The Hip

3 – The Hip

Chapter 3
The Hip
David W. Stoller
Thomas Sampson
Miriam Bredella
The hip—consisting of the acetabulum, femoral articulation, supporting soft tissue, muscle, and cartilage structures—is a functionally and structurally complex joint. Disease processes involving the hip joint include trauma, osteonecrosis, arthritis, infection, and neoplasia, conditions that are frequently not detected by conventional radiographic techniques until they have reached an advanced clinical stage. The various imaging modalities have different strengths and weaknesses in facilitating diagnosis. Plain films, for example, are limited in assessment of soft tissues and articular structures. Contrast arthrography is useful in evaluation of the joint spaces and for sampling of synovial fluid in cases of infection. Computed tomography (CT), by reformatting axial scans with sufficient bone detail to generate sagittal and coronal images, provides a multiplanar three-dimensional (3D) perspective on hip disease.1
Magnetic resonance (MR) imaging has also been successfully used to evaluate pathologic processes in the hip.2,3 The excellent spatial and contrast resolution provided by MR imaging facilitates early detection and evaluation of femoral head osteonecrosis, definition of hyaline articular cartilage damage in arthritis, identification of joint effusions, and characterization of osseous and soft tissue tumors about the hip. With direct, noninvasive MR imaging of bone marrow, fractures and infiltrative diseases can be identified earlier than with radiographic studies. In addition, the cartilaginous epiphysis in an infant or child, which is not visible on routine radiographs, can be demonstrated on MR images. The use of surface coils, including pelvic phased-array coils, produces more anatomic detail in imaging of the joint capsule and acetabular labrum.


Imaging Protocols for the Hip
With the body coil used in most MR examinations of the hip, and with a large (32- to 40-cm) field of view (FOV), both hips are seen and can be compared. Phased-array torso coils improve the signal-to-noise ratio (SNR) while still providing visualization of both hips.4 A phased-array torso, cardiac, or dedicated hip coil is used to provide high-resolution images of the symptomatic or affected hip. High-resolution images are acquired at FOVs of 14 to 18 cm.5
T1- or proton density (PD)-weighted images can be acquired in the axial, sagittal, or coronal planes. Examinations are performed with a 512 × 256 or 256 × 256 acquisition matrix, using 1 or 2 excitations (NEX). Thin (3- to 4-mm) sections are obtained either contiguously or with a minimal interslice gap. Three-millimeter sections are preferred in pediatric patients, or when precise assessments are required to display articular cartilage surfaces and the labrum.
Fat-suppressed PD-weighted fast spin-echo (FS PD FSE) images are routinely acquired to evaluate trauma, arthritis, infection, and neoplasia. If FS PD FSE imaging is not adequate or available, short TI inversion recovery (STIR) and FSE STIR sequences are useful in identifying bone marrow pathology and muscle hemorrhage and edema.6,7,8 Coronal, sagittal, and axial surface coil imaging is useful in identifying capsular and labral abnormalities at FOVs of 14 to 18 cm.
Axial oblique images parallel to the femoral neck are used to assess femoroacetabular impingement (FAI). On these scans the relationships of the femoral neck, the dysplastic femoral bump, and the femoral head are visualized on the same image. Unilateral small FOVs (14 to 18 cm) are used to evaluate the acetabular and femoral head chondral surfaces. The changes seen in FAI can also be assessed on unilateral high-resolution coronal plane and radial images that display the acetabular chondral surface, the chondrolabral junction, and the acetabular labrum (Fig. 3.1). The lateral labrum is best visualized on coronal images, although changes seen in the anterior and posterior labrum require verification on axial and sagittal images. Radial imaging is not required but can be helpful in evaluating anterior labral tears, which may be difficult to appreciate on coronal images. Routine radial images are not needed with proper correlation of axial and sagittal images.
FS PD FSE imaging is accurate in identifying areas of synovial thickening and is sensitive to intralabral, intrasubstance chondral changes and to subchondral edema. MR arthrography9 may be used to supplement routine FS PD FSE images. An additional FS T1-weighted coronal image is used to appreciate surface chondral contour and labral morphology. Capsular distention improves visualization of loose bodies. T2* gradient-echo contrast, although not routinely used, is the most sensitive and specific technique for the evaluation of chondrocalcinosis and calcium pyrophosphate dihydrate deposition disease. Gradient-echo techniques may be used selectively to appreciate trabecular architecture changes in osteomyelitis and to depict subchondral trabecular changes adjacent to the site of femoral impingement in FAI.
Related Muscles
The hip muscles10 can be grouped according to their function as follows:
  • The flexor muscles, including the iliopsoas, rectus femoris and sartorius
  • The extensor muscles, including the gluteus maximus and the hamstring muscles (the biceps femoris, semimembranosus, and semitendinosus)
  • The abductor muscles, including the gluteus medius and minimus
  • The adductor muscles, including the adductor brevis, longus, and magnus muscles, the pectineus, and the gracilis
  • The muscles of external rotation, including the obturator internus and externus, the superior and inferior gemellus, the quadratus femoris, and the piriformis
  • The muscles of internal rotation, including the gluteus medius and minimus (secondary function), the tensor fasciae latae, the semimembranosus, the semitendinosus, the posterior pectineus, and the adductor magnus
They may also be grouped by regional location, as follows:
  • The muscles of the iliac region, including the psoas major (Fig. 3.2), psoas minor (Fig. 3.3), and iliacus (Fig. 3.4)
  • The anterior muscles of the thigh, including the sartorius (Fig. 3.5), the rectus femoris (Fig. 3.6), the vastus lateralis (Fig. 3.7), the vastus medialis (Fig. 3.8), and the vastus intermedius (Fig. 3.9). The vastus lateralis, vastus medialis, vastus intermedius, and rectus femoris are the quadriceps muscles.
  • The medial muscles of the thigh, including the gracilis (Fig. 3.10), the pectineus (Fig. 3.11), the adductor longus (Fig. 3.12), the adductor brevis (Fig. 3.13), and the adductor magnus (Fig. 3.14)
  • The muscles of the gluteal region, including the gluteus maximus (Fig. 3.15), the gluteus medius (Fig. 3.16), the gluteus minimus (Fig. 3.17), the tensor fasciae latae

















    (Fig. 3.18), the piriformis (Fig. 3.19), the obturator internus (Fig. 3.20), the gemellus superior (Fig. 3.21) and gemellus inferior (Fig. 3.22), the quadratus femoris (Fig. 3.23), and the obturator externus (Fig. 3.24)

  • The posterior muscles of the thigh, including the biceps femoris (Fig. 3.25), the semimembranosus (Fig. 3.26), and the semitendinosus (Fig. 3.27).
FIGURE 3.1 ● (A, B) Coronal plane images of the hip using a phased-array surface coil. Subtle acetabular sclerosis is identified on the coronal PD FSE image (A), and the full-thickness acetabular roof chondral defect is conspicuous on the FS PD FSE images (B and D). Although PD-weighted images are used more frequently than T1-weighted images, subchondral sclerosis is more apparent on T1-weighted contrast. (C) Radial image locations are prescribed from this FS PD FSE axial image centered on the femoral head. (D) High-resolution coronal FS PD FSE image (MR arthrogram) showing the potential to separate chondral surfaces of the acetabulum and femoral head.
FIGURE 3.2PSOAS MAJOR The psoas major flexes the femur (thigh) and vertebral spine on the pelvis when the leg is fixed. The psoas major and iliacus form the iliopsoas muscle group. Iliopsoas muscle tendon strain is the result of forceful contraction of the iliopsoas when the thigh is fixed or in the extended position.
FIGURE 3.3PSOAS MINOR The psoas minor flexes the pelvis on the spine and assists the psoas major in flexing the spine. The psoas minor may be absent in 40% of individuals.
FIGURE 3.4ILIACUS The iliacus muscle flexes the femur (thigh) and tilts the pelvis anteriorly when the leg is fixed.
FIGURE 3.5SARTORIUS The sartorius flexes and externally rotates the hip and flexes the leg on the thigh. The anterior superior iliac spine at the origin of the sartorius is a common location for an avulsion fracture. These injuries are usually seen in athletes (sprinters, jumpers, soccer players, and football players).
FIGURE 3.6RECTUS FEMORIS The rectus femoris flexes the thigh (hip) and extends the leg (knee). Of the four quadriceps muscles (the vastus lateralis, vastus medialis, vastus intermedius, and rectus femoris), only the rectus femoris has an origin that crosses the hip joint. Soccer, football, and basketball players and track and field athletes are at risk for distal musculotendinous junction injuries and proximal intrasubstance tears of the musculotendinous junction of the indirect head of the rectus.
FIGURE 3.7VASTUS LATERALIS The vastus lateralis extends the leg and flexes the thigh (hip) and is one of the quadriceps muscles (vastus lateralis, vastus medialis, vastus intermedius, and rectus femoris). Quadriceps muscle fibers are predominantly type II and are adapted for rapid forceful activity. The vastus lateralis obliquus (VLO) fibers of the vastus lateralis muscle interdigitate with the lateral intermuscular septum and insert onto the patella. In a lateral retinacular release, the VLO may be selectively sectioned without involving the main vastus lateralis tendon proper.
FIGURE 3.8VASTUS MEDIALIS The vastus medialis extends the leg and pulls the patella medially. The quadriceps muscle group includes the vastus lateralis, the vastus medialis, the vastus intermedius, and the rectus femoris. The quadriceps muscles converge distally, forming the quadriceps tendon, which inserts on the proximal pole of the patella. The vastus medialis assists in preventing patellar dislocations and may be weak in patellofemoral disorders. Therefore, vastus medialis obliquus injuries are frequently associated with transient patellar dislocation.
FIGURE 3.9VASTUS INTERMEDIUS The vastus intermedius extends the leg and covers the articularis genu. Quadriceps (vastus lateralis, vastus medialis, vastus intermedius, and rectus femoris) injuries, including strains and tendon ruptures, result from eccentric muscle contractions. The articularis genu muscle represents a few separate muscle fibers deep to the vastus intermedius and is responsible for contracting the knee joint capsule superiorly in extension.
FIGURE 3.10GRACILIS The gracilis muscle adducts the thigh and flexes and internally rotates the leg and can be used for anterior cruciate ligament reconstructions. The gracilis is the one muscle of the medial aspect adductors of the thigh that does not attach to the linea aspera of the femur (as opposed to the adductor longus, magnus, and brevis and pectineus muscles).
FIGURE 3.11PECTINEUS The pectineus muscle adducts, flexes, and medially rotates the thigh. The adductor muscles, the pectineus, and the gracilis represent the muscles of the medial aspect of the thigh.
FIGURE 3.12ADDUCTOR LONGUS The adductor longus adducts and assists in the flexion of the thigh. The adductor group muscles (longus, magnus, and brevis) originate at the symphysis pubis and inferior pubic ramus and insert on the linea aspera of the femur.
FIGURE 3.13ADDUCTOR BREVIS The adductor brevis muscle adducts and assists in flexing the thigh.
FIGURE 3.14ADDUCTOR MAGNUS The adductor magnus adducts the femur (thigh). The proximal portion flexes the thigh and the distal portion extends it.
FIGURE 3.15GLUTEUS MAXIMUS The gluteus maximus extends the thigh and assists in adduction and lateral rotation of the femur (thigh). Trunk extension is accomplished by action on its insertion.
MR Anatomic Atlas of the Hip
Coronal Images
The coronal plane (Fig. 3.28) is used in the evaluation of the acetabular labrum, the hip joint space, and the subchondral acetabular and femoral marrow. Acetabular and femoral head articular cartilage may be more difficult to separate on coronal images than on sagittal images:
  • The fibrocartilaginous limbus, or acetabular labrum, is visualized as a low-signal-intensity triangle interposed between the superolateral aspect of the femoral head and the inferolateral aspect of the acetabulum.
  • The joint capsule is visualized as a low-signal-intensity structure circumscribing the femoral neck. In the presence of fluid, the capsule distends and the lateral and medial margins become convex.
  • Anterior coronal images demonstrate that the articular cartilage of the femoral head can be seen medially at the ligamentum teres insertion site. The reflected head of the rectus femoris is shown lateral to the proximal portion of the iliofemoral ligament.
  • Anteriorly, the iliopsoas muscle and tendon are in a 7-o—clock position relative to the femoral head.
  • The low-signal-intensity iliofemoral ligament is present on the lateral aspect of the femoral neck, near the greater trochanter.
  • The superior acetabular labrum is located deep to the proximal portion of the iliofemoral ligament along the lateral inferior margin of the acetabulum. The orbicular zone may be identified as a small outpouching on











    the medial aspect of the junction of the femoral head and neck.

