The femoral head is inspected for fractures, avascular necrosis (AVN), or edema from any number of causes, including transient osteoporosis of the hip, subchondral fractures, or overlying chondral degeneration (Fig. 3.31). The femoral neck, the greater and lesser trochanters, and the acetabulum are also examined for fractures. In the setting of recent-onset atraumatic hip pain, the differential diagnosis for diffuse bone marrow edema seen throughout the femoral head includes a subchondral (insufficiency) fracture, transient osteoporosis of the hip, infection, and avascular necrosis. On T1- and T2-weighted images, a subchondral fracture appears as a dark trabecular fracture line just deep to the subchondral plate at the superior margin of the femoral head. The subchondral fracture line may be extremely small and difficult to find. To avoid a misdiagnosis of transient osteoporosis, a careful search for a subtle subchondral trabecular fracture line should be performed whenever prominent edema is visualized in the femoral head.

In addition, the shape of the acetabulum is examined for evidence of a shallow contour or decreased acetabular coverage of the femoral head, suggestive of developmental dysplasia. It is not uncommon to find unilateral mild adult developmental dysplasia, and comparison with the opposite hip on large-FOV coronal images is useful in the detection of subtle







asymmetry in acetabular contour. Acetabular dysplasia is associated with labral tears and early osteoarthritis (OA), a condition known as lateral rim syndrome. Even a mildly abnormal shallow acetabulum predisposes to the development of premature degenerative chondral changes and labral tears. A shallow acetabulum is best visualized on anterior coronal images. Marrow signal throughout the pelvis and femur is often heterogeneous, as the pelvis is a common reservoir for red marrow.

Cartilage covers not only the articular surface of the acetabulum but also the femoral head to the level of the femoral head-neck junction (sparing only the fovea on the medial femoral head). Cartilage surfaces are examined for the presence of thinning, fibrillation, fissuring, or defects. The subjacent bone is also examined for evidence of subchondral cystic change and edema (Fig. 3.32). In the presence of chondral degeneration, the remainder of the joint space, which extends inferiorly to the junction of the femoral neck and trochanter, is examined for loose bodies. Commonly, early chondral degeneration is initially visualized in the anterior superior quadrant of the hip, accompanied by bone marrow edema in the anterior superior acetabulum and tearing of the anterior superior labrum.

In FAI, cartilage loss and subchondral edema involving the anterior and lateral acetabulum, as well as associated labral tearing, are accompanied by hypertrophic changes and subcortical cystic change at the anterolateral femoral head-neck junction. The latter of these findings has been referred to as a dysplastic bump. This combination of findings is most likely due to repetitive microtrauma of the lateral femoral head-neck junction as the femur swings up and abuts the lateral acetabulum during flexion with internal rotation.

The normal labrum is seen as a dark-signal triangle covering the articular cartilage at the lateral peripheral margin of the acetabulum (Fig. 3.33). By viewing successive anterior-to-posterior coronal images, the anterior superior, superior, and posterior superior labra are visualized. Interpretation of MR findings in the acetabular labrum is comparable to examination of the labrum in the shoulder. Normally the dark-signal-intensity triangle of the labrum is seen firmly attached to the acetabulum. Linear or irregular fluid signal extending through the substance of the labrum indicates a labral tear. Labral tears are also characterized by fluid signal undermining the attachment between the labrum and the acetabulum (indicative of partial or complete detachment) and by expansion of the labrum by fluid signal, often extending to the surface of the labrum and into a paralabral cyst. Complete absence of the labrum, often with replacement by a large bony acetabular spur, suggests longstanding chronic labral tearing with eventual resorption of the torn and degenerated labrum. Labral tears usually involve the anterior half of the labrum but may also involve the labrum circumferentially, and they occasionally affect the posterior labrum alone.

When present, paralabral cysts are strongly suggestive of an adjacent labral tear. Paralabral cysts, which range in size from a few millimeters to several centimeters, may manifest as a single cyst extending a neck back to the labrum, as a multiloculated cyst, or occasionally as a collection of tiny cysts (each measuring a few millimeters) lining up in an arc along the circumference of the labrum.

The inferior portion of the acetabulum is not covered by the labrum; in its place, the transverse ligament spans the inferior aspect of the acetabulum.

As described earlier, there are four major muscle groups about the hip (Fig. 3.34). The anterior muscle group includes the sartorius, rectus femoris, and iliopsoas. The medial group, the adductors, includes the gracilis, pectineus, adductor longus, adductor brevis, and adductor magnus. The lateral group includes the tensor fasciae latae and the gluteus maximus, medius, and minimus, as well as the obturator internus and externus, the gemelli, and the quadratus femoris. The posterior group, the hamstring muscles, includes the biceps femoris, semimembranosus, and semitendinosus.

Laterally, the gluteus minimus and medius insert anteriorly and posteriorly, respectively, on the greater trochanter. Medially, the adductor muscles can be strained, partially torn, or completely avulsed (with bony avulsion fragments) from the inferior pubic ramus. Posteriorly, the hamstring tendon origin at the ischium is a frequent site of tendinosis, tears, and bony avulsion, particularly in high-level athletes. Anteriorly, the rectus femoris and sartorius may be avulsed from their insertions on the anterior inferior and anterior superior iliac spines, respectively. This injury is seen most often in children and adolescent athletes.

