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Osteonecrosis of the Hip

Silent Killer of Function

symptoms-of-arthritis: Symptoms Of Osteoarthritis This is a conceptual review on the topic of osteonecrosis of the hip, also know as avascular necrosis or AVN. We will cover in detail the origins, diagnosis, and treatment of this potentially disabling disease. It is our hope this can serve as a guide for those suffering with this condition as well as those treating it.

About the Authors

Doctors John Fernandez, MD, Mark Cohen, MD, and Robert Wysocki, MD are board-certified, fellowship-trained orthopaedic surgeons and microsurgeons. They have a combined experience of over 30 years with a particular dedication in the treatment of this condition. They have founded one of only a few centers around the country and the only one in Chicagoland that performs some of the available treatments for osteonecrosis of the hip, such as vascularized fibula grafting. Any questions or comments can be directed here or emailed to us at hipavn@gmail.com

Dr. John J. Fernandez, MD, FAAOS Dr. Mark S. Cohen, MD, FAAOS

Introduction

Osteonecrosis of the hip, also know as avascular necrosis (AVN) is a multifactorial disorder, which results in significant disability and social costs. Estimates affirm 300, 000-600, 000 people are afflicted with osteonecrosis in the United States and 10, 000-20, 000 new cases are discovered each year [1]. Failed cases result in collapse of the femoral head and degeneration, and may account for 10% or more of total hip arthroplasties [3]. The majority of patients are male (4:1) and present at a young age, usually in their 30's [2]. Because of its multifactorial character and range of presentations, a consensus on treatment has not emerged. Failed treatment results in hip arthroplasty with all its inherent limitations and complications. This is less than ideal given the younger age of these patients. This makes the treatment of osteonecrosis very challenging.

Etiology

The final common pathway for osteonecrosis of the hip is a disruption in the blood supply to the femoral head. This can be attributed to a single event or a series of events. The causes of osteonecrosis can be categorized as traumatic, nontraumatic, and idiopathic. Traumatic events such as hip fractures and dislocations result in physical disruption of the blood supply to the femoral head. This carries with it a variable incidence of osteonecrosis depending on severity and delay of treatment. Dysbarism, or decompression sickness, can also be considered a traumatic or mechanical event leading to osteonecrosis. It can be seen in people using compressed air such as divers, pilots, tunnel workers, and miners. Nontraumatic etiologies include exposure to corticosteroids and alcohol and may account for 90% of nontraumatic cases [4]. Other conditions and diseases have demonstrated an increased incidence of osteonecrosis and are listed as nontraumatic risk factors [Table 1].

Table 1: Risk Factors

Corticosteroids

Alcohol

Smoking

Sickle-cell disease

Lupus

Coagulopathies

Lipid disorders

Pancreatitis

Organ transplantation

Myeloproliferative disorders

While it is estimated 8-10% of those using corticosteroids develop osteonecrosis, the relationship is not completely understood. There does appear to be a dose dependent correlation. Higher doses and longer duration seem to be important predictors (greater than 20 mg /day). Lower doses (less than 6 mg/day) even over longer periods did not seem to have an effect. Single boluses of steroids also have not been show to have an influence [5, 6]. Additionally there is the confounding variable of the conditions being treated that may have their own association with osteonecrosis. Alcohol also seems to show a dose dependent link to osteonecrosis. Those consuming less than 400 mL per week have a three-fold risk compared to nondrinkers, and with consumption greater than 400 mL there is an eleven-fold risk [4, 7]. In 10-20% of cases there is no identifiable risk factor and these are categorized as idiopathic. As we learn more about the origins of osteonecrosis this idiopathic group is shrinking.

Pathophysiology

The unique anatomy of the blood supply to the femoral head leaves it susceptible to disruption. The blood supply can be compromised from external mechanical disruption, external compression, or internal occlusion. The pathophysiology varies with the possible causes. While mechanical disruption from traumatic events is well understood, atraumatic mechanisms are varied and poorly understood.
Alterations in lipid metabolism have been a leading proposed mechanism. This may lead to fat cell hypertrophy and increased intraosseous pressure causing external compression and failure of the microcirculation. Similarly fat embolism as a cause has been linked to lipid abnormalities [8]. Blood dyscrasias and coagulopathies can result in hypercoagulable states and ultimately thrombosis of the vessels [Table 2]. Up to 50% of patients can have clotting abnormalities compared to 2-6% of the normal population [2].

Table 2: Coagulopathies

Protein S deficiency

Protein C deficiency

Factor V Leiden disease

Once the blood supply is disrupted cellular death ensues within 6-12 hours. Edema from cell death further increases local intraosseous pressure leading to further compromise. In response to the injury a repair process is initiated creating a reactive zone of tissue between the normal bone and the osteonecrotic segment [Figures 1 and 2]. Osteoclasts begin to resorb the necrotic bone and osteoblasts follow behind with new bone formation (creeping substitution). Small lesions can be successfully repaired this way. Larger lesions pose a challenge, as it is difficult for the repair process to quickly penetrate the deeper portions of the lesion. This leaves only a peripheral zone of repair at the boundries of the lesion.

Figure 1. Coronal section of femoral head. Note reactive zone of bone
with discoloration (black arrows) outlining white osteonecrotic area.