  • The intraarticular femoral fat pad is located between the medial femoral head and the acetabulum and displays increased signal intensity on T1-weighted images.
  • The obturator externus muscle crosses the femoral neck on posterior coronal images.
  • Inhomogeneity of marrow signal intensity in the acetabulum, ilium, and ischium is a normal finding on T1-weighted images, representing normal red and yellow marrow inhomogeneity.
FIGURE 3.16GLUTEUS MEDIUS The gluteus medius abducts and medially rotates the thigh when the extremity is extended.
FIGURE 3.17GLUTEUS MINUMUS The gluteus minimus abducts and medially rotates the thigh when the extremity is extended.
FIGURE 3.18TENSOR FASCIAE LATAE The tensor fasciae latae assists in flexion, abduction, and medial rotation of the femur (thigh) and counteracts the posterior pull of the gluteus maximus on the iliotibial tract.
FIGURE 3.19PIRIFORMIS The piriformis rotates the femur (thigh) laterally and abducts the thigh in flexion.
FIGURE 3.20OBTURATOR INTERNUS The obturator internus rotates the femur (thigh) laterally and abducts the femur in flexion.
FIGURE 3.21GEMELLUS SUPERIOR The gemellus superior rotates the femur (thigh) laterally.
FIGURE 3.22GEMELLUS INFERIOR The gemellus inferior rotates the femur (thigh) laterally.
FIGURE 3.23QUADRATUS FEMORIS The quadratus femoris adducts and rotates the femur (thigh) laterally.
FIGURE 3.24OBTURATOR EXTERNUS The obturator externus adducts and rotates the femur (thigh) laterally.
FIGURE 3.25BICEPS FEMORIS The biceps femoris extends the thigh and flexes the leg in external rotation of the tibia, contributing to lateral stability of the knee. The muscles of the hamstring group (biceps femoris, semimembranosus, and semitendinosus), except for the short head of the biceps femoris, all cross the hip and the knee joint. Musculotendinous junctions extend the entire length of the muscle and serve as potential sites for strains. The short head is innervated by the peroneal branch of the sciatic nerve; the other hamstring muscles derive innervation from the tibial branch of the sciatic nerve.
FIGURE 3.26SEMIMEMBRANOSUS The semimembranosus extends the thigh and flexes the leg. It is part of the hamstring muscle group (biceps femoris, semimembranosus, and semitendinosus) in the posterior thigh. Except for the short head of the biceps, the origins of the hamstring tendons are from the ischial tuberosity and are involved in ischial avulsion fractures in the young athlete.
Axial Images
The axial plane (Fig. 3.29) displays the relationship between the femoral head and the acetabulum and the supporting musculature. Axial images made at the level of the acetabular roof may show a partial volume effect with the femoral head. Signal intensity inhomogeneity within the acetabulum is secondary to a greater distribution of red (hematopoietic) marrow stores:
  • The hip musculature demonstrates intermediate signal intensity on T1-weighted images. The gluteal muscles—the gluteus medius laterally, the gluteus minimus deep, and the gluteus maximus posteriorly—can be differentiated from one another by high-signal-intensity fat along fascial divisions. The tensor fasciae latae muscle is seen anterior to the gluteus medius and is bordered anteriorly by subcutaneous fat. The iliopsoas muscle group is anterior to the femoral head in a 12-o—clock position. The sartorius muscle is the most anterior, and the rectus femoris is positioned between the more lateral tensor fasciae latae and the medial iliopsoas. The obturator internus muscle is visualized medial to the anterior and posterior acetabular columns.
  • The sciatic nerve, located directly posterior to the posterior column of the acetabulum, demonstrates intermediate signal intensity. It exits the pelvis through the greater sciatic foramen (the greater sciatic foramen is bordered by the ilium, the rim of the greater sciatic notch, the sacrotuberous ligament, and the sacrospinous ligament) inferior to the piriformis muscle.
  • Entrapment of the sciatic nerve at this location may be associated with the piriformis syndrome. Asymptomatic hypertrophy of the piriformis muscle in this syndrome is best appreciated on axial images. The piriformis originates from the anterior sacrum and greater sciatic notch and inserts on the upper border of the greater trochanter. The piriformis divides the greater sciatic foramen into superior and inferior portions.
  • The external iliac vessels, which are of low signal intensity, are medial to the iliopsoas muscle and anterior to the anterior acetabular column.
  • The low-signal-intensity tendon of the rectus femoris blends with the low-signal-intensity cortex of the anterior inferior iliac spine. The tendon of the reflected head of the rectus femoris muscle is anterolateral to the iliofemoral ligament and follows the contours of the lateral acetabulum.
  • At the level of the femoral head, the more distal femoral artery and vein are visualized.
  • The femoral head articular cartilage demonstrates intermediate signal intensity, and the anterior and posterior fibrocartilaginous acetabular labrum may also be identified at this level. The acetabular labrum is triangular, with the apex oriented laterally.
  • At the level of the greater trochanter and femoral neck, the obturator internus is identified medial to the pubis and ischium.
  • The iliofemoral ligament is of low signal intensity and blends with the dark (i.e., low signal intensity) cortex of the anterior femoral neck.
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  • The sciatic nerve, lateral to the ischial tuberosity, is encased in fat between the quadratus femoris muscle anteriorly and the gluteus maximus muscle posteriorly.
  • The iliotibial tract can be seen peripherally as a thin, low-signal-intensity band surrounded by high-signal-intensity fat on the medial and lateral surfaces.
  • The low-signal-intensity obturator vessels are encased in high-signal-intensity fat and can be identified posterolateral to the pubic bone, between the pectineus and obturator internus muscles.
  • The adductor muscles anteromedially, the obturator externus and the quadratus femoris muscles medially, the ischial tuberosity attachment of the long head of the biceps femoris, and the semitendinosus tendons posteriorly can be visualized at the level of the proximal femur.
  • The ischiofemoral ligament is identified anterior to the quadratus femoris, medial to the ischium, and applied to the posterior hip capsule.
  • The sacrotuberous ligament is seen posteromedial to the ischium.
FIGURE 3.27SEMITENDINOSUS The semitendinosus, which is part of the hamstring muscle group, extends the thigh and flexes the leg. It may be used for anterior cruciate ligament reconstructions, posterolateral knee reconstructions, and tenodesis for patellar subluxation. It is the most posteromedial tendon on axial knee images at the joint line. Hip hyperflexion and simultaneous knee extension is a mechanism of injury for proximal hamstring injuries in adults and apophyseal avulsions in young skeletally immature athletes.
FIGURE 3.28 ● Normal coronal anatomy of the hip. (A, B) In the setting of pubic rami fractures, the sacrum and sacroiliac joints should be examined for the presence of fractures or a diastasis completing the pelvic ring fracture. (C, D) Sacral insufficiency fractures or sacroiliitis is seen only on images with a large field of view. Occasionally they are the only significant finding in a patient with unilateral hip pain. (E, F) Images with a large field of view should also be used to examine the pelvic viscera, especially in women, for adenopathy, masses, and adnexal or uterine pathology. (G, H) Articular cartilage covering the acetabulum and femoral head is clearly displayed. A small portion of the medial femoral head (the fovea) and a large portion of the medial acetabulum (the acetabular fossa) are devoid of cartilage. (I, J) Early signs of degenerative arthrosis may be seen in the anterior superior quadrant of the hip, including cartilage thinning and fraying, subchondral edema in the anterosuperior acetabulum, and anterosuperior labral tearing. (K, L) The anterior superior portions of the bilateral acetabuli are visualized on images obtained with a large field of view. These images allow appreciation of subtle differences in symmetry of the acetabular contour. Even mild acetabular dysplasia may be accompanied by unilateral labral tears and chondral degeneration. (M, N) Osseous spurring at the symphysis pubis is a common finding. Occasionally, acute or insufficiency fractures occur immediately to the left or right of the symphysis pubis, and are seen only on images obtained with a large field of view.
FIGURE 3.29 ● Normal axial anatomy of the hip. (A, B) At this level, the sciatic nerve can be seen exiting the sciatic foramen, deep to the piriformis muscle. Asymmetric enlargement of the piriformis muscle or masses in this region can cause impingement of the sciatic nerve, the so-called piriformis syndrome. (C, D) At this level the transition from the acetabular roof to the top of the femoral head is visualized. The thin arc of dark signal along the lateral margin of the acetabular roof represents the superior margin of the labrum. High signal in the superior labrum can be identified as a labral tear, and accompanying paralabral cysts are commonly identified extending superficial to the labrum. (E, F) The anterior labrum and the posterior labrum on axial images are identified as dark-signal triangles at the lateral margin of the acetabuli. Labral tears present as linear or irregular fluid signal extending through the substance of the labrum, or as expansion of the labrum by fluid signal extending to the surface of the labrum. Fluid signal interposed between the labrum and the acetabulum at the labral attachment indicates labral detachment.(G, H) Tendinosis of the gluteus medius and minimus insertions on the greater trochanter is visualized as thickening and increased signal of the tendons. Trochanteric bursitis can be identified either superficial or deep to the gluteus medius and minimus insertions. (I, J) A fluid collection anteromedial or anterolateral (or both) to the iliopsoas tendon is compatible with iliopsoas bursitis. Occasionally, iliopsoas bursitis may be present adjacent to an anterior labral tear, in which case it may be difficult to distinguish from a paralabral cyst. (K, L) The common hamstring origin on the ischium comprises the biceps femoris and semitendinosus tendons. The common hamstring tendon is a frequent site for tendinosis or partial tears, and the pathology is commonly symmetric.
Sagittal Images
Lateral sagittal images (Fig. 3.30) display the gluteus medius muscle and the tendon attachment to the greater trochanter. The ilium, the anterior inferior iliac spine, the acetabular roof, and the femoral head are seen on the same sagittal section. The intermediate-signal-intensity hyaline cartilage of the femoral head and acetabulum can be separately defined, and the posterior gluteal and anterior rectus femoris muscles are displayed in the long axis:
  • The tendon of the obturator externus is anterior and inferior to the greater trochanter.
  • The piriformis tendon is situated between the iliofemoral ligament anteriorly and the gluteus medius tendon posteriorly.
  • The iliofemoral ligament extends inferiorly, directly anterior to the anterior acetabular labrum.
  • The iliopsoas muscle and tendon course obliquely anterior to the iliofemoral ligament, anterior to the femoral head.
  • The ischiofemoral ligament is closely applied to the surface of the posterior femoral head, anterior to the inferior gemellus muscle and obturator internus tendon.
  • The femoral physeal scar is seen as a horizontal band of low signal intensity in an anterior-to-posterior orientation.
Distally, the vastus musculature is seen anterior to the proximal femoral diaphysis, and the biceps femoris is viewed posteriorly. The sciatic nerve can be followed longitudinally between the anterior quadratus femoris and the posterior gluteus maximus. The low-signal-intensity attachment of the sartorius to the anterosuperior iliac spine is shown anteriorly on sagittal images. The low-signal-intensity iliopsoas tendon spans the hip joint anteriorly, crossing to its insertion on the lesser trochanter. The adductor muscle group is displayed inferior to and medial to the iliopsoas tendon and the pectineus muscle.
On medial sagittal images, the acetabulum encompasses 75% of the femoral head, and the low-signal-intensity transverse acetabular ligament bridges the uncovered anterior inferior gap. On extreme medial images through the hip joint, the ligamentum teres may be seen within the acetabular fossa. At this level, the ischial tuberosity can be seen posterior and inferior to the acetabular fossa.
Imaging Checklist for the Hip
The femur is examined in all three planes for the presence of osteonecrosis, fractures, or edema. The cartilage surfaces covering the femur and acetabulum are also inspected for cartilage fissures, fraying, thinning, or defects. Chondral debris or loose bodies, if present, are identified within the joint recesses. The labrum, which covers the anterior, superior, and posterior acetabulum, is assessed for tears, detachment, fraying, and degeneration. The acetabulum is evaluated for an abnormally shallow contour suggestive of dysplasia. The muscles and tendons about the hip are examined for the presence of tears or strain. Also, the areas overlying the greater trochanter and medial iliopsoas tendon are inspected for trochanteric bursitis and iliopsoas bursitis, respectively. The remainder of the pelvic bones, including the symphysis pubis, the superior and inferior pubic rami, the ilium, the sacroiliac joints, and the sacrum, are then examined on large-FOV coronal images.
Coronal Plane Checklist
1. Femur and Acetabulum
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.

FIGURE 3.30 ● Normal sagittal anatomy of the hip. (A and B) On medial sagittal images, the course of the obturator internus, piriformis, and the adductor muscles can be followed and analyzed for strain injury or tears. (C and D) Tendinosis and tears of the common hamstring tendon origin on the ischial tuberosity are optimally viewed at this location and are extremely common in middle aged and elderly patients. (E and F) Although thinning and fraying of the articular cartilage can occur anywhere in the joint, chondral degeneration is most commonly seen first in the anterior superior quadrant, often accompanied by anterior labral tears, subchondral edema, and cystic change in the anterior acetabulum. When any one of these findings is present, a careful search for the others should be performed. (G and H) Linear tears of the anterior labrum can be mimicked by fluid filling a normal recess between the anterior labrum and the anterior joint capsule. Imaging in the axial and coronal planes is used to distinguish between a true tear and the normal recess, since a tear is visualized and confirmed in the axial and coronal planes, whereas a recess is only seen prominently in the sagittal plane. (K and L) The gluteus medius and minimus tendons have been referred to as the “rotator cuff” of the hip. The gluteus medius tendon inserts posteriorly on the greater trochanter, and the gluteus minimus tendon inserts anterolaterally on the greater trochanter. (I and J) Loose bodies commonly lodge in the joint recesses anterior and posterior to the femoral neck (deep to the iliofemoral and ischiofemoral ligaments). They are commonly seen (particularly in the sagittal plane) in patients with chondral degeneration. (M and N) Acute tears of the gluteus medius and minimus often mimic symptoms of a proximal femoral fracture. Chronic partial tears and tendinosis are frequently associated with trochanteric bursitis, and are common in middle-aged and elderly patients.
FIGURE 3.31 / Femur and Acetabulum.
2. Cartilage Surfaces
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.
3. Labrum
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.
FIGURE 3.32 / Hip Cartilage.
FIGURE 3.33 / Labrum.



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.
FIGURE 3.34 / Muscle and Tendon Insertions.
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.
4. Muscle and Tendon Insertions
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.
5. Greater Trochanter
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.
6. Other Pelvic Bones
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.

FIGURE 3.35 / Greater Trochanter.
Axial Plane Checklist
1. Labrum
The anterior and posterior labrum are best visualized on axial images (Fig. 3.37). Abnormalities of the superior labrum can also be detected.
2. Cartilage Surfaces
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.
3. Femur and Acetabulum
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.
4. Muscles and Tendons
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.
5. Iliopsoas and Trochanteric Bursae
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.

FIGURE 3.36 / Pelvic Bones.
FIGURE 3.37 / Labrum.
FIGURE 3.38 / Cartilage.
FIGURE 3.39 / Femur.
FIGURE 3.40 / Muscles.
FIGURE 3.41 / Iliopsoas.
FIGURE 3.42 / Hip Capsule.
6. Joint Capsule
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.
Sagittal Plane Checklist
1. Labrum
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.

FIGURE 3.43 / Labrum.
FIGURE 3.44 / Cartilage.
2. Cartilage Surfaces
The sagittal plane affords an additional opportunity to evaluate the femoral head and acetabular cartilage surfaces and associated subchondral changes (Fig. 3.44).
3. Femur and Acetabulum
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.
4. Muscle and Tendon Insertions
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.
FIGURE 3.45 / Femur and Acetabulum.
Sample MRI Report, Right Hip
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.
FIGURE 3.46 / Muscles.
FIGURE 3.47 / Sample Hip Case.
FIGURE 3.48 ● (A) Articular surfaces of the hip joint comprise the acetabulum of the hip bone and the head of the femur. (B) A sagittal MR arthrogram of the hip demonstrating capsular distention and the articular relationship of the femoral head (H) to the anterior (A) and posterior (P) aspects of the acetabulum and ilium (I). Fat-suppressed T2-weighted fast spin-echo.