The insertions of the gluteus medius and minimus tendons are the major structures to be evaluated at the greater trochanter (Fig. 3.35). The gluteus medius tendon inserts posterosuperiorly on the greater trochanter and the gluteus minimus tendon inserts anterosuperiorly. The trochanteric bursa lies alongside the lateral margin of the greater trochanter, and distention of this bursa with fluid (compatible with bursitis) is evaluated on coronal and axial images. Mild trochanteric bursal inflammation from friction over the greater trochanter is common, particularly in elderly patients, and is visualized as mild fluid signal interdigitating around the distal gluteus medius and minimus tendons. Trochanteric bursitis is commonly accompanied by tendinosis, strain, or tears of the gluteus medius and minimus tendons at their insertion on the greater trochanter. Tears and strain of these tendons, particularly in older patients, can mimic pain from fractures. The gluteus medius and minimus tendons have been referred to as the “rotator cuff” of the hip, and tendinosis and partial tearing of these tendons are extremely common in middle-aged and older patients.

Large-FOV coronal images that include both hips are optimal for evaluating the other pelvic bones and articulations (Fig. 3.36). On images throughout the anterior pelvis, the symphysis pubis is examined for osseous spurring, the pubic rami are examined for fractures (insufficiency, stress, or posttraumatic),
and the ilium is analyzed for marrow-signal abnormalities, tumor, and fractures. The sacroiliac joints are examined for arthritis, posttraumatic changes, and infection. The sacrum is also a common location for both posttraumatic and insufficiency fractures.

The anterior and posterior labrum are best visualized on axial images (Fig. 3.37). Abnormalities of the superior labrum can also be detected.

The cartilage covering the medial and superolateral femoral head is well depicted, and the cartilage covering the anterior and posterior acetabular articular surfaces is also visualized (Fig. 3.38). Normally there is no cartilage covering the articular side of the medial acetabulum, which is the location for the acetabular fossa (filled with fat). In the setting of chondral degeneration, loose bodies are vigorously sought within the joint.

Axial images are used for further evaluation of the extent of AVN involving the femoral head (Fig. 3.39). Fractures of the femur and acetabulum are also further characterized. Osteomyelitis involving the central marrow cavity of the femur is also optimally visualized. The dysplastic bump and subcortical cystic changes within the superoanterior femoral head-neck junction, associated with FAI, are also depicted.

The gluteus medius and minimus tendon insertions are seen nearly in cross-section, allowing further localization and characterization of tendon tears and strains (Fig. 3.40). The adductors, the rectus femoris, the sartorius, and the iliopsoas are also imaged in cross-section. The insertion of the distal obturator internus and externus tendons on the medial posterior aspect of the greater trochanter is also visualized. The origin of the hamstring tendon from the ischium is also visualized in cross-section. The piriformis muscle and its relationship to the sciatic nerve posterior to the acetabulum are well demonstrated, which makes axial-plane images excellent for the identification of anatomic abnormalities contributing to suspected piriformis syndrome.

The iliopsoas tendon and muscle are evaluated as they course anterior to the acetabulum and hip joint (Fig. 3.41). The iliopsoas bursa (normally not seen if not distended with fluid) is located medial to the iliopsoas tendon and anterior to the hip joint. This bursa can become inflamed and distended with fluid with repetitive hip flexion, as part of a snapping hip syndrome,


or secondary to communication with the hip joint. Trochanteric bursitis suspected on coronal images is confirmed on axial images.

The capsule surrounding the hip joint comprises the iliofemoral ligament anteriorly and the ischiofemoral ligament posteriorly (Fig. 3.42). The capsule is examined for the presence of rupture, particularly in patients who have suffered hip dislocations.

Anterior superior labral tears and detachments are well displayed on sagittal plane images (Fig. 3.43). Anterior superior labral pathology is commonly accompanied by anterior superior chondral degeneration. The entire course of the labrum from anterior to posterior is evaluated. Normal fluid interposed between the anterior labrum and capsule may mimic a
labral tear; to avoid this pitfall, suspected labral tears should be confirmed in all three planes.

The sagittal plane affords an additional opportunity to evaluate the femoral head and acetabular cartilage surfaces and associated subchondral changes (Fig. 3.44).

Fractures, AVN, edema, or intraosseous masses involving the femur and acetabulum are also visualized in the sagittal plane (Fig. 3.45). Triangulation on axial and coronal images is used for further characterization of abnormalities.

The medial muscle and tendon group, including the obturator internus and externus, the superior and inferior gemelli, and the quadratus femoris, is visualized in cross-section, allowing localization of pathologic changes to specific muscles within this group (Fig. 3.46). The iliopsoas tendon and associated iliopsoas bursitis are also well displayed. The distal insertions of the gluteus minimus and medius tendons onto the greater trochanter are examined for tears and tendinosis.

Chronic right hip pain. Evaluate for avascular necrosis.