Figure 2: Core biopsy sample from femoral head. Avascular segment
between black arrows (note dense, sclerotic bone). Reactive zone between
white arrows (fracture in sample from stress riser effect between normal
and abnormal bone). Normal bone noted to right side of sample.

The necrotic segment of bone loses the ability to repair itself. If the involved bone is in an area of stress such as the subchondral region of the femoral head, stress fractures ensue. As the stress fractures propagate the subchondral bone collapses [Figure 3]. The interface at the site of collapse can sometimes be seen on radiographs (crescent sign). The bone collapse leads to deformity and abnormal mechanical loading of the cartilage itself, which is intrinsically unaffected. Chondrolysis then occurs and subsequently degeneration with total joint involvement.

Figure 3: Coronal section of femoral head. Note subchondral
fracture (black arrows). This corresponds to radiographic
"crescent sign". Cartilage is fractured (white arrow) leading
to collapse and incongruity.

Clinical Presentation

Patients usually present with hip pain, deep and throbbing, referable most commonly to the groin but can be referred to the buttock, thigh, or knee. The pain is worse with increasing weight bearing activities and can also be worse at night. There can be mechanical symptoms such as popping and catching, and a sense of weakness. Physical examination findings are limited and at best reveal increased pain on forced internal rotation and extension of the hip. Long standing cases can result in a loss of motion to internal rotation and extension through the hip. Alterations in gait pattern can be present (antalgic or Trendelenburg gait). Bilateral involvement is seen in 40-80% of cases [9]. In some cases there is "silent" involvement without clinical symptoms but positive diagnostic studies.

Diagnostic Studies

Plain radiographs are usually the first studies requested leading to a diagnosis. At a minimum the following views should be performed: AP of the pelvis, AP of the hip, and frog-leg lateral. Radiographic findings can include sclerosis of bone, intraosseous cysts, subchondral fracture (crescent sign), and joint space narrowing and degeneration. Bone-scanning should only rarely be utilized as it has been supplanted by magnetic resonance imaging. It is less specific and has a higher false-negative rate. In one study magnetic resonance imaging revealed positive findings in 73% of negative bone scans [20]. It can be used when access to magnetic resonance imaging is limited in patients with unilateral symptoms and negative radiographs with few risk factors. Findings include increased isotope uptake in the reactive bone regions at the borders of the lesion with relative decreased uptake within the lesion. Magnetic resonance imaging has the highest sensitivity and specificity of all modalities approaching 99% [10]. T1-weighted images can reveal a line of low-intensity signal representing the interface between normal bone and ischemic bone [Figure 4]. T2-weighted images can additionally demonstrate a double-density line with a high-intensity signal within a low-intensity signal representing hypervascular granulation tissue (double-line sign). The superior qualities of magnetic resonance imaging can allow for more accurate quantification and location of the lesion.

Figure 4: Coronal MRI of hip demonstrating low-intensity signal
"line" marking boundry between normal bone and osteonecrotic
lesion.

Computed tomography can more accurately assess any collapse that may be present. This can lead to more accurate classification of disease in up to 31% of cases, i.e. stage II to stage III [11]. Intraosseous pressure measurements, venography, and core biopsy have been relegated to historical relevance only and are no longer implemented in the primary work-up of osteonecrosis. Laboratory studies should also be considered including sickle cell testing in African Americans, lipid/cholesterol testing, and testing for coagulopathies.

Classification

The original classification system was described by Ficat and Arlet [12] and is based on four radiographic stages [Table 3]. Steinberg et al. [13] developed a classification based on both MRI and radiographic findings. They made a distinction between subchondral collapse with or without flattening of the femoral head. Additionally they attempted to quantify the amount of head involvement and or collapse as 30%. The Japanese Investigation Committee [14] classification emphasizes the location and size of the lesion in relation to the dome of the acetabulum with smaller, medial lesions doing best, and larger, lateral lesions doing worst.

Table 3: Ficat and Arlet Classification

Stage I: normal radiographs

Stage II: sclerocystic changes of bone

Stage III: subchondral collapse of femoral head

Stage IV: narrowing / degeneration of joint

We prefer to utilize the International classification system as proposed by ARCO [15] [Table 4]. This system utilizes a four-part system based on Ficat and Arlet, with the lesion quantification of Steinberg et al., and lesion location of the Japanese Investigation Committee.

Table 4: International Classification

Stage 0: Bone biopsy abnormal; all other tests normal

Stage 1: MRI/bone scan positive; radiograph normal

A: 30% femoral head

Stage 2: MRI/bone scan positive; radiographs abnormal; no collapse

A: 30% femoral head

Stage 3: evidence of femoral head collapse; positive crescent sign

A: 4-mm depression femoral head

Stage 4: joint space narrowing, degeneration of joint

* lesions are also subdivided by location, i.e. medial, central, or lateral (Type A, B, C)

Quantifying the extent of disease can be difficult with radiographs. We prefer to use the method of Koo and Kim [16], which utilizes an "index" of necrosis. The maximum lesion as seen on the coronal and sagittal MR images is measured as an arc using degrees with the apex in the center of the head. These numbers are divided by 180 and multiplied by one another to arrive at a number approximating the volumetric percentage of femoral head involvement [Figure 5]. They showed that small lesions medial 2/3

>50

sedentary

poor

Hip Arthroplasty

References

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