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.
  • Degenerative arthritis of the right hip, with severe anterior superior chondral loss, anterior and superior labral tearing, an adjacent large paralabral cyst, and subchondral cystic changes involving the anterior acetabulum
  • P.101

  • Dysplastic bump in the anterolateral femoral head-neck junction associated with cam-type femoroacetabular impingement
  • No evidence of avascular necrosis
Anatomy of the Hip
The femoral head represents a multiaxial, synovial ball-and-socket joint (Fig. 3.48).11 The acetabulum, which provides bony coverage of 40% of the femoral head (Fig. 3.49), has a horseshoe-shaped lunate surface. The acetabular fossa lies in the inferomedial portion of the acetabulum. This region is occupied by the pulvinar (fat pad) and round ligament (ligamentum teres) (Fig. 3.50). The stellate lesion or crease (Fig. 3.51) is a bare area above the anterosuperior margin of the acetabular fossa within the articular area of the acetabulum.
The dense fibrocartilaginous labrum of the acetabulum increases the depth of the acetabulum (Fig. 3.52). In some patients the labrum is intra-articular in location, and in these patients it may be a predisposing factor in the development of OA. Arthroscopically, three distinct gutters can be identified peripheral to the labrum: a perilabral sulcus and the anterior and posterior synovial gutters, which are the margins of the hip joint.12 The innominate (hip) bone comprises the ilium, ischium, and pubic bones. At birth, the triradiate or Y cartilage, located at the center of the acetabulum, separates the ilium, ischium, and pubis.13,14 The fovea capitis, a small depression on the medial femoral head, is the site of attachment of the ligamentum teres originating in the acetabular fossa (Fig. 3.53). The ligamentum teres demonstrates a banded, pyramidal morphology. The transverse acetabular ligament bridges the notch at the inferomedial acetabulum and together with the acetabular labrum forms a complete ring around the acetabulum (Fig. 3.54). The femoral head, covered by articular cartilage, forms two thirds of a sphere proximal to its transition into the femoral neck. There is no articular cartilage surface over the fovea capitis. The insertion of the ligamentum teres into the fovea fills what has been referred to as a “bare area.”12 The femoral head articular cartilage surface measures 3 mm in its thickest regions posteriorly and superiorly, thinning to 0.5 mm along its peripheral and inferior margins.
The inelastic fibrous joint capsule of the hip is reinforced by the iliofemoral, pubofemoral, and ischiofemoral ligaments (thickenings of the hip capsule) (Figs. 3.55 and 3.56). The iliofemoral ligament, or ligament of Bigelow, is the strongest and thickest of the capsular ligaments and has an inverted Y-shape anteriorly. The pubofemoral and ischiofemoral ligaments are less substantial. Deep circular fibers form the ischiofemoral ligament from the zona orbicularis. Arthroscopically, the zona orbicularis may be mistaken for the acetabular labrum (Fig. 3.57).12 Twisting and shortening of the capsule limit full hip extension. The main hip abductors, the gluteus minimus and gluteus medius, insert on the greater trochanter (Fig. 3.58). The iliopsoas tendon, a major hip flexor, passes anterior to the hip joint and attaches to the lesser trochanter (Fig. 3.59).
Normal Labral Variants
The normal lateral acetabular labrum15 as assessed on coronal images correlates with the labrum on lateral peripheral sagittal images. The far anterior labrum is difficult to evaluate on anterior coronal images but is easy to visualize on axial and sagittal images. Pitfalls in interpreting the appearance of the normal labrum may occur when the labrum is visualized in close proximity to a capsular structure. Common labral variations include the following:
  • The posterior inferior sublabral sulcus (Fig. 3.60) should not be misinterpreted as a posterior labral tear on axial images.15,16 When depicted, this sublabral groove is seen on one or two axial oblique images superior to the transition between the transverse ligament and the posteroinferior labrum. This sulcus is in fact characterized as a labrocartilaginous cleft and can be shown arthroscopically.
  • An anterosuperior cleft (Fig. 3.61) may be seen as a normal variant in the presence of a normal lateral acetabular labrum. On anterior coronal or sagittal images, this cleft is seen as a partial undercutting of the labrum on a single image. The extension of fluid into this cleft occurs from the femoral side. It may be more commonly seen in labral hypertrophy associated with mild developmental dysplasia of the hip (DDH).
  • A transverse ligament-labral junction sulcus is a normal sulcus or recess that may be seen between the transverse ligament and the labrum either anteriorly (Fig. 3.62) or posteriorly (Fig. 3.63). The perilabral sulcus (Fig. 3.64) represents a normal space between the acetabular labrum and capsule visualized on coronal images. The capsule attaches directly to the osseous rim of the acetabulum. A normal sulcus may exist at the junction of the transverse ligament and labrum (see Fig. 3.62) on medial sagittal images. A normal perilabral sulcus is present on coronal images between the capsules and labrum and does not represent a pathologic detachment. This sulcus is a distinct and normal potential separation from the labrum (Fig. 3.65). The




    perilabral sulcus is more conspicuous on MR arthrography. In comparison and contrast with the glenohumeral joint of the shoulder, the acetabular labrum of the hip is not critical in providing stability. However, it does maintain a role in creating the vacuum seal of the hip joint.

  • An enlarged or hypertrophied labrum may occur in patients with mild DDH.17 We have observed a femoral head chondral crease (Fig. 3.66) in these patients, creating a demarcation trough medial to a femoral head bump immediately proximal to the physeal scar. Patients who demonstrate femoroacetabular impingement (or lateral acetabular rim syndrome in DDH) also have direct impingement between the lateral acetabular labrum and the femoral head.
FIGURE 3.49 ● A normal cortical articular ridge of the acetabulum (arrow) is seen on (A) T2*-weighted coronal and (B) 3D CT images. This bony ridge should not be mistaken for osseous pathology. The acetabular notch (open arrow) is shown on the 3D CT rendering. (A: TR, 400 msec; TE, 20 msec; flip angle, 25°). (C) Arthroscopic view of acetabular notch.
FIGURE 3.50 ● (A) Arthroscopic anatomy demonstrating the labrum, ligamentum teres, and articular cartilage of the lunate surface of the acetabulum. (B) Arthroscopic view of the ligamentum teres with the hip in internal rotation.
FIGURE 3.51 ● (A) The stellate crease (arrows) is shown above the acetabular fossa (F) and within the lunate surface of the acetabulum. The stellate crease, (lesion) represents a bare area deficient in hyaline cartilage and not degeneration. Arthroscopically, this bare area may appear as an indentation. The femoral head (H) is indicated. Anterior is down and posterior is up. (B) The articular lunate surface of the acetabulum. The osseous acetabular rim is angled anteroinferior relative to the sagittal plane. The adult aperture angle is 17°.
Osseous Components
The calcar femorale (Fig. 3.67), the weight-bearing bone in the femur, radiates from the inferomedial femoral cortex toward the greater trochanter. Weight-bearing stress trabeculae form the boundaries of Ward—s triangle in the femoral neck and head. On conventional radiography, Ward—s triangle appears as a region of decreased bone density distal to the intersection of femoral neck weight-bearing trabeculae.
The secondary ossification centers of the femoral head, the greater and lesser trochanters, appear at 4 to 7 months of fetal development. In the adult, the mean femoral neck shaft angle is 125°, and femoral anteversion averages 14°. The neck shaft and femoral anteversion angles decrease during skeletal maturation. The intertrochanteric line between the greater and lesser trochanters is the attachment site of the iliofemoral ligament. Therefore, it can be seen that 95% of the femoral neck is intracapsular. This has implications for the hip joint in cases of osteomyelitis of the proximal femoral metaphysis. Since this area is intra-articular, the hip joint may become secondarily infected.
Neurovascular Structures
The medial and lateral circumflex arteries (Figs. 3.68 and 3.69) provide most of the blood supply to the femoral head and proximal femur through anastomotic rings at the base of the femoral neck and head. Fractures involving the femoral neck can damage the blood supply to the femoral head, leading to osteonecrosis. The lateral part of the extracapsular arterial ring provides most of the blood supply to the femoral head. The obturator artery provides a variable vascular supply to the femoral head through the ligamentum teres.
The sciatic, femoral, and obturator nerves are the important neural structures about the hip:10
FIGURE 3.52 ● (A) Internal features are revealed by disarticulation of the joint after cutting the ligamentum teres and joint capsule. (B) The lunate-shaped articular surface covers the acetabular fossa and forms two thirds of a sphere.
FIGURE 3.53 ● (A) The joint capsule has been opened anteriorly and reflected to show the interior of the joint. The femur has been abducted and externally rotated. (B) Axial MR arthrogram identifying the fovea (F), ligamentum teres (arrows), posterior labrum (PL), obturator internus tendon (OI), and greater trochanter (GT). Fat-suppressed T2-weighted fast spin-echo image.
FIGURE 3.54 ● Transverse ligament. (A) Arthroscopic view. (B) Coronal T2* gradient echo image. (C) Sagittal FS PD FSE medially. (D) Sagittal FS PD FSE at posterior labrum-transverse ligament transition.
FIGURE 3.55 ● (A) The inverted Y-shaped iliofemoral ligament spirals from the superior acetabulum to the anterior femoral neck. The weaker pubofemoral ligament blends with the medial aspect of the iliofemoral ligament. The iliofemoral ligament fibers are taut in full hip extension. (B) Anterior surface of the joint capsule, associated ligaments, and adjacent structures.
FIGURE 3.56 ● (A) The ischiofemoral ligament, which reinforces the posterior capsule, originates from the ischial portion of the acetabular rim. Its fibers spiral laterally and superiorly across the femoral neck to blend with the fibers of the zona orbicularis. (B) Posterior surface of the joint capsule and the ichioremoral ligament.
FIGURE 3.57 ● (A) Coronal MR arthrogram displaying hip joint and capsular anatomy. The distal insertion of the capsule is at the base of the femoral neck. The zona orbicularis (zo) is seen as an area of capsular thickening and tightening over the middle of the femoral neck. The transverse ligament (tl), iliofemoral ligament (IF), and ligamentum teres (lt) are identified. The acetabular labrum is absent. This coronal MR section cuts through the supra-articular recess, the intra-articular recess, and the recess colli (the recess at the base of the femoral neck). Fat-suppressed T2-weighted fast spin-echo image. (B) Coronal FS PD FSE image showing the zona orbicularis fibers at the base of the femoral neck circumferentially surrounding the posterior capsule. The zona orbicularis represents a deep layer of circularly oriented fibers that do not directly attach to the femur. (C) Arthroscopic view of the zona orbicularis.
FIGURE 3.58 ● A coronal section through the hip joint shows its anatomic relations.
FIGURE 3.59 ● (A) A transverse section through the hip joint shows its anatomic relations. (B) Arthroscopic view of the iliopsoas tendon relative to its lesser trochanter insertion. The iliopsoas flexes, laterally rotates, and adducts the thigh.
FIGURE 3.60 ● The posterior inferior sublabral sulcus or groove does not extend completely underneath the labrum and is not analogous to the sublabral foramen. (A) Axial color illustration. (B) Axial FS PD FSE image. (C) Coronal 3D color illustration of the posteroinferior sulcus. (D) Arthroscopic view of the posterior inferior sulcus.
FIGURE 3.61 ● Coronal (A) and sagittal (B) FS PD FSE images of an anterosuperior cleft in a patient with mild DDH and a hypertrophied labrum. The cleft does not extend completely through the lateral or anterior labrum.
FIGURE 3.62 ● Normal transverse ligament labral sulcus. (A) Coronal color illustration. (B) Coronal FS T1 MR arthrogram. (C) Sagittal (lateral) color illustration. (D) Sagittal FS PD FSE image.
FIGURE 3.63 ● Sagittal FS PD FSE image showing the posterior transverse ligament of the labral sulcus.
FIGURE 3.64 ● (A) Coronal section through hip joint. (B) Coronal FS PD FSE image showing the perilabral sulcus between the capsule and lateral acetabular rim and labrum. (C) Normal chondrolabral junction and perilabral sulcus.
FIGURE 3.65 ● 3D image showing correlation between capsule and labrum and a corresponding coronal section of the perilabral sulcus lateral to the acetabular rim and labrum.
FIGURE 3.66 ● Femoral head chondral crease with adjacent bump proximal to the physis in a mild DDH case with a hypertrophied labrum. (A) A mild crease is shown on this coronal FS PD FSE image. (B) This coronal FS PD FSE image shows a prominent femoral head crease secondary to impingement between the hypertrophied labrum and the articular surface of the lateral femoral head proximal to the physeal scar in another DDH patient. (C) Arthroscopic view of femoral head crease demarcating the femoral head articular cartilage medially from the lateral bump. The crease or cleft is opposite the lateral edge of the hypertrophied labrum. The normal perilabral sulcus is also shown between the labrum and capsule.
FIGURE 3.67 ● Relationship of the femoral neck and calcar.
FIGURE 3.68 ● Anterior (A) and posterior (B) perspectives of femoral head arterial supply. The arteries are derived from an anastomosis of three sets of vessels, the retinacular vessels (from the medial circumflex femoral artery and, to a lesser extent, the lateral circumflex femoral artery), the terminal branches of the medullary artery of the femoral shaft, and the artery of the ligamentum teres from the posterior division of the obturator artery.
FIGURE 3.69 ● Vascular supply of the hip joint. The relationship of the obturator artery and the small foveolar artery contained within the ligamentum teres is shown.















  • The sciatic nerve (Fig. 3.70) is composed of the upper sacral plexus roots from the anterior and posterior divisions of L4, L5, S1, S2, and S3. The two peripheral nerves, the tibial (anterior divisions) and the common peroneal (posterior divisions), are contained within the same connective tissue sheath as the sciatic nerve.
  • The femoral nerve is derived from the posterior branches of the second, third, and fourth lumbar nerve roots (the hip). The femoral nerve overlies the iliopsoas muscle proximal to its entry into the thigh through the femoral triangle.
  • The obturator nerve is formed from the anterior divisions of L2, L3, and L4 and crosses the quadrilateral surface of the acetabulum medial to the obturator internus muscle. The obturator neurovascular bundle exits the pelvis through the obturator canal in the superolateral aspect of the obturator foramen.
Arthroscopically Relevant Anatomy
The radiologist should be familiar with the orthopaedic terminology describing locations and pathology of the acetabulum (Fig. 3.71). The lateral acetabulum is directed superiorly and the medial acetabulum is directed inferiorly. The key structures and disorders identified on an arthroscopic overview include:18,19
  • The acetabular notch and fat pad, loose bodies, synovial tissue, and notch osteophytes
  • Tears or avulsions of the ligamentum teres
  • The posterior labrum
  • The lateral labrum
  • The anterior labrum
  • Labral hypertrophy
  • Soft, blistered, or delaminated acetabular cartilage
  • Perilabral sulcus, cysts, spurring, and labral tears
  • Femoral head fovea and ligamentum teres
  • Transverse acetabular ligament
  • Zona orbicularis
  • Iliopsoas tendon reflection or capsule
Bone Marrow
The normal proximal femur marrow (Fig. 3.72) with red to yellow marrow conversion is visualized as fat-signal intensity in the greater trochanter and femoral epiphysis.20 Fatty or yellow marrow conversion occurs in Ward—s triangle of the femoral neck in middle-aged patients. Melorheostosis (Fig. 3.73), with peripherally located cortical hyperostosis about the hip, is hypointense on all pulse sequences and may be seen on both the acetabular and femoral sides of the hip.




Pathology of the Hip
Avascular Necrosis
FIGURE 3.70 ● (A) Posterior color illustration of the neural structures of the posterior proximal thigh. The sciatic nerve is sectioned. The sciatic nerve arises from the lumbosacral plexus and is composed of the ventral rami of the fourth and fifth lumbar roots and the first, second, and third sacral roots. It is shown exiting the pelvis through the sciatic notch inferior to the piriformis muscle. The sciatic nerve is completely motor in function. (B) Coronal T1 FSE image of the normal sciatic nerve.
FIGURE 3.71 ● In a lateral arthroscopic approach the lateral acetabulum is directed superiorly. The left hip is demonstrated.
FIGURE 3.72 ● Coronal PD FSE image showing the normal distribution of yellow marrow fat signal intensity in the greater trochanter and femoral epiphysis. In the femoral neck and proximal femoral diaphysis, red marrow is seen with intermediate or lower in signal intensity.
FIGURE 3.73 ● Hypointense sclerotic melorheostosis involving the acetabulum, femoral head, and ilium. Melorheostosis may cross the joint and can be associated with bone pain, limited range of motion, and joint effusion. The cortical hyperostosis (candle wax morphology) occurs in a dermatomal distribution. Subsequent evaluations may demonstrate flexion contractures, although this process is often an incidental finding. Coronal PD FSE image.
Avascular necrosis, also referred to as aseptic necrosis, osteonecrosis, or ischemic necrosis, most commonly involves the femoral head (Fig. 3.74). Osteonecrosis is considered to be a more general term, used to indicate cellular necrosis of bone and marrow elements. The term “avascular necrosis” is used to refer to these changes when they occur in the epiphyseal region or subchondral bone. A bone infarct represents osteonecrosis of the metaphyseal or diaphyseal bone, although some infarcts involve the deep subchondral bone of the epiphyseal region. The changes seen in bone infarcts are morphologically different from those of AVN of the femoral head.
Etiology and Clinical Features
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
  • The classic presentation includes hip, groin, or gluteal pain, with or without referred thigh or knee pain. Groin pain is characteristic of hip pathology. The C sign is pain described by a cupped hand placed above the greater trochanter, indicating deep joint pain.
  • The pain is described as deep and throbbing and is worse with ambulation or activity, particularly twisting motions such as occur in turning or changing direction.
  • The patient may describe pain with sitting and difficulty ascending and descending stairs.
  • Hip rotation and range of motion are decreased, particularly in the presence of a joint effusion.
  • There may be a catching or popping sensation.
  • A Trendelenburg gait is often noted.
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.
FIGURE 3.74 ● Crescentic subchondral involvement of the femoral head prior to segmental flattening of the articular surface.