There is a linear oblique tear and partial detachment of the anterior superior labrum (Fig. 3.47A, coronal image). The tear extends into the superior labrum (Fig. 3.47B, axial image), and there is a septated, lobulated 2.5-cm paralabral cyst adjacent to the anterior superior labrum (Fig. 3.47C, coronal image). In addition, there is severe complete to near-complete chondral loss involving the anterior and superior femoral head and acetabular articular surfaces (Fig. 3.47D, sagittal image), with prominent subjacent subchondral cystic change within the anterior acetabulum (Fig. 3.47E, sagittal image). There is a small dysplastic bump along the anterolateral femoral head-neck junction with mild subcortical bone marrow edema (Fig. 3.47F, axial image).

The findings are compatible with femoroacetabular impingement, with moderately severe degenerative arthritis. There is a small to moderate joint effusion with reactive synovitis (Fig. 3.47G, coronal image). There is no evidence of a loose body within the joint or of acetabular dysplasia.

There is no evidence of a fracture or avascular necrosis. Large field of view coronal images demonstrate that the degenerative changes are asymmetric, involving the right hip only, and the left hip joint appears grossly normal. Large field of view images also demonstrate that the sacrum, sacroiliac joints, and symphysis pubis are normal. The pelvic viscera are normal.

The gluteus medius and minimus tendon insertions are normal, and there is no evidence of trochanteric bursitis. The remainder of the muscles and tendons about the hip are normal.

AVN is usually caused by trauma, typically occurring after a displaced femoral neck fracture and less frequently after a fracture-dislocation of the hip. Necrosis results when the vascular supply to the femoral head is disrupted at the time of injury.

Nontraumatic AVN occurs in a younger patient population and is commonly bilateral.²¹ Although the etiology is not well understood, one popular theory suggests a vascular etiology secondary to fat embolism, which leads to inflammation and focal intravascular coagulation.²² Nontraumatic AVN is associated with a variety of clinical conditions, including sickle cell anemia and other hemoglobinopathies, systemic lupus erythematosus, alcoholism, hypercortisolism, Gaucher—s disease, obesity, coagulopathies, hyperlipidemia, organ transplantation, pancreatitis, dysbaric phenomena such as Caisson—s disease, and thyroid disease. In 5% to 25% of cases there is a history of corticosteroid use. In a significant number of cases, none of the known risk factors can be identified, and the disease is considered idiopathic.^23,24,25 An increased risk of contralateral AVN has been noted.

Clinical findings in AVN typically include the following signs and symptoms:²⁶

Overall, AVN is responsible for 10% of total hip replacements, 10% of nondisplaced femoral neck fractures, 15% to 30% of displaced fractures, and 10% of dislocations.

Early diagnosis is important in improving the chances of saving the femoral head because prophylactic treatment (discussed below) is more successful in the initial stages of AVN. It is particularly important in evaluating a patient with asymptomatic nontraumatic AVN on the contralateral side. Although the anterolateral portion of the femoral head is characteristically involved in AVN, no specific area of the femoral head is protected or spared in this disorder.²⁷ The articular cartilage is intact at the initial presentation of the wedge-shaped subchondral bone infarct. An ineffective healing response with resorption of bone predominates. Partial resorption of necrotic bone and replacement with fibrous granulation tissue characterize the lack of central repair and incomplete peripheral repair of the necrotic focus. The deposition of viable bone on necrotic bone forms thickened trabeculae, which produce a mixed sclerotic and lucent or cystic radiographic appearance. Collapse of unsupported articular cartilage, secondary to subchondral fracture, leads to subsequent joint destruction (Fig. 3.75).

In addition to MR imaging, radiography, CT, and bone scans are all used to identify and stage AVN.

There are a number of staging and classification systems used to describe AVN.^{22,34,35,36,37} The international system, the Ficat and Arlet system, a combined system, and the Mitchell systems are described below. The specificity of radiographic staging of AVN is improved by the use of CT, which is also helpful in defining the associated sclerotic arc, in detecting acetabular dome and femoral head contour changes, in assessing the joint space, and in evaluating the extent of femoral head involvement.³⁸ Disruption of the normal pattern of bony trabeculae can be observed on CT scans in osteonecrosis of the femoral head.³⁹ Clumping and fusion of peripheral aspects of the femoral head asterisk may be identified prior to conventional radiographic sclerosis or subchondral fracture. These CT changes do not, however, reflect the early vascular marrow histologic processes in AVN. With MR imaging it is possible to identify early changes and to stage all aspects of the disease.

Many MR findings can also be correlated with pathologic changes. Common gross pathologic and surgical features and corresponding MR findings include:

Another pattern of MR signal intensity, diffuse low signal intensity on T1-weighted images with increased signal intensity on T2-weighted images, has been described by Turner et al.⁴⁷ The area of diffuse low signal intensity on T1-weighted images extends from the femoral head and neck into the intertrochanteric area. Although no focal findings were identified initially, AVN was subsequently demonstrated by core biopsy and focal MR morphologic patterns specific for osteonecrosis. The diffuse pattern of low signal intensity in and adjacent to the femoral head was shown to be transient in five of six patients and may represent a bone marrow edema pattern (see discussion below) preceding focal anterosuperior femoral head osteonecrosis. A bone marrow edema pattern may represent the early stages of a reversible form of AVN. These changes have also been reported in the acetabular bone prior to the development of sclerosis and granulation tissue at the interface surrounding devitalized or necrotic bone. When there is also increased uptake on corresponding radionuclide bone scans, careful observation may be required to differentiate diffuse MR patterns of early AVN from transient osteoporosis of the hip. Most cases of diffuse femoral head and/or femoral neck edema are associated with either a subtle subarticular fracture or an ischemic focus and do not represent transient osteoporosis of the hip. Red marrow adjacent to the base of Ward—s triangle should not be mistaken for an extended column of AVN-associated marrow edema (Fig. 3.87).

