 17 hips at an average follow-up of 53 months. ³¹ Randomized trials evaluating the efficacy of these agents in preventing femoral head collapse are necessary.

Intertrochanteric osteotomy is an effective treatment option for carefully selected patients with ON of the femoral head. The goal of osteotomy in these patients is to reposition the necrotic segment away from the weight-bearing surface and bring normal articular cartilage supported by healthy bone into the weight-bearing

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area. The ideal patient for this procedure is a young adult possessing a mobile hip with a small isolated lesion who does not require corticosteroids or abuse alcohol. ²⁰,³² The type of osteotomy will be contingent on the size and location of the lesion and may include intertrochanteric, rotational transtrochanteric, valgus flexion, or varus intertrochanteric osteotomies. Outcomes following osteotomies are better in small or medium-size lesions of early stage whereas these procedures are less predictable following femoral head collapse. ²⁰These technically demanding procedures should be performed only by experienced surgeons, and subsequent conversion to a total hip arthroplasty may be difficult.

Collapse of the femoral head and the development of arthrosis are indications for reconstructive procedures. Failure rates for total hip arthroplasties (THA) and hemiarthroplasties in this cohort are higher than failure rates for other diagnoses, which is most likely attributable to the relative youth of the patients and the lack of other factors limiting physical activity. ³³ Accordingly, temporizing procedures have evolved to address this difficult-to-treat group of patients. Joint resurfacing, or surface arthroplasty, has been proposed as a means of providing pain relief to patients who are deemed too young for conventional arthroplasty. Hemiresurfacing uses a cemented hemispheric femoral head prosthesis that is matched to the patient's native acetabulum. This mode of resurfacing may be considered for patients with little or no acetabular disease. In the presence of significant articular cartilage degeneration, a total resurfacing procedure (which incorporates a prosthetic acetabular component in addition to the femoral resurfacing) may be considered. Although these resurfacing procedures have demonstrated clinical promise, the current short- and long-term results for resurfacing procedures remain variable. ³³,³⁴,³⁵

In patients with extensive femoral head involvement and end-stage arthrosis, total hip replacement is indicated. Although early studies evaluating THA in patients demonstrated high failure rates, newer surgical techniques have yielded more favorable results. ³⁶,³⁷ With the advent of highly cross-linked polyethylene, metal-on-metal, and ceramic-on-ceramic weight-bearing surfaces, patients with ON may have more favorable success rates with total hip arthroplasty, obviating the need for multiple surgeries. A treatment algorithm based on radiographic stage and clinical symptom proposed by Lieberman et al. is outlined in Table 4-3. ⁹

Reference

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8. Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am. 1995;77(3): 459–474.
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31. Lieberman JR, Conduah A, Urist MR. Treatment of osteonecrosis of the femoral head with core decompression and human bone morphogenetic protein. Clin Orthop Relat Res. 2004;429:139–145.
32. Shannon BD, Trousdale RT. Femoral osteotomies for avascular necrosis of the femoral head. Clin Orthop Relat Res. 2004;418: 34–40.
33. Schmalzried TP. Total resurfacing for osteonecrosis of the hip. Clin Orthop Relat Res. 2004;429:151–156.
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Suggested Readings

Kim YH, Oh SH, Kim JS, et al. Contemporary total hip arthroplasty with and without cement in patients with osteonecrosis of the femoral head. J Bone Joint Surg Am. 2003;85-A:675–681.

Kim SY, Kim TG, Kim PT, et al. Vascularized compared with nonvascularized fibular grafts for large osteonecrotic lesions of the femoral head. J Bone Joint Surg Am. 2005;87:2012–2018.

Lavernia, CJ, Sierra RJ, Grieco FR. Osteonecrosis of the femoral head. J Am Acad Orthop Surg. 1999;7(4):250–261.

Lieberman JR. Core decompression for osteonecrosis of the hip. Clin Orthop Relat Res. 2004;418:29–33.

Lieberman JR, Berry DJ, Mont MA, et al. Osteonecrosis of the hip: Management in the 21st century. J Bone Joint Surg Am. 2002;84-A:834–853.

Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am. 1995;77:459–474.

Shannon BD, Trousdale RT. Femoral osteotomies for avascular necrosis of the femoral head. Clin Orthop Relat Res. 2004;418:34–40.