Diagnosis and Pathology
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.
Plain films, usually anteroposterior (AP) and frog lateral views, are used in staging AVN but are not sensitive to early changes. Involvement of the femoral head is usually more distinct than evidence of joint space narrowing or acetabular findings. Femoral head sclerosis may be noted, and subchondral collapse, when found, is a sign of advanced disease. With MR imaging, plain films can be used to stage disease according to the Ficat classification (see below).
Computed Tomography
CT is also used for staging disease and is more accurate than conventional radiographs for more extensive disease (stage II and higher). It is less sensitive than MR, however. Osteoporosis is the first sign of disease. Sclerosis and distortion of the central bony asterisk, normal thickening of trabeculae in the center of the femoral head, can also be seen.
Bone Scans
Nuclear scintigraphy with technetium-labeled phosphate analogues, such as methylene diphosphonate (99mTc-MDP), may be used for the early detection of osteonecrosis.28 Although bone scans allow earlier detection of changes than conventional radiographs, they are not as sensitive as MR imaging. During the acute phase of the disease, decreased uptake of bone tracer is associated with vascular compromise. Increased accumulation of radiopharmaceutical tracer occurs with chronic vascular stasis in repair and in revascularization. Dynamic scanning is useful to assess regional blood flow in this setting. The specificity of marrow scanning with technetium sulfur colloid (99mTc-sulfur colloid) is variable and depends on the status of the underlying disease and on the pattern of marrow composition.
MR Imaging
MR imaging is more sensitive than conventional radiography, CT, or radionuclide bone scintigraphy in detection of AVN of the hip.29,30 In differentiating AVN from non-AVN disease of the femoral head, MR imaging has a specificity of 98% and a sensitivity of 97%.31 MR is also effective in assessing joint effusions, marrow conversion, edema, and articular cartilage congruity, none of which is possible with bone scintigraphy, standard radiographs, or CT.
Imaging protocols for evaluation of patients with AVN include T1- or PD-weighted images and contrast-enhanced T1-weighted fat-suppressed images. A T1-weighted axial localizer and coronal images are acquired with either a T1- and T2-weighted spin-echo sequence, an FS PD FSE sequence, or a STIR (FSE STIR) sequence. Sagittal plane imaging may be helpful in defining early changes of cortical flattening associated with subchondral collapse. STIR sequences, which negate yellow marrow-fat signal, provide excellent contrast for the detection of marrow replacement, fluid, and necrotic tissue.
FIGURE 3.75 ● Segmental flattening with loss of the spherical shape of the femoral head. Subchondral collapse produces the characteristic crescent sign.


Premature fatty marrow conversion associated with AVN can be detected using chemical-shift imaging techniques. On fat- and water-selective images, fatty and hematopoietic marrow and distribution of water within the ischemic focus can be differentiated. Gradient-echo coronal images, although not as sensitive for fluid within reparative tissue and necrosis, demonstrate associated hip joint effusions, subchondral fluid, and changes in articular cartilage contours. When compared with coronal images acquired with a body coil, sagittal images acquired with a surface coil and a small FOV may provide superior AP and superoinferior localization of AVN by demonstrating joint-space narrowing, articular cartilage fracture, and the double-line sign.32 On T2-weighted or FS PD FSE images, the double-line sign is visualized as an inner border of high signal intensity, paralleling the low-signal-intensity periphery. It can be observed in up to 80% of lesions and cannot be solely attributed to a chemical-shift artifact or misrepresentation.
Early osteonecrosis may present with an ischemic focus that mimics a subchondral stress or insufficiency fracture. Femoral head and neck edema may be mistaken for transient osteoporosis of the hip (Fig. 3.76). Bone marrow edema, which is a nonspecific finding, does correlate with pain and has a stronger association than joint effusion. Bone marrow edema may also occur in later stages of ischemia.
AVN may also present with a more medial and non-weight-bearing focus (Fig. 3.77). A deeper subchondral ischemic area (Fig. 3.78) may have features of both AVN and bone infarction. A deep subchondral infarct that extends to the subchondral plate, however, is equivalent to other forms of AVN, and these patients are at risk for progression and subsequent subchondral fracture.
General MR characteristics of AVN include the following:
  • A hypointense peripheral band (primarily granulation tissue and to a lesser extent sclerosis) outlining a central region of bone marrow represents the reactive interface between necrotic and reparative zones, as seen on T1-weighted images.
  • There may be associated bone marrow edema of head and neck of the femur.
  • A joint effusion may be seen and is hypointense on T1-weighted images and hyperintense on FS PD FSE images.
  • Post-contrast enhancement corresponds to a reparative zone, seen as a hypointense band. There may be decreased enhancement with gadolinium in early AVN, and there is no enhancement with nonviable trabeculae and marrow.
  • The alpha angle, determined on coronal images, is used to assess the largest area of necrosis (with the vertex of the angle at the center of the femoral head).33 Alpha angles greater than 75° are associated with a poor prognosis.33 (See discussion below on alpha angles.)
  • A wedge-shaped subchondral infarct may also be seen.
FS PD FSE images allow further characterization of AVN, but determination of the percentage of femoral head volume involved requires the use of at least two imaging planes. In the double-line sign there is a combination of a hypointense peripheral border (sclerosis) and a hyperintense inner border (granulation tissue) visualized on FS PD FSE images. AVN may exist in the absence of a double-line sign. Hyperintense effusion and marrow edema require characterization with FS PD FSE sequences.
FIGURE 3.76 ● Bilateral AVN (after renal transplant). The right hip is asymptomatic and there is a diffuse edema pattern of the left femoral head and neck associated with ischemic change and subchondral fracture. Coronal FS PS FSE image.



Staging and Classification
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.
FIGURE 3.77 ● Medial osteonecrosis on coronal T1-weighted (A) and FS PD FSE images (B). Osteonecrosis involving the one third or less of the weight-bearing portion of the femur is less likely to progress to femoral head collapse.
FIGURE 3.78 ● Early AVN focus extending toward the subchondral plate. Central marrow fat signal intensity is shown within the ischemic zone.
International Classification
The international system consists of four stages:
  • Stage 0: Bone biopsy shows osteonecrosis, but imaging findings are normal.
  • Stage I: Bone scans are positive; MR imaging may or may not show early changes of AVN.
  • Stage II: Mottled femoral head with sclerosis/cyst/osteopenia on radiographs. There is no collapse; bone scans are positive.
  • Stage III: Crescent sign lesion and depression of the femoral head articular surface
  • Stage IV: Flattening of the articular surface and joint space narrowing with secondary acetabular changes
FIGURE 3.79 ● Coronal T1-weighted (A) and FS PD FSE (B) images show osteonecrosis with approximately 70% femoral head involvement without associated articular collapse. Marrow edema extends into the intertrochanteric area.
Ficat and Arlet Staging System
The most popular of the staging systems for AVN is that of Ficat and Arlet,35 modified to include preclinical and preradiologic stages of the disease.34 This modification is important because the disease can be present in the absence of clinical and radiologic signs (stage 0). In stage I and stage II disease, the joint remains normal and the femoral head is spherical (Fig. 3.79):
  • Stage 0: Diagnosed on the basis of scintigraphic or MR imaging when a painful contralateral hip is being evaluated. There are no clinical or radiographic changes found. There is a double-line sign on the MR image in the asymptomatic hip in this stage.
  • Stage I: The trabeculae appear normal or slightly porotic. MR imaging may show a single line on T1-weighted images and the double line sign on FS PD FSE images. The double-line sign is specific and pathognomonic for AVN. The hyperintensity at the periphery of the necrotic focus is probably caused by hypervascular granulation tissue, a hyperemic response adjacent to thickened trabeculae.27 Pathologic specimens from lesions in these early stages show viable bone on necrotic bone with marrow spaces infiltrated by mononuclear cells and histiocytes, explaining the imaging changes.
  • P.126

  • Stage II: There is sclerosis and porosis of the trabeculae, and a shell of reactive bone demarcates the area of infarct. Within this area, the trabeculae and marrow spaces are acellular. There may be an extended pattern of associated marrow edema from the nonischemic region of the femoral head into the femoral neck (Fig. 3.80).
  • Stage III: The onset of stage III disease is marked by the loss of the spherical shape of the femoral head (Fig. 3.81). The AP radiograph may appear normal, but the lateral view often reveals a crescent sign, or radiolucency, under the subchondral bone. This represents a fracture between the subchondral bone and the underlying femoral head (Fig. 3.82). The crescent sign is the



    earliest indication of mechanical failure from accumulated stress fractures of nonrepaired necrotic trabeculae.27 At this stage, there is also separation of the subchondral plate from the underlying necrotic cancellous bone. The necrotic area becomes radiodense (Fig. 3.83) as a result of mineral deposition in the marrow spaces. The joint space remains preserved or may actually increase in height.

  • Stage IV: The femoral head undergoes further collapse, leading to articular cartilage destruction and joint space narrowing (Fig. 3.84). Segmental collapse and subchondral fracture may result in pain and disability. Frequently this is the stage at which the patient presents for evaluation, although attention is sometimes sought earlier. Pain may be attributed to increased intraosseous pressure and microfractures.
FIGURE 3.80 ● Extended pattern of marrow edema in association with osteonecrosis. Edema of the femoral neck is hypointense on T1-weighted image (A) and hyperintense on FS PD FSE image (B). (C, D) A separate case of AVN with an ischemic focus demonstrating attenuated fat signal with adjacent reactive femoral head and neck edema. The marrow edema does not extend into the ischemic region. (C) Coronal T1-weighted image. (D) Coronal FS PD FSE image.
FIGURE 3.81 ● AVN with subchondral fracture. The focus of osteonecrosis involves a portion of the weight-bearing surface. (A) Coronal T1-weighted image. (B) Sagittal T1-weighted image. (C) Sagittal FS PD FSE image.
FIGURE 3.82 ● AVN. (A) T1-weighted coronal image demonstrates high-signal-intensity cortical necrosis (large arrow), low-signal-intensity sclerotic peripheral interface between necrosis and viable marrow (small arrow), and low-signal-intensity subchondral fracture (open arrow) (TR, 600 msec; TE, 20 msec). (B) A macroslide of a gross specimen shows corresponding subchondral collapse (open arrow), reactive periphery (white arrow), and cortical necrosis (black arrow).
FIGURE 3.83 ● Hypointense ischemic area on coronal T1-weighted (A) and FS PD FSE (B) images.
Combined Classification System
A separate classification system incorporates components from several different systems and includes the four stages of the Ficat and Arlet classification, quantification of the extent of femoral head involvement (determined by MR imaging as less than 15%, 15% to 30%, or more than 30%), and assess-ment of the location of the necrotic focus (medial, which is rarely progressive; central, which carries a prognosis of intermediate severity; or lateral, which has the worst prognosis).27
Mitchell Staging System
Mitchell et al. have described an MR classification system for AVN based on qualitative assessment of alterations in the central region of MR signal intensity in the osteonecrotic focus.28,40 Although the Mitchell system is useful in characterizing MR signal, the Ficat system as modified for MR findings is more useful in describing the progression of ischemia that results in changes in femoral head morphology:
  • Class A: In MR class A disease (Fig. 3.85), the osteonecrotic lesion demonstrates signal characteristics analogous to fat. There is a central region of high signal intensity on images obtained with short TR/TE settings (T1-weighted images) and intermediate signal intensity on images obtained with long TR/TE settings (T2-weighted images).
  • Class B: Class B hips demonstrate the signal characteristics of blood or hemorrhage (i.e., high signal intensity on both short and long TR/TE sequences).
  • Class C: Hips identified as class C demonstrate the signal properties of fluid (i.e., low signal intensity on short TR/TE sequences and high signal intensity on long TR/TE sequences).
  • Class D: Class D hips exhibit the signal characteristics of fibrous tissue (i.e., low signal intensity on short and long TR/TE sequences) (Fig. 3.86).
In all four classes, a peripheral band of low signal intensity outlines the central focus of AVN. This border is most visible on T1-weighted images in class A and B hips (the central focus of necrosis is bright in signal intensity) and on T2-weighted images in class C hips. Manipulation of TR/TE pulse parameters does not affect the low-signal-intensity border.
FIGURE 3.84 ● Osteonecrosis in a dysplastic hip with a shallow acetabulum. There is frank subchondral collapse and femoral head cystic change. Changes in the acetabulum represent superimposed degenerative arthritis with joint space narrowing. (A) T1-weighted coronal image. (B) FS PD FSE coronal image. (C) FS PD FSE sagittal image.
FIGURE 3.85 ● Coronal T1 FSE (A) and FS PD FSE (B) images showing AVN with associated synovitis. The central AVN focus demonstrates marrow fat signal intensity. Synovitis demonstrates intermediate signal intensity.



Symptoms of AVN correlate well with MR classification. They are least severe in class A hips and most severe in class D hips. MR signal intensity, therefore, can be seen to follow a chronologic progression from acute (i.e., class A) to chronic (i.e., class D) AVN. Compared with conventional radiographic staging, approximately 50% of radiographic stage I and over 80% of stage II lesions demonstrate fat-like central signal intensity on MR scans and are classified as MR class A. Class A lesions are infrequent in more advanced radiographic stages.
FIGURE 3.86 ● AVN associated with acetabular degenerative changes. Note the hypointense sclerotic reaction of the femoral head. (A) Coronal T1-weighted image. (B) Coronal FS PD FSE image.
Pathologic Correlation
Many MR findings can also be correlated with pathologic changes. Common gross pathologic and surgical features and corresponding MR findings include:
  • Necrosis of cancellous bone and yellow bone marrow, which occurs prior to the development of capillary and mesenchymal ingrowth, corresponds to the central region of hyperintensity.41
  • P.131

  • A sclerotic margin of reactive tissue at the interface between necrotic and viable bone corresponds to the hypointense peripheral band.
  • Thickened trabecular bone and the high water content of mesenchymal tissue are seen as low signal intensity on T1-weighted images and intermediate to high signal intensity on T2-weighted images.
  • Inflammation with granulation tissue or hyperemia inside the reactive bone interface is thought to produce the double-line sign. It is present in 80% of cases of AVN.28
  • Softening within the necrotic cancellous bone at the interface with viable bone appears as resorption of the necrotic focus. There may be rim enhancement of granulation tissue at the reactive interface, with a lack of contrast enhancement with the central nonviable marrow.
  • Collapse of the femoral head load-bearing segment and collapse of the femoral head with articular cartilage destruction, loose bodies, and marginal osteophytes. Collapse is visualized as a subchondral fracture.
  • Areas of vascular engorgement and inflammation are indicated by decreased signal intensity on T2-weighted images and are associated with successful core decompression treatments.
  • A breach in the overlying articular cartilage is associated with fluid signal intensity in the subchondral fracture on FS PD FSE images.42
  • With intravenous gadolinium administration, enhanced and nonenhanced areas correspond to viable and necrotic bone, respectively.43,44
  • Perfusion, as assessed on gadolinium-enhanced T1-weighted images, and marrow composition, as measured with hydrogen-1 MR spectroscopy, were shown to be inversely related to marrow fat content in healthy subjects and were higher in patients at risk for AVN (e.g., patients with systemic lupus erythematosus).45
  • Joint effusions demonstrate low signal intensity on T1-weighted images and high signal intensity on T2-weighted images and are commonly associated with more advanced stages of AVN.46 It is not known whether the presence or absence of a joint effusion is of prognostic significance for the course and treatment of the disease. However, joint effusion is also associated with a bone marrow edema pattern prior to the irreversible demarcation (double-line sign) of the necrotic focus.
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).
Importance of MR Imaging
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.