One of the most important contributions MR imaging has made to the detection of AVN is identification of an osteonecrotic lesion in patients with normal bone scintigraphy and conventional radiography.^1,48 Scintigraphy, responding to the death of hematopoietic cells (within 6 to 12 hours of the initial ischemic insult) or osteocytes (within 12 to 48 hours), may show a focus of decreased radiopharmaceutical uptake very early after the ischemic insult. Bone scans become negative once bone remodeling occurs with disease progression, however, and the osteonecrotic focus may be missed. MR imaging, which is sensitive to changes in marrow fat signal intensity, will be negative until there is death of marrow fat cells, up to 5 days after the initial ischemic insult. Unlike scintigraphy, however, MR remains positive throughout the course of AVN or until the lesion is healed. Contrast-enhanced imaging may allow even earlier identification of changes in AVN, as discussed below.

The finding of a symptomatic hip joint effusion prior to any alteration in marrow signal intensity may correspond to an elevation of intraosseous intramedullary pressures. Focal MR abnormalities, subsequent to the presentation of diffuse bone marrow edema, can be observed as early as 6 to 8 weeks from the time of detection. The demonstration of marrow necrosis and acellular lacunas can help to differentiate osteonecrosis in its early stages from transient osteoporosis of the hip. Bone marrow edema may represent a marker for progression to advanced osteonecrosis.⁴⁹ Bone marrow edema and joint effusions occur most frequently in stage III AVN, although bone marrow edema has a stronger association with hip pain.⁵⁰ Bone marrow edema of the proximal femur, however, has also been associated with pain in the early stage of osteonecrosis of the femoral head.⁵¹

Genez et al. determined that in the early stages of AVN there may be histologic findings of osteonecrosis in the absence of abnormal MR findings.⁵² It has been found that administration of intravenous gadolinium improves the early detection of AVN by demonstrating areas of decreased enhancement, despite normal findings on T1- and T2-weighted images. In a study of renal transplant patients (at risk because of corticosteroid treatment) it was found that with contrast-enhanced images it was possible to identify early changes of AVN in 6% of
100 asymptomatic patients.⁵³ In another study of renal transplant recipients, followed for 22 months using serial radiographs and MR, untreated AVN was shown to have a benign course without progression from Ficat stage 0.⁵⁴ Jiang and Shih reported that the presence of a complete or dense physeal scar on MR scans was associated with a high risk for AVN of the femoral head.⁵⁵ Segmental or incomplete scars in AVN were uncommon. The sealed-off or complete scar was shown to be a risk factor in patients with or without a history of steroid or alcohol abuse (associated lipogenic factors). Because it is possible to identify MR changes of focal osteonecrosis when radionuclide scans are negative and CT and plain film findings are normal,⁵⁶ a limited or modified MR examination could be used as a low-cost screening tool in at-risk populations.

Another advantage of MR imaging is the ability to perform chronologic or temporal staging and assessment of the percentage of marrow involvement, information that may facilitate therapy choices. In the later stages of AVN (i.e., stages III and IV) core decompression is frequently used to palliate pain without altering disease progression. A 3D MR rendering can be used to evaluate the volume of osteonecrotic involvement of the femoral head relative to its cross-sectional area. This technique is also useful in differentiating and separating the necrotic zone of involvement and for identifying its location in the femoral head and its relationship to the weight-bearing surface. Information from quantitative assessment of femoral head involvement may assist in deciding whether to perform a core decompression or a rotational osteotomy.

Disarticulation of the femur and femoral head from the acetabulum may facilitate superior surface viewing of the femoral head and the associated necrotic focus. Separate disarticulation and composite volume rendering can be performed to display associated joint effusions. Volume transmission enables viewing of the femoral head through the acetabulum using various degrees of pelvic rotation in horizontal and vertical planes. In a quantitative approach to the assessment of the early stages of AVN, weight-bearing areas of involvement are an important and reliable parameter to monitor in follow-up.⁵⁷

Without treatment, AVN progresses to destruction of the femoral head and joint OA. Unfortunately, even early identification and intervention may not alter the result. The likelihood of disease progression is greater with nonsurgical approaches to management.

Treatment options include the following:

The aim of treatment is to save the femoral head, not replace it, because most patients with nontraumatic AVN are relatively young. Unfortunately, surprisingly little has been written about the natural history of the disease. Although some clinicians still recommend restricted activity and protected weight-bearing as initial therapy, Steinberg et al. have published a retrospective study of 48 patients treated nonoperatively,⁵⁸ and their results indicate that limiting weight-bearing has no beneficial effect on the outcome: disease was progressive in 92% of patients. A subsequent study showed disease progression in over 80% of patients, regardless of the stage of disease at presentation, and progression of the disease in all patients who presented with some collapse of the femoral head.²¹

Because of the high rate of progression, many clinicians recommend early surgical intervention. Conservative or prophylactic procedures include core decompression (Fig. 3.88) with or without bone grafts,^{21,34,59,60,61,62,63,64} osteotomy,^24,65 and electrical stimulation.^59,66,67

The rationale for core decompression, the most commonly used of these procedures, is to alleviate the elevated intraosseous pressure, permitting neovascularization. Success rates reported in the literature vary dramatically (from 40% to 90%) depending on the criteria used to grade results. Smith et al.⁶⁸ found that core decompression was successful in 59% of Ficat stage I lesions (success being defined as no subsequent operation or radiographic evidence of progression), but they recommended an alternative treatment for stage IIB or III lesions and possibly even stage IIA lesions.