FIGURE 3.87 ● Osteonecrosis with adjacent column of red marrow. Red or hematopoietic marrow should not be mistaken for an extended edema pattern, which is partially shown in the medial femoral head/neck junction. (A) Coronal T1-weighted image, (B) Coronal FS PD FSE image.
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:
  • Conservative management, observation, and protected weight-bearing, which is of limited utility
  • Surgical management, including core decompression (with or without bone grafts), osteotomy, electrical stimulation, and arthroplasty
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.
FIGURE 3.88 ● Post-core decompression for an ischemic focus with associated subchondral fracture without femoral head collapse. Arthroscopy has been performed for stage IV or post-collapse patients who are also candidates for osteotomy or vascularized graft. Delamination of articular cartilage is treated with débridement and core decompression, although improvement may be limited. (A) Coronal T1-weighted image. (B) Sagittal FS PD FSE image.
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.
Legg-Calvé-Perthes Disease
Legg-Calvé-Perthes disease (LCP) is a childhood hip disorder that results in infarction of the bony epiphysis of the femoral head (Fig. 3.90). Children 4 to 8 years of age are the most commonly affected, with a median age of 7 years. Approximately 1 in 1,200 children under the age 15 years is affected.
FIGURE 3.89 ● Post-core decompression for pain reduction and to delay femoral head collapse in a separate case. A fibular strut graft can also be used to prevent femoral head collapse. (A) Coronal T1-weighted image. (B) Coronal FS PD FSE image.
Diagnosis, Etiology, and Clinical Features
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:
  • Insufficiency of the capital epiphyseal blood supply, with the physis acting as a barrier; ischemia may be arterial or venous and leads to intraepiphyseal infarction
  • Medial and lateral overgrowth of articular cartilage
  • Infarction and trabecular fracture, with decreased epiphyseal height
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:
  • A limp with groin, thigh, or knee pain (referred). Children who present with knee pain must be carefully examined for hip pathology.
  • As the disease progresses, a flexion and adduction contracture may develop, resulting in decreased range of motion.
  • Lateral overgrowth of the femoral head cartilage may cause loss of abduction. Attempts at abduction lead to hinging and possible subluxation of the femoral head.
  • Eventually, the hip may move only in the flexion-extension plane, resulting in a painful gait and muscle atrophy.


Diagnosis of LCP is usually made from plain films. Typical radiographic features include:
  • Effusion, fragmentation, and flattening of a sclerotic capital epiphysis
  • Metaphyseal irregularity, including cystic changes and rarefaction of the lateral and medial metaphysis
  • Widening of the inferomedial joint space with an intact subchondral plate
  • A subchondral fracture line
  • A small epiphysis
FIGURE 3.90 ● Color coronal section showing subchondral necrosis of the proximal femoral epiphyses in LCP.
Conventional film findings may be negative early in the course of the disease, and scintigraphy and MR imaging may provide additional information.
Staging and Classification
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.
FIGURE 3.91 ● Earliest changes of LCP are irregularity of the hypointense subchondral plate of the capital epiphysis and associated joint effusions. (A) Coronal T1-weighted image. (B) Coronal FS PD FSE image.


Catterall Classification
In Catterall—s system the distribution of epiphyseal abnormalities is based on assessments made on AP and lateral radiographs. Four groups have been defined:78
  • Group I: There is involvement of the anterior aspect of the epiphysis without a metaphyseal reaction, sequestrum, or subchondral fracture line. Less than 25% of the epiphysis is involved.
  • Group II: There is more extensive or severe involvement of the anterior aspect of the epiphysis, with preservation of the medial and lateral segments. A sequestrum is present, as is an anterolateral metaphyseal reaction. There is a subchondral fracture line that does not extend to the apex of the femoral epiphysis. Less than half the epiphysis is involved.
  • Group III: The entire epiphysis is dense and there is a diffuse metaphyseal reaction with femoral neck widening. A subchondral fracture line is visualized posteriorly. Most of the epiphysis is involved.
  • Group IV: There is total involvement of the epiphysis, with flattening, mushrooming, and eventual collapse of the femoral head. An extensive metaphyseal reaction and associated posterior remodeling can be seen.
Using this system, it should be possible to separate group I cases (without sequestrum or metaphyseal lesions) from groups II and III (with viable bone posteriorly and medially) and from group IV (with involvement of the entire epiphysis and collapse and loss of epiphyseal height). The more advanced the stage at the time of presentation, the poorer the prognosis. It is important to understand that the disease is progressive, and final radiographic staging may take up to 9 months. Risk factors for progression include lateral subluxation, calcification lateral to the epiphysis, Gage—s sign (a radiolucent V in the lateral epiphysis), and a horizontal physis.
Salter-Thompson Classification
The Salter-Thompson system is based on the extent and location of subchondral fracture and is divided into two groups:79
  • Group A: Less than 50% of the span of epiphysis is involved.
  • Group B: There is fracture of more than 50% of the span of the epiphysis.
Herring System
The Herring system of classification is based on lateral pillar involvement (the lateral pillar is defined as the lateral 15% to 30% of epiphysis), and there are three groups:80
  • Group A: The lateral pillar is not involved.
  • Group B: Less than 50% of the lateral pillar is affected.
  • Group C: More than 50% of the lateral pillar is affected.
Waldenström's Radiographic Staging
Waldenström has developed a five-tier staging system based on overall radiographic findings:
  • Initial stage: Increased head-socket distance, subchondral plate thinning, and a dense epiphysis
  • Fragmentation stage: Subchondral fracture, an inhomogeneous dense epiphysis, and a porous appearance, with metaphyseal cysts
  • Reparative stage: Normal bone in areas of resorption and removal of sclerotic bone. The epiphysis has a more homogenous appearance.
  • Growth stage: Re-ossification; the normal femoral shape is approached.
  • Definitive stage: The final shape is determined, with joint congruency or incongruency.
Pathologic Features and Staging
Pathologically, the early stages of the disease are characterized by overgrowth of the articular cartilage medially and laterally.81,82 Infarction within the femoral head can lead to trabecular fracture and decreased epiphyseal height. The pathologic stages based on epiphyseal involvement are:
  • Initial stage: There is necrosis of epiphyseal bone and marrow, vascular invasion of dead bone, and hypertrophy of epiphyseal cartilage.
  • Fragmentation stage: The dead bone is resorbed, the unossified physeal cartilage in the metaphysis may produce cysts, and there is cartilage hypertrophy.
  • Reparative stage: Dead bone is replaced.
Green et al. have correlated the degree of epiphyseal extrusion with prognosis: when more than 20% of the epiphysis is extruded laterally, the prognosis is poor; when more than 50% of the femoral head is also involved, only 8% have good results.83 On radiographic examination, increased bony tissue density is found in the area of infarction, representing appositional new bone and calcification of necrotic marrow. Revascularization occurs through creeping substitution of necrotic bone with fibrocartilage, causing the fragmented appearance seen on plain-film radiographs during this phase of the disease. The thickened articular cartilage is repaired from subchondral bone and from within the abnormal cartilage anteriorly and laterally. Unossified cartilage that streams down from the growth plate can lead to metaphyseal cysts. In the late stages, the fibrocartilage is reossified. The last area to heal is superior and anterior.
Histologic changes in the epiphysis include disordered collagen fibrosis, increased proteoglycan concentration, and decreased structural glycoproteins. Infarction is characterized by histologic evidence of necrosis of epiphyseal bone and marrow, invasion of new blood vessels, and resorption of dead bone and new bone formation.
MR Imaging
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).

FIGURE 3.92 ● T1-weighted coronal images in LCP. (A) Normal femoral head capital epiphyses. (B) The earliest MR signs of LCP include peripheral irregularity of marrow-fat-containing epiphyseal ossification center (white arrows). Low-signal-intensity foci or linear segments are seen within the right and left ossification centers (black arrows). No subarticular collapse is present, and conventional radiographs are normal (TR, 500 msec; TE, 20 msec).
FIGURE 3.93 ● Coronal T1-weighted images show the spectrum of LCP from (A, B) early to (C, D) late advanced involvement. (A) Small, laterally displaced ossific nucleus with loss of yellow marrow signal intensity (long black arrow) is present early in the disease. Normal contralateral epiphyseal cartilage (curved arrow) and high-signal-intensity marrow (short black arrow) are seen. (B) Complete loss of right femoral epiphyseal marrow signal intensity (arrow) occurs as the disease progresses. (C) Bilateral low-signal-intensity osteonecrotic foci in the femoral epiphysis (arrows) become apparent later in the disease. Articular cartilage is thinner in the older child. (D) Advanced remodeling with coxa plana and coxa magna of the femoral heads (arrows) is indicative of late advanced involvement. (TR, 600 msec; TE, 20 msec.)
FIGURE 3.94 ● LCP with hypointense ischemic capital epiphysis associated with medial metaphyseal irregularity. Coronal FS PD FSE image.
Typical features seen on T1- or PD-weighted images include:
  • Hypointense intra-articular effusion
  • Hypointense irregularity along the periphery of the ossific nucleus. Before diffuse loss of signal intensity of the ossific nucleus is observed, low-signal-intensity irregularity occurs along the periphery of the fat-containing ossific nucleus, and linear areas of low signal intensity may traverse the femoral ossification center. These changes correlate with positive bone scintigraphy in stage I disease.
  • Replacement of the initial low-signal-intensity focus with high-signal-intensity marrow fat is associated with revascularization of a necrotic epiphysis after treatment with varus osteotomy.
  • Coxa plana and coxa magna as a result of late remodeling
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:
  • In the early stages of disease, physeal cartilage may or may not be hyperintense on T2-weighted images.
  • Loss of containment of the femoral head in the acetabulum is indicated by intermediate-signal hypertrophied synovium in the iliopsoas recess, seen as a frond-like structure adjacent to the inferomedial joint space. Rush et al. reported these findings in 7 of 20 cases.86 Thickening of the intermediate-signal epiphyseal cartilage also contributes to loss of containment.87
  • Hyperintense joint effusion
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.
FIGURE 3.95 ● An 11-year-old girl with chronic changes of LCP on the right. There is enlargement of the right capital epiphysis with decreased superolateral coverage, and loss of epiphyseal height on coronal T1-weighted (A) and T2* (B) images. The T2* coronal image (B) shows flattening of the femoral head and acetabulum. A sagittal T2* image (C) identifies the hyperintense anterior epiphyseal involvement (arrows). The overlying articular cartilage appears more congruent than the necrotic focus within the capital epiphysis.
FIGURE 3.96 ● An 11-year-old with LCP. A coronal T1-weighted image (A) and a sagittal FS PD FSE image (B) show total epiphyseal necrosis, fragmentation, and flattening. Joint effusion is hyperintense on the FS PD FSE image (B). Presentation after 8 years of age is associated with a poor prognosis.



Separate prognostic criteria have been developed for children who present after skeletal maturity. Mose90,91 states that evaluation of the shape of the femoral head is predictive of the eventual outcome. Stulberg—s classification90,91 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
FIGURE 3.97 ● Transient osteoporosis of the hip with partial marrow-sparing of the greater trochanter and medial femoral head. No subchondral fracture is identified. (A) Coronal color section. (B) Coronal T1-weighted image. (C) Coronal FS PD FSE image.


Bone Marrow Edema Pattern (Including Transient Osteoporosis of the Hip, Transient Bone Marrow Edema Syndrome, and Osteonecrosis)
The term bone marrow edema pattern refers to nonspecific MR signal intensity changes, including hypointensity on T1-weighted images and hyperintensity on conventional T2-weighted, FS PD FSE, or STIR images.93 Bone marrow edema encompasses the entities of transient osteoporosis of the hip, transient bone marrow edema syndrome, and osteonecrosis. A nonspecific bone marrow edema pattern may also be observed in cases of occult osseous trauma, infection, and neoplasms, although these entities can usually be distinguished.
Transient Osteoporosis of the Hip
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.
Diagnosis, Etiology, and Clinical Features
The disease process is self-limited and of unknown etiology. It was originally described in women in the third trimester of pregnancy with a predilection for the left hip, although it is most commonly found in healthy middle-aged men in the third and fourth decades. These may both, in fact, represent populations at risk for stress or insufficiency fractures. TOH is characterized by progressive bone demineralization. Clinical features include:
  • Acute onset of groin pain, which is exacerbated by weight-bearing
  • Decreased range of motion
  • Limp
  • History negative for infection or trauma
  • Resolution of symptoms after 6 to 10 months and restoration of mobility
One joint is usually affected, with diffuse involvement of the femoral head and variable extension to the femoral neck and intertrochanteric region. The laboratory evaluation is unremarkable except for intermittent elevation in the sedimentation rate. Pathologic and histologic findings include:
  • Elevation of pressure within bone marrow
  • Normal appearance of articular cartilage, cortex, and subchondral bone
  • A small joint effusion
  • Synovial inflammation
  • Possible necrosis of fat cells
  • Fibrovascular regenerative tissue
  • Increased osteoid
  • Edema, although it is difficult to document increased free water histologically
  • Hydroxyapatite shift and reduced mineral content
Radiographs are usually normal in the first few days, and although plain films reveal osteopenia around the hip joint, these changes may lag 3 to 6 weeks behind the development of groin pain. Radiographic changes frequently develop after positive findings are made on bone scintigra-phy, which shows intense homogeneous uptake within the femoral head and neck. Although demineralization is present in the active phase of the disease, the radiographic picture eventually returns to normal. Morphologically, changes are variable within the confines of the femoral head and neck, and there may be partial marrow sparing in the greater trochanter.
MR Appearance
MR imaging is useful for characterization of the low signal intensity seen on T1-weighted images and the uniform increased signal intensity seen on conventional T2-weighted, FS PD FSE, or STIR (including FSE STIR) images (see Fig. 3.97). Signal intensity changes may be seen extending from the femoral head to the intertrochanteric line.95 Associated joint effusions are commonly seen on T2-weighted and STIR images.96,97 Resolution of clinical and MR abnormalities usually occurs within 6 to 10 months. Since biopsy reveals histopathologic evidence of increased bone turnover and a mild inflammatory reaction, the signal intensity changes in transient osteoporosis of the hip are thought to be related to an increased amount of free water.
Typical findings on T1- or PD-weighted FSE images include:
  • Diffuse or large areas of hypointensity within the femoral head and neck, sometimes extending to the intertrochanteric region and/or the acetabulum
  • A narrow line of sclerosis associated with a subchondral stress fracture
  • A homogeneous and well-marginated edema pattern
  • There may be a hypointense joint effusion.
  • There may be marrow sparing in the medial and lateral-most margins of the femoral head and greater trochanter secondary to higher concentrations of fatty marrow.
  • Resolution is associated with web-like or reticular areas of hypointensity.


Typical findings on FS PD FSE or STIR images include:
  • Hyperintensity in the femoral head and neck, which is most conspicuous on FS PD or STIR images, sometimes accompanied by acetabular hyperintensity
  • A hypointense fracture line parallel to the subchondral plate (high-resolution imaging is necessary for visualization)
  • Marrow edema, which can be seen as early as 48 hours after the onset of clinical symptoms
  • Marrow sparing may be seen in the anterior, posterior, medial, or lateral aspect of the femoral head.
  • The anatomic distribution of marrow hyperintensity may vary on sequential studies.
  • The edema interface is well defined without a demarcating hypointense line or band (no double-line sign).
  • The cortex and subchondral plate are normal, as are adjacent soft tissues.
  • There is a small to moderate hyperintense joint effusion.
FIGURE 3.98 ● A 40-year-old male patient with subtle subchondral stress fracture easily mistaken for transient osteoporosis. (A) Coronal T1-weighted image. (B) Coronal FS PD FSE image. (C) Sagittal FS PD FSE image.
After contrast administration there is heterogeneous, prominent enhancement.
Transient Bone Marrow Edema Syndrome
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.
Slipped Capital Femoral Epiphysis
Slipped capital femoral epiphysis (SCFE) is a childhood disorder of the hip characterized by posterior inferior displacement of the proximal femoral epiphysis.99
Diagnosis, Etiology, and Clinical Features
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.
MR Imaging
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:
  • Posterolateral labral injuries (compared to posterosuperior labral tears in young patients with occult hip pain)
  • Erosion of the anterosuperior acetabular cartilage
  • A transverse cleft in the anterior femoral head
  • Metaphyseal cartilage damage
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

FIGURE 3.99 ● SCFE. (A, B) The femoral epiphysis is displaced posteriorly, medially, and inferiorly relative to the neck. There is widening of the physis with associated joint effusion. There is a relative decrease in the height of the epiphysis (similar to changes seen on conventional radiographs) and loss of intersection of the epiphysis by the lateral cortical (long axis) line of the femoral neck. The subsequent remodeling of the femoral neck creates a Herndon bump directly lateral to the physeal scar, similar to the location of the dysplastic femoral bump in FAI. (A) Coronal T1-weighted image. (B) Coronal FS PD FSE image. (C) A separate case showing a more severe Salter-Harris type I fracture contributing to varus hip deformity. Coronal T1-weighted image.
Developmental Dysplasia of the Hip
In developmental dysplasia of the hip (DDH), also known as infantile hip dysplasia, there is inadequate contact between the acetabulum and the femoral head. The left hip is affected in 40% to 60% of cases and bilateral involvement occurs in 20%. Infants at risk for DDH include those with a positive family history, breech presentation, torticollis, scoliosis, metatarsus adductus, and structural abnormalities such as underdevelopment of the anterior capsule, ligament of Bigelow, or rectus muscle.99 Early diagnosis and treatment are important, because in the first 6 weeks postpartum the acetabulum is susceptible to remodeling.
Diagnosis, Etiology, and Clinical Features
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:
  • An hourglass joint capsule with compression between the limbus and the ligamentum teres
  • A thick and tight transverse ligament
  • Medial flattening of the femoral head
  • Deficiency of the superior and posterior acetabular rim
  • Hyperplasia of the ligamentum teres
  • Hypertrophy of the pulvinar
Clinical Tests
Ortolani—s and Barlow—s tests are used to assess the dislocated and dislocatable hip, respectively, in the newborn. In Ortolani—s test, hip abduction at 90° flexion with anterior pressure directs the dislocated femoral head into the acetabulum. In Barlow—s test, an unstable femoral head can be dislocated by application of posterior pressure in adduction. A positive finding is indicated by a palpable click or clunk using either test.
Radiographic diagnosis of DDH is more accurate than either of the clinical tests. It should be noted, however, that in children under 6 months of age, radiography may produce a false-negative diagnosis. In addition, a 45° bilateral abduction and internal rotation view or Van Rosen view may prematurely reduce the positionally unstable hip.
Conventional radiographic assessment of the ossific nucleus relative to Hilgenreiner—s line (through triradiate cartilage) demonstrates its location in the lower medial quadrant. Perkins— line (perpendicular to Hilgenreiner—s line) is seen through the lateral acetabular rim. Shenton—s line, connecting the medial border of the femoral metaphysis and the superior border of the obturator foramen, should form a smooth uninterrupted arc in the normal hip, with no subluxation or dislocation. The femoral capital epiphysis is seen in the inner lower quadrant. There may be lateral subluxation of the capital epiphysis (2 mm or more from teardrop to metaphysis) and superior subluxation (a change of 2 mm or more from Hilgenreiner—s line to the metaphysis compared with the normal side). A center-edge angle less than 25° is also associated with instability. The acetabular index (i.e., the slope of the ossified acetabular roof), which is 27° to 30° at birth, is an unreliable measurement in newborns and changes with rotation of the pelvis.
Secondary signs include excessive femoral head ante-version and delayed ossification of the femoral capital epiphysis.
Ultrasonography is often used to evaluate the cartilaginous femoral head prior to the appearance of the ossific nucleus, subluxation, dislocation, the pulvinar, an inverted labrum, a hypoplastic ossific nucleus, acetabular dysplasia, and ossification in children up to 6 months of age. In fact, this technique may also be used in older children. Sonographic findings of increased thickness of the acetabular cartilage are reported to be an early sign of DDH.109 The iliac bone, the acetabulum, the labrum, and the femoral capital epiphysis can all be assessed on ultrasound scans. Osseous dysplasia of the acetabular rim and coverage of the acetabular roof can also be evaluated. Ultrasound is also used to classify hips, as described below.
CT Examination
CT, using a limited number of axial or coronal CT scans with reformations and optional 3D renderings, may be a more appropriate modality for children in plaster


casts or with equivocal conventional radiographs.110,111 The sector angle should be used to evaluate acetabular coverage (from the capital epiphysis to acetabular rim relative to the horizontal axis).

MR Imaging
MR imaging can be successfully used in the detection and evaluation of DDH (Fig. 3.100).108,110,112 The femoral epiphyseal articular cartilage displays intermediate signal intensity on T1-weighted images and bright signal intensity on gradient-echo images. T1-weighted coronal and axial images display the exact position of the intermediate-signal-intensity capital epiphysis, which is particularly useful when the position of the capital epiphysis is uncertain on conventional radiographs and when serial follow-up examinations are required. MR examination can be used for children in or out of plaster casts, eliminating the need to repeatedly expose the child to ionizing radiation. It is also useful when the ossific nucleus is not yet visible on plain radiography or CT. T2-weighted images are helpful when evaluating complications associated with DDH, such as ischemic necrosis and associated effusions, which are not effectively detected with ultrasound or conventional radiography. 3D MR rendering is useful in displaying complex femoral head and acetabular spatial relationships, as well as associated dysplasia.113 Calculation of the acetabular index may be performed on coronal MR images by measuring Hilgenreiner—s line through the triradiate cartilage and the tangent through the acetabular roof. The acetabular index should be less than 30°; however, as mentioned earlier it is an unreliable measurement in newborns.
Additional findings on T1- or PD-weighted FSE images include:
  • Hypointense joint effusions
  • Superolateral dislocation (on coronal plane images)
  • AP relationship and dysplasia of acetabulum (on axial images)
  • Mild acetabular dysplasia (on coronal images)
  • Hyperintense fat signal of the pulvinar
On FS PD FSE images the epiphyseal articular cartilage demonstrates intermediate signal intensity and joint effusions are hyperintense. On T2* GRE images the epiphyseal articular cartilage is hyperintense. Associated ischemic necrosis is hypointense on T1- and PD-weighted images and hypointense in chronic ischemia on FS PD FSE images.
With MR imaging, failure to achieve adequate reduction of the dislocated hip can be determined without the use of invasive arthrography.114 Important elements in evaluating failure of reduction include the following:
  • An hourglass configuration of the acetabulum or an inverted, hypertrophied limbus must be excluded. With inversion, the intermediate-signal-intensity limbus is often seen in the lateral aspect of the joint, with increased fat (i.e., high signal intensity on T1-weighted images) noted medially.
  • On coronal and sagittal images an interposed iliopsoas tendon can be seen crossing the joint space. This prevents reduction of the femoral head in the acetabulum and may create an hourglass configuration of the joint capsule.
  • Supralateral subluxation or dislocation is best identified on coronal MR images, and AP relationships and dysplasia of the acetabular wall are best demonstrated on axial plane images.
  • MR allows direct visualization of the fat-suppressed pulvinar fibrofatty tissue.
  • There is hypertrophy of the hypointense ligamentum teres.
  • The labral limbus is deformed and has a horizontal slope instead of the normal downward lateral slope.
  • On coronal images the limbus of the acetabular roof is inverted with inferomedial displacement and a superoinferior long axis orientation.
  • The coronal plane is the most useful for evaluating acetabular labral coverage beyond the lateral margin of the bony acetabulum relative to the femoral capital epiphysis (see Fig. 3.100). This is important in determining the coverage of the femoral head and the possible need for increased coverage through surgical osteotomy. If adequate coverage is provided by the bony acetabulum and acetabular labrum together, more conservative management of DDH may be appropriate.
MR imaging is also useful in the long-term follow-up and postoperative evaluation of patients with DDH. There is no artifact from plaster or fiberglass abduction spica casts, allowing noninvasive evaluation of the femoral head. Sequelae of DDH may require reconstruction of the acetabulum using a pelvic osteotomy or shelf procedure to redirect, reposition, and augment the hip socket. Later in life, patients often develop secondary OA requiring total hip replacement.
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):
  • Type 1: The alpha angle is greater than 60° in the mature hip. This is considered a normal hip.
  • Type 2a: The alpha angle is 50° to 59° in the immature hip (infants less than 3 months of age).
  • Type 2b: In infants more than 3 months of age with an alpha angle of 50° to 59°, the hip is considered abnormal.
  • Type 2c: The alpha angle is 43° to 49° and the hip is considered critical and subject to subluxation.
  • Type 3: The alpha angle is less than 43°, the acetabular head is eccentric, and the hip is subject to dislocation.
  • Type 4: The alpha angle is less than 43°, and there is severe dysplasia and an inverted labrum.
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.

FIGURE 3.100 ● DDH. (A) Pseudo-coverage of the capital epiphysis by an everted labrum. Coronal radiograph (B) shows complete lateral uncovering of the femoral capital epiphysis associated with a shallow acetabulum. A corresponding T2* coronal MR image (C), however, demonstrates improved coverage by a mildly deformed but primarily everted labrum (arrows).
DDH in the Adolescent and Adult
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 acetabular labrum
  • The articular cartilage of the acetabular roof
  • The ligamentum teres
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.

FIGURE 3.101 ● (A) DDH associated with longitudinal tearing of a hypertrophied labrum. The shallow slope of the acetabulum is demonstrated. The transverse angle of the osseous acetabular rim affects the degree of lateral coverage and is increased in adult DDH. (B) The normal angle of 40° is shown in contrast to (A).
FIGURE 3.102 ● (A) Labral hypertrophy in DDH. (B) Mild labral hypertrophy and marked hypertrophy of the ligamentum teres in DDH. Coronal FS PD FSE images.
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.
FIGURE 3.103 ● Chronic untreated DDH with superiorly displaced aspherical femoral head and deficient acetabular roof. Coronal T1-weighted image.
Miscellaneus Pediatric Hip Conditions
Multiple epiphyseal dysplasia is an autosomal dominant condition affecting the epiphyseal chondrocytes of the growth plate with resultant joint incongruity and premature degenerative arthritis. MR imaging demonstrates irregularity of the femoral head and articular and cortical surfaces. Joint-space narrowing and secondary degenerative joint disease are present by the third or fourth decade of life.
Proximal focal femoral deficiency is a term used to describe a unilateral lack of or shortening of the proximal segments of the femur.99 The radiographic classification system (classes A through D) is based on the presence or absence of femoral head or acetabular dysplasia, and on the shape of the femoral segment.116 MR imaging is used to evaluate the pseudoarthrosis and subtrochanteric varus deformity. On MR examination, fibrous and osseous connections between the femoral head and shaft can be differentiated. In coxa vara, MR imaging is successful in displaying articular cartilage and epiphyseal morphology (Fig. 3.104).
Diaphyseal sclerosis, or Engelmann—s disease, is characterized by long bone sclerosis involving both endosteal and cortical surfaces with relative sparing of the epiphysis and metaphysis. Bilateral symmetry and varying degrees of pain are usually associated with this condition. Although MR imaging is not indicated as the initial study of choice, its use allows the assessment of low-signal-intensity cortical thickening without repeated exposure to ionizing radiation.
Muscle and Tendon Disorders and Hip Pain in the Athlete
Structure of Skeletal Muscle
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:
  • Parallel fibers (fusiform muscles)
  • Oblique fibers (pennate and bipennate muscles)
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.


Overuse Syndromes
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.
FIGURE 3.104 ● (A) Coxa vara with multiple epiphyseal dysplasia. (B) T1-weighted image documents the cartilaginous continuity (curved arrow) between the capital epiphysis and femur.
FIGURE 3.105 ● The structure of skeletal muscle. The endomysium surrounds the individual muscle fibers. The perimysium surrounds groups of fascicles made up of fibers. The epimysium surrounds the entire muscle.
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 Strains
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 system117,118 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
Diagnosis, Etiology, and Clinical Features
Muscle strains occur most often in young athletes, especially speed runners (sprinters), and football, basketball, and soccer players. They occur more often in males, probably because of participation in sports requiring highly eccentric muscle activities. Risk factors include improper warm-up, fatigue, and previous orthopaedic injury. Approximately 30% of sports-related injuries are muscle strains.
Clinically the patient presents with:
  • Muscle pain
  • Weakness, possibly associated with separation of muscle from tendon or fascia (absent in mild or first-degree strains with no myofascial disruption)
  • Edema and swelling
  • Loss of function in third-degree strains with complete myofascial separation
Associated gross pathologic and histologic findings include irregular thinning of the myotendinous junction, hematoma, partial or complete tears of the MTU, avulsion fractures, a hemorrhagic response at the injured fibers, muscle fiber necrosis, edema, and appearance of macrophages and other inflammatory cells and fibroblastic activity. Random disruption of Z lines, caused by damage to the contractile elements of muscle, may also be found.
Early reports indicated that the midsubstance location was the most common site of muscle strain,119 and a grading system similar to that used for ligament injuries was developed for this type of strain:120,121
  • Grade 1: Minimal disruption of the musculotendinous junction (Fig. 3.106). Clinically, a grade 1 strain may simply result in a muscle spasm or cramp.
  • Grade 2: A partial tear with some intact musculotendinous fibers (Fig. 3.107). Clinically, there is discomfort during sports activity or training, but it usually resolves with rest.
  • Grade 3: Complete rupture of the MTU (Fig. 3.108)
  • Grade 3B: Avulsion fracture at the tendon origin or insertion
A simpler grading system of MTU strains has been advanced in which injuries are characterized as mild, moderate, or severe.117,118 According to this scheme, if weakness is absent, the strain is mild, or first degree, and is believed to represent injury in the absence of myofascial disruption. To be


categorized as a mild strain, pathologic findings must be restricted to mild inflammatory cell infiltration, edema, and swelling. In moderate, or second-degree, strains, weakness is associated with a variable degree of separation of muscle from tendon or fascia. In severe, or third-degree, strains, myofascial separation is complete and there is an associated lack of muscle function.