Beltran et al. have correlated collapse of the femoral head after core decompression with the extent or percentage of involvement of AVN as determined preoperatively by MR imaging.⁶⁹ When less than 25% of the weight-bearing surface was involved, femoral head collapse did not occur after core decompression. With 25% to 50% involvement, femoral head collapse occurred in 43% of hips. With greater than 50% involvement, femoral head collapse occurred in 87% of hips. Mean time to collapse was 6.7 months after diagnosis and treatment. Therefore, if a large area or volume of the femoral head is involved, subchondral collapse may occur with core decompression, despite the absence of subchondral fracture on conventional films.

In untreated patients, Shimizu et al. reported a 74% rate of femoral head collapse by 32 months if the necrotic focus involved one-fourth the femoral head diameter, or at least two thirds of the weight-bearing area.⁷⁰

Cancellous, cortical, muscle pedicle, and microvascular bone grafts have been used with core decompression. The use of a cortical graft for necrotic bone was first described by Phemister,⁷¹ and the procedure was modified by Bonfiglio and Voke.⁵⁹ Urbaniak et al. first used a vascularized fibular graft after coring of the femoral head.⁷² Long-term follow-up results with free vascularized fibular grafting indicated a decreased need for pain medication (86%) and a high rate of patient satisfaction (81%).⁷³ Brown et al. used a 3D model to incorporate biomechanical variables in coring and bone grafting of a necrotic femoral head.⁷⁴ For coring, they recommended that the tract not extend near the subchondral plate. The greatest structural benefit with cortical bone grafting was shown for grafts that penetrated deep into the superocentral or lateral aspect of the lesion with subchondral plate abutment. Increased stresses on necrotic cancellous bone occurred in central or lateral grafts that were placed proximal to the subchondral plate.⁷⁴

A variety of proximal femoral osteotomies have been used with varying results.^25,63 The principle underlying osteotomy involves redirecting stresses from structurally compromised trabeculae. These procedures are most successful in cases with limited femoral head involvement. Patients who remain on corticosteroids or who have persistent
metabolic bone disease do not benefit greatly from osteotomy.

Pulsed electromagnetic fields and implantable direct current stimulators have also been used in the treatment of AVN, also with varying results.^63,66,67

Once the femoral head has collapsed, the success of prophylactic procedures diminishes significantly (Fig. 3.89). The chance of saving the femoral head is small, and most patients go on to require femoral head replacement. In general, total hip replacement is more reliable than bipolar endoprostheses.⁷⁵ Hip fusion is also an alternative in young patients with unilateral disease, especially the heavy, active male.

Although the etiology is unclear, certain risk factors have been identified, including gender (boys are affected four to five times more often than girls), socioeconomic class (high incidence in low socioeconomic classes and in children with low birthweight), and inguinal hernia and genitourinary anomalies in children.^76,77 There is no specific history of trauma. Other etiologic factors include:

LCP is a progressive, dynamic condition, and the results of the physical examination depend on the stage of the disease at the time of presentation. Early in the disease (Fig. 3.91), the physical findings are similar to those of irritable hip syndrome. There is bilateral involvement in 15% to 20% of children. Common clinical features include:

Diagnosis of LCP is usually made from plain films. Typical radiographic features include:

Conventional film findings may be negative early in the course of the disease, and scintigraphy and MR imaging may provide additional information.

The most commonly used classification systems for LCP are based on radiographic estimates of the amount of femoral head involvement. Catterall has defined four groups,⁷⁸ Salter and Thompson have described two groups, and Herring has defined three groups based on such estimates. Waldenström has also staged the disease based on radiographic findings.

MR imaging is used to identify both morphologic and signal characteristics of the femoral epiphysis in the early stages of radiographically negative disease (Fig. 3.92) and in more advanced disease (Fig. 3.93). In addition to a hypointense epiphyseal marrow center on T1- and T2-weighted images, associated findings include an intra-articular effusion and a small, laterally displaced ossification nucleus.^84,85 Sagittal T1- and

T2-weighted images also are useful for displaying acetabular and femoral head cartilage. Metaphyseal irregularities and subchondral hyperintensity are identified on FS PD FSE coronal images (Fig. 3.94).

Typical features seen on T1- or PD-weighted images include:

FS PD or T2-weighted FSE images are used to assess articular cartilage thickness and chondral irregularities. Characteristic changes on these images include the following:

Since articular cartilage demonstrates increased signal intensity on T2*-weighted images (Fig. 3.95), this sequence is useful in evaluating the thickness of the articular cartilage, which may be increased in the initial stages of LCP. FS PD FSE or STIR (including FSE STIR) sequences are more accurate than gradient-echo techniques, however, in demonstrating degenerative changes of the articular cartilage with the influx of fluid in areas of articular cartilage irregularity. The physeal cartilage may also demonstrate increased signal intensity on T2-weighted images in early-stage disease.⁸⁷ Coronal or sagittal images may be used to display both acetabular and femoral head cartilage surfaces. Measurements of acetabular and femoral head articular cartilage show an increased thickness in affected hips.

Ranner, in a study of 13 patients with LCP among 45 patients presenting with acute hip pain, demonstrated that MR imaging was as sensitive as isotope bone scans and allowed more precise localization of involvement than conventional radiography.⁸⁸ Although revascularization of the necrotic focus may be more accurately determined with nuclear scintigraphy, MR imaging is preferable for evaluating the position, form, and size of the femoral head and surrounding soft tissues. Bone marrow edema, detected on MR scans in pediatric patients with symptomatic hips, may resolve without resultant osteonecrosis. Cartilaginous physeal and metaphyseal abnormalities identified on MR imaging are common in LCP and frequently result in growth arrest. Transphyseal bone bridging and metaphyseal extension of physeal cartilage were seen in 63% and 81% of cases, respectively, and were strong predictors of abnormal growth.⁸⁷ Epiphyseal abnormalities, seen in a majority of cases, are not associated with growth disturbances.

It is important to determine prognosis at the time of presentation, because more than 50% of patients with LCP do well with no treatment.⁸⁹ The younger the child and the earlier the stage at the time of presentation, the better the prognosis. Children who present after 8 years of age tend to do poorly (Fig. 3.96), as do those who present with both epiphyseal and metaphyseal changes. Catterall has identified clinical and radiographic “head at risk” signs that he correlated with the chance of developing significant femoral head deformity.⁷⁸ Clinically, progressive loss of movement, adduction contracture, flexion with abduction, and obesity are all poor prognostic signs. The epiphyseal signs are calcification lateral to the epiphysis and a lytic area laterally (Gage—s sign). In the metaphysis, horizontal inclination of the growth plate and diffuse metaphyseal reaction are risk factors. Two or more of these signs correlate with a poor prognosis.⁷⁸ Lateral subluxation of the femoral head is also associated with a poor outcome. In general, girls do not do as well as boys and may have a more severe form of the disease. The natural history of the disease usually includes the development of leg length inequality and thigh atrophy.

Separate prognostic criteria have been developed for children who present after skeletal maturity. Mose^90,91 states that evaluation of the shape of the femoral head is predictive of the eventual outcome. Stulberg—s classification^90,91 also predicts long-term performance. Coxa plana and coxa magna are poor prognostic signs, as are arthritis (defined by a 2-mm or more deviation off the Mose circular template—Mose “fair” to “poor” outcome), greater than 20% epiphyseal extrusion, or more than 50% femoral head involvement.

Decisions about whether to treat a particular patient can be difficult. Approximately 50% of patients improve with no treatment, and some clinicians recommend conservative treatment (e.g., observation, bed rest, abduction, stretching, and bracing). Surgical treatment consists of femoral/pelvic osteotomies to contain the hip.

Catterall recommends definitive treatment for all “at risk” cases, for groups II and III disease in patients older than 7 years of age, and for group IV cases in which serious deformity has not occurred.⁷⁸ A more conservative approach can be taken with group I cases and group II and III cases that are not “at risk.” Arthrography may be helpful in determining incongruity of the femoral head. After healing is established radiographically, treatment is not required because the femoral head will not deteriorate further. Radiographic signs of healing are an increase in the height and size of viable bone on the medial side of the epiphysis and an increase in the height and quality of new bone formed laterally.

The principles of treatment involve restoring hip motion and decreasing the forces across the hip joint. To accomplish this, the femoral head must be positioned within the acetabulum. This can be achieved with physical therapy and bracing or femoral osteotomy. Neither treatment modality is clearly superior, and both have advantages and disadvantages. In the long term, approximately 86% of patients develop OA, but most are able to function relatively well until the fifth or sixth decade of life.⁹²

Transient osteoporosis of the hip (TOH) has also been referred to as transient osteonecrosis or algodystrophy. TOH represents a self-limited diffuse bone marrow edema of the femoral head and neck (Fig. 3.97)⁹⁴ and must be differentiated from AVN, tuberculosis, stress fracture, malignancy, synovial chondromatosis, and pigmented villonodular synovitis (PVNS). With the use of phased-array hip surface coils it is possible to identify subtle subchondral subarticular stress (Fig. 3.98) and insufficiency fractures that were previously overlooked, resulting in the inappropriate diagnosis of TOH.

Transient bone marrow edema syndrome refers to a reversible bone marrow edema pattern without the associated radiographic changes of osteopenia. Transient bone marrow edema syndrome, like transient osteoporosis of the hip, is self-limited and may in fact represent a form of transient osteoporosis of the hip. Evaluation of associated subchondral stress or insufficiency fractures requires the use of high-resolution techniques.