FIGURE 3.106 ● Bilateral adductor longus grade 1 muscle strain with diffuse hyperintense muscle edema. Coronal FS PD FSE image.
FIGURE 3.107 ● Adductor longus muscle strain with characteristics of both grades 1 and 2 strain. There is diffuse muscle edema with partial (myotendinous) tearing. Proximal focal hyperintensity represents hemorrhage. (A) Coronal FS PD FSE image. (B) Coronal FS T1-weighted contrast-enhanced image. (C) Axial FS T1-weighted contrast-enhanced image.
Although initially appealing, such a grading system for characterizing muscle injuries may be deceptively simplistic. In fact, the clinical evaluation of muscle strains is admitted to be very difficult,121,122,123,124 even more so than injuries of tendons or bones.121 Only when the muscle bunches up on contraction is complete muscle rupture a straightforward clinical diagnosis. However, associated edema or hematoma may prevent palpation of the fascial defect.117,125 In addition, the fact that synergists are recruited when a single muscle is disrupted hinders the detection of muscle strains and limits the accuracy of clinical assessment. It may also be difficult to evaluate a muscle strain when the affected muscle is located in a deep site relative to intact, normal muscles. Furthermore, the apparent degree of weakness is dependent upon the presence of spasm, pain, guarding, and hematoma, all of which can occur in the absence of a fascial tear. Further complicating the clinical picture is the fact that on the one hand large fascial tears may be associated with relatively little muscle abnormality, and on the other the MTU may be functionally impaired because of muscle spasm, even when it is structurally intact.121 Fluid collections also frequently accompany strains, making the assessment of the injured muscle even more problematic.118 Fluid collections themselves may be a cause of swelling and weakness in the absence of fascial tear.
FIGURE 3.108 ● Grade 3 tear of the iliopsoas in its distal MTU. Axial FS PD FSE image.
Differential Diagnosis
The most important differential diagnoses include infection and deep venous thrombosis. Infection is characterized by focal involvement with or without a superficial tract and extensive subcutaneous edema. On MR examination infection is visualized with hyperintense to intermediate fluid signal intensity on FS PD/T2 FSE or STIR images. Deep venous thrombosis is characterized by an enlarged, thrombosed popliteal vein and watershed hyperintensity in the gastrocnemius/soleus muscle complex on T2-weighted images.
MR Imaging
By providing objective morphologic data, MR imaging allows accurate assessment of the integrity of strained muscles, the MTU, the tendon, and the tendo-osseous unit. Edema within or around the muscles, depending on the stage of healing, is also identified on MR images.126,127 The MTU is frequently found to be the point of rupture, the extent of associated tendinous injury can be evaluated, and appropriate therapy needs can then be addressed. The use of MR imaging to distinguish focal hematomas from swollen, edematous muscles may also be useful in guiding clinical management. The former may be treated by drainage, whereas the


latter are often treated with wrapping procedures for compression and support of the injured area.128

In general, muscle tears and avulsions demonstrate high signal intensity in areas of edema or hemorrhage on conventional T2, FS T2 FSE, and STIR sequences.129,130,131 Axial plane imaging is useful for the demonstration of associated muscle retraction and atrophy, which show high signal intensity on T1-weighted images. Coronal or sagittal images provide a longitudinal display of the entire muscle group on a single image. A comparison with the contralateral extremity is important in evaluating the relative symmetry of muscle groups.
Additional findings on T1- or PD-weighted images include:
  • Blurring of muscle fiber striations
  • Hypointense to hyperintense hemorrhagic fluid collections
  • Hypointense subcutaneous tissue edema
Expected findings on FS PD FSE images vary depending on the severity of the injury:
  • Grade 1: Hyperintense edema with or without hemorrhage and preservation of muscle morphology (Fig. 3.109). On FS PD, T2 FSE, and STIR images there is an edema pattern, displayed as interstitial hyperintensity with a feathery distribution (Fig. 3.110). Hyperintense subcutaneous tissue edema and intermuscular fluid can also be seen.
  • Grade 2: Hyperintense hemorrhage with tearing and disruption of up to 50% of the muscle fibers. Interstitial hyperintensity with focal hyperintensity represents hemorrhage in the muscle belly with or without intramuscular fluid (Figs. 3.111 and 3.112). A hyperintense focal defect and partial retraction of muscle fibers may also be visualized. Associated myotendinous and tendinous injuries as well as hyperintensity and interruption and widening of the MTU are also found.
  • Grade 3: Complete tearing with or without muscle retraction (Fig. 3.113). A fluid-filled gap can be seen, which is hyperintense on FS PD FSE and STIR images. Associated adjacent hyperintense interstitial muscle changes may also be depicted.
FIGURE 3.109 ● Grade 1 muscle strain of obturator externus, adductor brevis adductor longus, and pectineus muscles. Axial FS PD FSE image.
FIGURE 3.110 ● Feathery edema pattern and mild intramuscular fluid (a grade 2 characteristic) in a grade 1 to 2 biceps femoris muscle strain. Coronal FS PD FSE image.
Although conventional radiography should remain the initial diagnostic examination for excluding posttraumatic myositis ossificans secondary to muscle trauma, MR scans have shown small areas of calcification or ossification as signal void or low signal intensity on T1- and T2-weighted images.
MR imaging pitfalls or “look-alikes” in exertional muscle injury span all categories of disease. For example, the MR signal changes seen with muscle damage may be very similar to changes caused by other forms of trauma or pathology, including neoplasm, radiation, denervation, bacterial infection, polymyositis, hemorrhage, and even acute exercise. Muscle and soft tissue inflammation may appear similar to a grade 1 muscle strain. Acute fasciitis is visualized as a diffuse increase in signal intensity conforming to the involved muscle group. Corresponding gallium scintigraphy and CT may be negative. Soft tissue edema in infection demonstrates low signal intensity on T1-weighted images and increased signal intensity on T2-weighted images. If soft tissue infection is suspected, MR evaluation may be the examination of choice.
Both treatment choices and eventual outcome are dependent on the degree of muscle injury. With untreated or unsuccessfully treated strains there may be progression from incomplete to complete extension of injury, fibrous or fatty replacement, muscle ossification, or even compartment syndrome. Hamstring injuries recur in up to 25% of cases. Potential complications include fibrosis and muscle retraction, reinjury, myositis ossificans, and malunion or nonunion of osseous avulsions.
Therapy options include conservative and surgical treatment. Conservative treatment, which is appropriate for small



fascial or tendinous tears, includes the RICE protocol (rest, ice, compression, elevation); nonsteroidal anti-inflammatory drugs; protective exercises and passive stretching to prevent stiffness, atrophy, and weakness; and isometric and/or isotonic exercises. Treatment of grade 2 strains centers on identifying the offending activity. The injury usually responds to cutting back or altering the training schedule. Cycling or swimming can be temporarily substituted for running to maintain aerobic conditioning. Physiotherapy is beneficial in decreasing muscle spasm and ultimately in regaining flexibility and strength. In general, the recovery period lasts from 2 weeks for grade 1 injuries to over 2 months for grade 2 strains. Grade 3 strains are more difficult to treat and usually require 6 to 8 weeks of rest. Return to full activity is allowed when pain has resolved and muscle strength has returned; this can be effectively judged by using Cybex testing.

FIGURE 3.111 ● (A) Coronal color illustration anterior view of a partial tear of the proximal adductor magnus. Coronal (B) and axial (C) FS PD FSE images showing grade 2 adductor magnus strain with proximally localized intramuscular fluid.
FIGURE 3.112 ● Grade 2 biceps femoris muscle strain with a hematoma at the musculotendinous junction associated with a second-degree injury. Transient sciatica may occur in grade 2 to 3 injuries secondary to compressive sciatic neuropathy. (A) Coronal FS PD FSE image. (B) Axial T2 FSE image.
FIGURE 3.113 ● Sagittal (A) and axial (B) FS PD FSE images demonstrating distal biceps femoris MTU tear with retraction.
Surgical treatment may be necessary when a muscle is completely or nearly completely ruptured, for rupture of the musculotendinous complex from its origin or insertion, and for repair of avulsions with more than 2 to 3 cm displacement of the bone fragment. Fibrosis and retraction of the muscle may cause an inferior functional result, even after only a short delay.121 Because weakness from muscle strains can devastate an athlete—s performance or cause disability in workers, and because these injuries may be recurrent, precise definition of the injured muscles is important for optimal management.117 Regardless of which of the various classification schemes may be used, it is most important for the radiologist to localize the lesion, estimate the volume and severity of muscle involvement, and determine the presence or absence of clinically important associated abnormalities.
Muscle Contusions
Muscle contusions are differentiated from strain-related damage by the mechanism of injury.129,132,133 Contusions are caused by compressive or concussive direct trauma to the tissue, typically with a blunt object,132 although hematoma from lacerations in penetrating injuries may also occur. Muscle contusions often occur in athletes who engage in contact sports in which a body part or object strikes the muscle, causing the injury.132 Clinically there are fluid collections, swelling and weakness, and bruising of the superficial tissue. When associated with metabolic disorders, muscle contracture and rhabdomyolysis may also be part of the clinical presentation. Muscle edema, atrophy, and fatty infiltration suggest a myopathic or neurogenic association. The proposed criteria for diagnosis


of muscle contusion include superficial capillary rupture, interstitial hemorrhage, edema, and an inflammatory reaction.132,134

Jackson and Feagin133 suggested the following grading system for the severity of contusions based on the relative restriction of the range of motion of the adjacent joint. In addition, they correlated prognosis with the grade of injury:
  • Mild contusion: Active or passive range of motion is limited by less than one third of normal. Patients have an average of 6 days of disability.
  • Moderate contusion: Active motion is limited to one third to two thirds of the normal range of motion, usually due to the presence of muscle spasms. Patients have an average of 56 days of disability.
  • Severe contusion: Active motion is limited by greater than two thirds of the normal range of motion. Patients have longer than 60 days of disability.
Although the MR imaging appearance of muscle contusion is a direct reflection of the combination of factors just described,132,134 it is highly variable and often cannot be distinguished from a grade 1 or grade 2 muscle strain. Muscle strains, however, typically involve superficial muscle layers, whereas muscle contusions frequently involve deep muscle belly fibers. In football players the vastus intermedius (Fig. 3.114) and vastus lateralis (Fig. 3.115) are commonly affected. Diffuse feathery muscle edema and intramuscular hematoma contribute to increased muscle girth without architectural disruption of muscle fibers. Significant trauma results in proliferative repair of muscle tissue with the activation of perimysial tissue inducible osteoprogenitor cells. The process of repair starts peripherally and proceeds in a centripetal direction. On histologic evaluation a zone of osteoblasts and immature osteoid can be seen surrounding a central core of necrosis and hemorrhage. Mature bone may be present as a peripheral shell.
FIGURE 3.114 ● (A) In comparison to the rectus femoris, the vastus muscles do not cross the hip joint. Note the potential exposure of the vastus lateralis and intermedius to muscle contusion with trauma. Anterior view color illustration of the thigh with resected rectus femoris. Axial PD FSE (B) and FS PD FSE (C) images showing a muscle contusion in a football player involving the vastus intermedius.
A known complication of muscle contusion is the development of myositis ossificans (Fig. 3.116),132,134 which is the localized formation of nonneoplastic heterotopic bone and cartilage in soft tissues.132,135 MR imaging may be used to characterize myositis ossificans, which is associated with myonecrosis and hematoma, and surrounding osteoid. There is an inhomogeneous mass with a hyperintense center on FS PD FSE images. MR imaging, however, may be nonspecific prior to the development of peripheral calcification. Peripheral hyperintensity of edema may be identified, which is distinct from peripheral calcification. Gradient echo imaging can be used to emphasize the magnetic susceptibility of calcification. Changes caused by a biopsy from the central zones of immature osteoid and necrosis may be mistaken for a sarcomatous process, including osteosarcoma. Posttraumatic myositis ossificans with heterotopic nonneoplastic bone formation may affect the iliopsoas muscle. Chronic groin pain in soccer players and ballet dancers


has been associated with myositis ossificans. Post-contrast-enhanced images define the central core and demonstrate the development of a zonal phenomenon. Adjacent muscle edema is often associated with myositis ossificans on FS PD FSE or STIR images and is a normal finding. The final zonal pattern demonstrates peripheral bone signal without surrounding edema. Rim enhancement alone can be seen in liposarcomas, and thus the zonal pattern or susceptibility of peripheral calcifications can be used to increase the specificity of diagnosis.

FIGURE 3.115 ● (A) The vastus lateralis muscle forms the lateral patellar retinaculum contribution and lateral aspect of the quadriceps tendon. A blow to the thigh, as may occur in football players, results in direct compression of the vastus intermedius or vastus lateralis muscle groups against the femur. Coronal PD FSE (B) and FS PD FSE (C) images depicting vastus lateralis contusion with intramuscular hematoma.
Interstitial Hemorrhage and Hematoma
Both interstitial hemorrhage and hematoma are commonly found in association with muscle injuries.126,130,132,134 Interstitial hemorrhage is bleeding that occurs between the damaged connective tissues, whereas a hematoma is a discrete collection of blood confined to a restricted location.130,132,134 An increase in the size of the affected muscle may be seen in both of these entities.130,132
The MR appearance varies depending on the static magnetic field strength of the MR system, the “timing” of the evaluation of the blood-containing tissue, and the relative degree of edema at the injury site.129,132 If MR imaging is conducted within 48 hours of injury, interstitial hemorrhage and hematoma have a signal intensity similar to muscle on T1-weighted pulse sequences and hyperintense on STIR pulse sequences.129,132 During the subacute or chronic stage (i.e., 7 to 300 days after injury), the water content decreases and the protein content increases, and the hematoma has moderately decreased T1 and T2 relaxation times. This produces a signal intensity similar to that of fat on a T1-weighted pulse sequence.


In addition, the tissues are affected by the presence of oxyhemoglobin, deoxyhemoglobin, and red blood cells.129,132,136 This results in T1 shortening due to oxidative denaturation of hemoglobin and the production of methemoglobin. The concentration of methemoglobin increases over an 80- to 90-hour period following the injury, and the shortening of the T1 relaxation time of the blood-containing tissue follows the time course of methemoglobin production.129,132,136

FIGURE 3.116 ● (A) Axial FS PD FSE image depicting myositis ossificans as a complication of a vastus intermedius muscle injury. Note the characteristic hypointense focus surrounded by hyperintense edema. The hypointense region corresponds to the peripheral rim of calcification seen on CT. (BD) Myositis ossificans of the iliopsoas muscle demonstrating signal void in areas of more mature osteoid and peripheral calcification and a rim enhancement pattern with contrast. (B) Coronal FS PD FSE image. (C) Axial FS PD FSE image. (D) Axial FS T1-weighted contrast-enhanced image.
In hematoma (Fig. 3.117), the overall effect on T1-weighted images is a pattern of heterogeneous signal intensity during the subacute stages. With T2-weighted pulse sequences acquired on an MR system with a high static magnetic field strength, there is a focal area of low signal intensity, corresponding to the preferential T2 shortening secondary to deoxyhemoglobin within intact red cells.129,132,136 In longstanding hematoma, T1-weighted images demonstrate low signal intensity.
In comparison, the signal characteristics of interstitial hemorrhage (i.e., low signal intensity on T1-weighted images and high signal intensity on T2-weighted images during the acute stage120,132,136) may be due primarily to the concomitant presence of edema, but this is poorly documented.