Osteonecrosis may also present with a diffuse bone marrow edema pattern that either partially obscures a poorly defined subchondral focal lesion (pseudohomogeneous bone marrow edema pattern) or precedes the development of a discrete well-demarcated focus of osteonecrosis. Patients with transient osteoporosis of the hip or transient bone marrow edema syndrome do not have the associated common risk factors usually seen in osteonecrosis. Histologically, transient osteoporosis of the hip and AVN may show similar findings of edema, necrosis, and a fibrovascular reaction. Transient osteoporosis of the hip may thus represent an early reversible form of osteonecrosis.⁹⁸ Initial reports show that treatment of bone marrow edema syndrome with drilling shortens the duration of pain and illness compared with conservative management.

Although the precise etiology is unknown, current theories indicate that obesity, trauma, and hormonal abnormalities are associated with the development of the disease.¹⁰⁰ Mechanically, a vertical growth plate and retroversion of the femoral neck appear to be risk factors.¹⁰¹ Histologically, the slip occurs through the zone of hypertrophy in the growth plate. Agamanolis et al. demonstrated a generalized chondrocyte degeneration throughout the growth plate, suggesting a primary pathology.¹⁰²

The child with SCFE usually presents with pain and a limp. Often the pain is located only in the thigh or knee, leading to frequently missed diagnoses. It is important to remember that knee pain in the child can be secondary to hip disease. On physical examination, there is frequently limitation of motion, especially internal rotation and abduction. As the examiner flexes the hip, it moves into external rotation, and the patient often holds the leg externally rotated when standing.

Initial evaluation should include both AP and frog lateral radiographs. Since the major direction of the slip is usually posterior, it is often most easily noted on a frog lateral view. Both hips should be evaluated, because slips are bilateral in 20% to 25% of cases. Commonly there is impaction of the articular cartilage between the acetabulum and femoral head, and increased friction on joint cartilage subsequent to the slippage during joint motion. Evacuation of hematoma by arthroscopic lavage is associated with decreased pain and earlier postoperative motion and weight-bearing.

SCFE can be classified according to either the duration of symptoms or the degree of slippage. Acute slips may be diagnosed in patients who have had symptoms for less than 3 weeks and in whom no chronic radiographic changes are found. Symptoms lasting 3 weeks or longer indicate a chronic slip, and chronic radiographic changes include resorption of the superior femoral neck and new bone formation on the inferior femoral neck. An acute-on-chronic slip has chronic symptoms and radiographic changes with acute progression of the slip. Slips are also classified as mild, moderate, or severe based on the degree of slippage.

Although MR imaging has played a limited role in the evaluation of SCFE, it is possible to display the morphology of the articular cartilage epiphysis prior to the development of bright-signal-intensity fat within the femoral ossification center.⁸⁸ The widened growth plate and epiphyseal slippage are clearly demonstrated on MR images (Fig. 3.99). MR imaging may also be useful in identifying associated osteonecrosis—reported in up to 15% of children—prior to its appearance on conventional radiographs.¹⁰³ Associated incongruity of the joint surfaces and changes in the articular cartilage covering of the femoral head and acetabulum are best seen on coronal and axial plane images. The relationship of the femoral epiphysis to its containment within the acetabulum is best displayed on axial images showing anterior and posterior position relative to the acetabulum.

Arthroscopy¹⁰⁴ is used in both evaluation of the articular cartilage and labral injury in SCFE and for decompression of the hematoma resulting from physeal fracture. Common findings include:

Treatment of SCFE is aimed at stabilizing the femoral capital epiphysis to allow early fusion of the growth plate. For

mild to moderate slips, the most common procedure is in situ pinning. Many types of hardware are used, including a variety of multiple pin techniques and single screws. With severe slips, some advocate a gentle closed reduction, open reduction, or cuneiform osteotomy.¹⁰⁵ The complication rate is high with internal fixation.¹⁰⁶ Chondrolysis may occur and has been attributed to pin penetration. Unrecognized pin penetration is a major problem. AVN, another serious complication of treatment in SCFE, may follow closed reduction, open reduction, osteotomy, or vascular damage from internal fixation. It is important to remember that this is an iatrogenic complication. Because of the high complication rate with internal fixation, bone graft epiphysiodesis has gained popularity in some centers.¹⁰⁷ In the long term, the resultant biomechanical abnormality predisposes the patient to degenerative arthritis.¹⁰⁸

DDH, which occurs in 1.5% of neonates, is considered a multifactorial/polygenic trait, and the etiology includes both genetic and environmental factors. DDH occurs more frequently in females (6:1 female to male ratio), and other risk factors include a positive family history, breech presentation, torticollis, and scoliosis. There are mechanical factors, such as acetabular dysplasia and laxity of joint capsule ligaments, as well as physiologic factors, such as elevated maternal estrogen level.

Typical pathologic and histologic findings include:

DDH is classified according to the configuration of the acetabulum and the limbus.¹¹⁵ The modified Graf classification defines four types based on the alpha (acetabular roof) angle (the alpha angle is the geometric complement of the acetabular index angle):

In dislocation of the femoral epiphysis, the femoral head is uncovered by the cartilaginous acetabulum and displaced superolaterally. The hourglass configuration of the joint capsule
is caused by compression between the limbus and the ligamentum teres. Constriction by the iliopsoas tendon may block attempts at reduction. Most cases of DDH present with a type 1 hip and positional instability. Failed hip reduction may be secondary to thickening of the ligamentum teres, an unfolded or blunted limbus, and severe deformity of the acetabulum or femoral head.

In the adolescent or young adult presenting with hip pain, the diagnosis of DDH is often associated with acetabular labral pathology. In the acetabular rim syndrome (Fig. 3.101), findings are similar to those described for femoroacetabular impingement (see discussion below) in the nondysplastic acetabulum, and the acetabular rim syndrome may also represent a precursor to the development of OA. As in FAI, DDH is not a direct cause of hip pain. The morphologic changes of DDH, however, make the hip more susceptible to intra-articular pathology, which may then produce symptoms. The structures vulnerable to injury in adult DDH include:

The shallow acetabulum in DDH is associated with a hypertrophied acetabular labrum (Fig. 3.102). It was initially thought that in children increased labral coverage would provide the support needed to maintain hip stability and obviate the need for an osteotomy. Although the enlarged labrum may not substitute for the lateral acetabulum in a child, it is thought to have a partial stabilizing and weight-bearing role in the DDH

patient. Unfortunately, the hypertrophic labrum is exposed to greater joint reaction forces and is at an increased risk for symptomatic tearing. The acetabular labrum may also become inverted, entrapped, and subsequently torn. Direct contact between the hypertrophied labrum and the femoral head chondral surface may produce a chondral crease demarcating a femoral head bump formed proximal to the physeal scar. This finding is associated with a lateral acetabular rim or the DDH equivalent of FAI. Anterior coronal MR images evaluated at the level of the anteriormost portion of the femoral head are sensitive to asymmetry in the slope of the acetabulum. The anterior acetabular roof should maintain a relatively horizontal slope and not open up or deviate from the horizontal plane.

Acetabular articular cartilage erosions occur in the lateral acetabular rim syndrome as a function of increased contact forces. There are acetabular chondral, subchondral, and femoral fibrocystic changes similar to those found in FAI in the adult patient.

The ligamentum teres may be hypertrophied (see Fig. 3.102) or elongated in association with lateral subluxation of the femoral head within the acetabulum. Calcification or ossification of the DDH labrum may be a response to buttress superolateral subluxation of the femoral head. Severe DDH is associated with remodeling of the femoral head and the development of a pseudocapsule as the femoral head is located superolateral to the shallow acetabulum (Fig. 3.103).

DDH may result in limb shortening, FAI, degenerative changes, or AVN. If diagnosis and treatment are delayed, the outcome is irreversible dysplasia. However, early diagnosis and treatment produce good results. The type of treatment is dependent on the age at diagnosis. In infants up to 5 or 6 months of age, conservative treatment (closed reduction with a harness) is usually sufficient. Conservative treatment may also be successful in somewhat older infants, but a spica cast or orthosis is required. Surgery may be necessary in older children, especially those who are walking. Surgical procedures include adductor tenotomy with release of the iliopsoas muscle, open reduction, and osteotomy. Both varus (derotational) and reconstructive (Salter opening wedge, triple innominate, and Chiari medialization of femoral head) osteotomies may be used.

The muscle fiber is the basic structural element of skeletal muscle. The contractile elements of skeletal muscle fibers are the Z-lines. The muscle-tendon unit (MTU) is a distal junction at risk for injury in muscle strains (see below). The muscle fiber arrangement relative to the long axis includes:

The surrounding connective tissue (Fig. 3.105) includes the perimysium, which surrounds fascicles (fascicles are arranged groups of fibers, and myofibrils are individual parts of the fibers that are a component of a fascicle); the endomysium, which surrounds the individual muscle fibers; and the epimysium, which surrounds the entire muscle.

Hip pain in the athlete is most commonly secondary to overuse, resulting in tendinitis, bursitis, or muscle strain. Runners are most prone to these types of injuries, which are often associated with repetitive drills or a change in the intensity or duration of a workout schedule. Muscle edema involving the adductor muscle groups can be demonstrated without tears in marathon and ultramarathon runners. The antagonist muscle groups are most susceptible to injury. Although the injury can occur anywhere within the muscle, the origin or insertion of the muscle is most likely to be affected. In the adductors, the resulting tendinitis and periostitis cause the so-called pulled groin. Similarly, the pulled hamstring usually is a result of periostitis-tendinitis at the ischial tuberosity, where the hamstring muscles originate.

In evaluating the athlete with hip pain, a careful history is critical. The physician needs a detailed account of the training
habits of the athlete and any recent modifications to that regimen. On physical examination, pain can often be elicited with deep palpation in the area of the musculotendinous junction or the muscle itself. In addition, pain with resistive muscle contraction can localize the traumatized muscle group.

Muscle strain ¹¹⁷ has been defined as an indirect injury to muscle caused by excessive stretch and overuse resulting in microtrauma, muscle, and myotendinous tearing. The MTU is the weakest link in the locomotor system^117,118 and is often the site of muscle failure. Muscles at risk include those with the highest proportion of fast-twitch, type II muscle fibers (e.g., rectus femoris, biceps femoris, and medial gastrocnemius muscles)^117,118 and those that cross multiple joints or have complex architecture. In addition, muscles that are subject to eccentric loading appear to be predisposed to strain.^117,118