Morel-Lavallée Lesion
FIGURE 3.117 ● Focal hemorrhage between the adductor brevis and adductor magnus muscle groups. (A) Coronal PD-weighted image. (B) Axial FS PD FSE image.
Morel-Lavallée lesions 137 are posttraumatic fluid collections that dissect deep to and along subcutaneous fatty tissue planes (the perifascial planes adjacent to the fascia lata and the iliotibial band) in the area of the trochanteric region and proximal thigh (Fig. 3.118). Morel-Lavallée effusions are usually associated with tangential trauma, as seen in high-speed motor vehicle accidents. Hemorrhage that dissects the superficial and deep fascia is also referred to as a degloving lesion. In the thigh the superficial fascia is also the deepest portion of the subcutaneous tissue, and the fascia lata, or deep fascia, covers the outer surface of the thigh muscles. Distally the fascia lata is reinforced as the iliotibial band. The frequency of Morel-Lavallée lesions in the trochanteric area and proximal thigh may be related to the firm attachment of the anterolateral fascia lata and iliotibial band and the secondary mobility and thus susceptibility of the regional skin and dermis, including the perforating vessels of the deep fascia.
Morel-Lavallée lesions have been grouped into types:
  • Type I: a fluid-like serohematic effusion (homogeneous and hyperintense on FS PD FSE images)
  • Type II: a subacute hematoma (a thick hypointense capsule with internal hyperintensity. Inhomogeneity of signal is associated with entrapped fatty globules, fluid-fluid levels, and internal septations)
  • Type III: a chronic, organizing hematoma (heterogeneity on FS PD FSE images with hemosiderin, granulation tissue, and necrotic debris)
  • Type IV: perifascial dissection and a closed fatty tissue laceration (hypointense on T1-weighted images and hyperintense on FS PD FSE images)
  • Type V: a perifascial pseudonodular lesion (variable signal intensity with or without peripheral enhancement)
  • Type VI: infection with or without thick capsular septations and a sinus tract (a thick capsule with contrast enhancement and adjacent hyperintense edema on FS PD FSE images)
Delayed-Onset Muscle Soreness
Muscle pain that occurs several hours to days after the precipitating activity is referred to as delayed onset muscle soreness. This is a nonacute injury and differs from muscle strain, in which pain usually occurs during or immediately following a muscle contraction.138,139,140 The associated painful symptoms typically increase in intensity during the first 24 hours after exertion, peak from 24 to 72 hours after the activity, and then subside. The degree of soreness is related to both the intensity of



the muscular contraction and the duration of exercise, with intensity appearing to be the more important factor.139,140,141,142,143

FIGURE 3.118 ● Type II Morel-Lavallée lesion with subacute hematoma dissecting into the plane between the fascia lata and the subcutaneous fat lateral to the greater trochanter. The lesion is superficial to the iliotibial band. In a type III lesion there is progression to a chronic organizing hematoma. (A) Color axial section illustrating the hemorrhage between subcutaneous tissue and the tensor fasciae latae. (B) Coronal FS PD FSE image. (C) Axial PD FSE image. (D) Axial FS PD FSE image.
Diagnosis, Etiology, and Clinical Features
A number of clinical and pathologic correlates are associated with delayed-onset muscle soreness, including increases in intramuscular fluid pressure, elevations in plasma enzymes, myoglobinemia, and abnormal muscle histology and ultrastructure.141,142,143,144 Muscle involvement may be diffuse, demonstrating hyperintense signal on STIR or FS PD FSE images (see discussion on MR Appearance below), and interstitial hemorrhage and hematoma may be present, as well as muscle hypertrophy. Biopsy of involved muscles may reveal free erythrocytes and mitochondria in the extracellular spaces, myofibrillar disorganization, and Z-band alterations, including misregistrations, bisections, and extensions.141,142,143 Disruption of sarcomeres may be seen at 24 to 48 hours, with regeneration beginning within 3 days after exertion.141,142,143 Exercise-induced muscle pain associated with delayed-onset muscle soreness may be related to disruption of the connective tissue elements in the muscles or their attachments and to the increase in intramuscular fluid pressure.138,139,140,141,142,143,144 Exertional rhabdomyolysis appears to be an extreme form of delayed-onset muscle soreness.134,145
MR Appearance
As with muscle strains, one of the major difficulties in the investigation of delayed-onset muscle soreness is the inability to localize precisely the involved muscle and to characterize the extent of injury. With MR imaging studies, however, it is possible to obtain information to better characterize the muscle abnormalities associated with delayed-onset muscle soreness.
In delayed-onset muscle soreness, as in muscle strains, muscle T1 and T2 proton relaxation times increase, consistent with the presence of edema.130,134,145,146 The overall MR imaging appearance is quite similar to that of muscle strains. In both conditions, perifascial fluid-like collections are sometimes seen in the early phase of injury.145,146 These recede concurrent with resolution of symptoms and normalization of creatine kinase and other enzyme levels.145,146 Unfortunately, the similarity in MR imaging appearances of strains and delayed-onset muscle soreness makes it difficult to distinguish between the two clinical syndromes on the basis of MR imaging changes alone.
Although the pathophysiology of delayed-onset muscle soreness is incompletely understood, all physical activity involves some combination of concentric (shortening), isometric (no change in length), and eccentric (lengthening) muscle actions (Fig. 3.119).138,139,144 Eccentric muscle action plays an important role in the development of delayed-onset muscle soreness, as well as the ability of MR imaging to confirm this impression and to study the natural history of this condition (Figs. 3.120 and 3.121). In studies on MR imaging of muscle injuries related to delayed-onset muscle soreness, eccentric actions were typically used to induce the damage.120,139,141,142,143,144 For muscles injured performing eccentric actions, there is a correlation between peak T2 increases and the decrease in muscle function. There is also a direct relationship between the volume of muscle damaged and the decrease in muscle strength.134,147 MR imaging signs of muscle injury persist for a prolonged time, despite a resolution of symptoms and return of muscle function to baseline values within a period of 10 to 12 days.147
Alterations in a cross-sectional muscle area have been shown to correspond with the accumulation of edema, which is known to occur as a result of performing eccentric actions.148 The accumulation of interstitial fluid seen with delayed-onset muscle soreness is probably a response to the myofibrillar disintegration that follows eccentric actions, which require extreme tension.148 On T2-weighted images, signal intensity gradually increases for a few days after the initial exercise, peaks after several days, and slowly decreases toward normal over a period as long as 80 days.148
Interestingly, studies show that there is a delay between the onset of severe symptoms in delayed-onset muscle soreness and the peak signal abnormalities seen on MR imaging. Clinical symptoms are not, therefore, a reliable means of assessing the severity or extent of muscle injury associated with delayed-onset muscle soreness.146,149 MR imaging may be used to detect subclinical muscle injuries and to monitor the course of delayed-onset muscle soreness, as well as other mechanisms of muscle damage.134,145,146,148
Different patterns of affected muscles, demonstrated by increased signal intensity, have been described in delayed-onset muscles soreness (Fig. 3.122).126,148 These different patterns may be related to the specific muscle group involved, the type of fiber composition of the muscles, the level of training of the individual, the type of activity that caused the soreness, and various biomechanical factors. There may also be collections or “streaks” of increased signal intensity seen in subcutaneous sites distal to the affected muscle.126 These have been ascribed to myoglobin.
Nurenberg et al.146 conducted a study to determine if there was a correlation between the degree of the delayed increase


in MR signal intensity of muscle after exertional injury and the amount of ultrastructural damage present. The highest correlations were found when T1-weighted and PD pulse sequences were used to evaluate signal intensity. These results differ from those of previous studies, which indicated that more prominent delayed signal intensity increases were found on T2-weighted images. The discrepancy in these findings can be explained by differences in the level of exertion, the severity of pain, and the extent of muscle involvement. More sustained exercise causes more severe muscle damage and edema (free water), resulting in greater increased signal intensity on T2-weighted images.146 Correlation between the graded amount of delayed-onset muscle soreness and the degree of ultrastructural injury is poor.146 However, there is good correlation between signal intensity changes and the degree of ultrastructural injury, suggesting that assessment of signal intensity associated with muscle injury may be used to determine the severity of damage.146

FIGURE 3.119 ● The two types of muscle action, concentric and eccentric. There is concentric action (shortening) in the right extremity as the weight is raised during performance of a biceps curl. There is eccentric action (lengthening) in the left extremity as the weight is lowered during the biceps curl. Eccentric actions are typically involved in the development of delayed-onset muscle soreness.
FIGURE 3.120 ● T2-weighted axial images obtained from the middle upper arm of the subject before (day 0) and serially after performance of eccentric muscle actions. The slight peripheral shading of the image obtained on day 0 was caused by contact of the subject—s arm with the bore of the magnet during imaging. Anatomy is best depicted on the day 1 image, which shows a subtle increase in signal intensity in the biceps and brachialis muscles. The day 3 image shows a more diffuse pattern and a greater increase in signal intensity in the brachialis and almost the entire biceps muscle. The lateral aspect of the biceps, however, appears to have been unaffected throughout the time of the MR evaluation. The peak increased signal intensity is seen on day 5, along with the greatest distortion in the anatomy of the affected muscles. On days 10 and 25, the increased signal intensity is diminished compared with day 5, and it is further reduced on days 40, 50, and 60. Note also the marked increase in the circumference of the affected muscles, which is most apparent on images obtained on days 3, 5, 10, and 25. The image obtained on day 80 shows a return to baseline with regard to signal intensity as well as the size of the affected muscles. This subject had severe symptoms of pain, soreness, and joint stiffness associated with eccentric muscular actions. (TR/TE, 2000/80 msec)
FIGURE 3.121 ● A graph of the muscle T2 relaxation times before (day 0) and after (days 1, 3, 5, 10, 25, 40, 50, 60, and 80) exercise involving eccentric actions. There was a statistically significant (P < 0.05) increase in T2 relaxation times for each subsequent postexercise imaging interval compared with T2 relaxation times before exercise (day 0). Values are given as means plus or minus the standard deviation. The “T” lines at the top of each bar represent the plus range of the standard deviation.
Muscle Contracture and Rhabdomyolysis
Muscle contracture refers to muscle shortening that occurs without repetitive action potentials. Indeed, this electrical difference


between cramp, with its high-frequency action potentials, and contracture is basic (Fig. 3.123).134,145 Muscle contracture occurs most often in metabolic disorders such as inherited defects of glycolytic enzymes (e.g., myophosphorylase deficiency or McArdle—s disease).134,145,150 After the contracture, patients typically develop elevated serum creatine kinase levels and, when severe, pigmenturia and acute renal failure. During the contracture, there typically is intense pain. In some diseases, such as phosphofructokinase deficiency, patients may have few or no symptoms and yet have marked rhabdomyolysis. In these patients, MR imaging may show extensive zones of myonecrosis and fatty infiltration.134,145,150 Although not specific, the coexistence of muscle edema, atrophy, and fatty infiltration is a significant finding and strongly suggestive of a myopathic or neurogenic disorder.134,145

FIGURE 3.122 ● Delayed-onset muscle soreness. T2-weighted axial images obtained from the middle upper arms of five different subjects on day 5 after performing biceps curl exercises involving eccentric actions. Note the variability in the pattern of increased signal intensity affecting the biceps and brachialis muscles. (TR/TE, 2000/80 msec)
FIGURE 3.123 ● Thigh muscle contracture in McArdle—s disease (A, B) Spin-echo images of the thighs show questionably increased signal intensity in the right adductor longus (arrows) (A: TR/TE, 1500/30 msec: B: TR/TE 1500/60 msec). (C) The abnormality was unequivocal using the STIR sequence (arrow). (D) STIR image 3 months later documents complete healing, without sequelae.
Rhabdomyolysis may occur in patients who do not have any metabolic disorder. Indeed, there are myriad predisposing causes for the development of rhabdomyolysis.134,151 However, the MR imaging appearance is typical and not different from the pattern of muscle edema seen in most other muscle injuries, including metabolic myopathies.134,145,151 Rhabdomyolysis has been associated to varying degrees with the use of lipid-lowering statin drugs. Disorders range from asymptomatic creatine kinase elevation to full-blown rhabdomyolysis. Fibric acid derivatives (fibrates) are also associated with primary muscle injury, especially when used in conjunction with statin drugs.
Sequelae of Muscle Injuries
One of the sequelae of muscle injury is further injury. For example, an incomplete muscle rupture may predispose to a complete rupture.152 In this context, it is interesting to note that MR alterations seen in both strains and delayed-onset muscle soreness persist for much longer than any other clinical evidence of injury.126,148 Clinical and scientific implications of this fact are being investigated. Obviously, it would be of great importance to known whether a persisting abnormality within the previously strained muscle of an athlete predicts that the strain will recur with resumption of intense exercise. Although the significance of the marked prolongation of MR abnormalities in muscle injuries is unclear, it remains a new opportunity for the noninvasive study of muscle healing.
One practical implication of the delayed disappearance of edema from muscle after excessive exercise is the MR detection of evidence of previous muscle injury beyond the patient—s memory of such an event. This implies a potential source of serendipitously observed MR abnormalities. On the other hand, this finding may be the only clue to the true origin of the patient—s musculoskeletal complaints.


Other sequelae of muscle injuries (including fibrosis, fatty replacement, and muscle ossification), although infrequent, are also detectable and differentiable using MR imaging. Fibrosis contributes to difficulties during surgery when treatment is delayed.121 As discussed earlier, fatty replacement of traumatized muscle is rare but occurs with regularity in patients with specific myopathies (Fig. 3.124).150 Ossification of muscle is not uncommon in muscle contusion and can be detected by MR imaging. This presents an exciting prospect for future investigations, because MR imaging also detects adjacent muscle edema that is undetectable by other means. Thus, the potential exists for detecting myositis before ossification occurs. In this way, it is hoped, an intervention might be optimally applied to the precise muscle at risk, so that ossification can be prevented.
Another complication of muscle injuries detectable by MR imaging is compartment syndrome.152 In this condition, edema or hemorrhage occurs within intact fascial boundaries, creating a closed compartment in which increases in muscle pressure impair blood and oxygen delivery. This may be an indication for immediate surgical decompression. Because lower extremity deep venous thrombosis and compartment syndrome may both present with painful swollen legs, the correct diagnosis is occasionally unclear. In this situation MR imaging simultaneously evaluates the status of vessels, subcutaneous tissues, and bone marrow in addition to the muscles. MR monitoring of exertion-induced changes in muscle relaxation times has been used to improve assessment of chronic compartment syndrome, the diagnostic criterion for which is said to be abnormal, progressive elevation of the muscle proton T1 relaxation time during recovery after exercise.152
Rectus Femoris Muscle Strain
The rectus femoris is most the frequently injured quadriceps muscle. Rectus femoris muscle strains are stretch injuries that occur during violent eccentric muscle contraction,153 and they are often associated with overuse, repetitive overload, and inadequate stretching and warm-up exercises. They are frequently seen in young athletes who participate in sprinting or kicking sports such as track and field, football, the martial arts, and soccer. Soccer, which requires sudden acceleration and bursts of speed, is most often associated with deep intramuscular tendon injuries of the indirect head.
Diagnosis, Etiology, and Clinical Features
Several anatomic features are relevant to proximal musculotendinous junction injuries. The quadriceps muscles, which have a majority of type II fibers (for rapid forceful activity), converge through a conjoined tendon to insert on the superior aspect of the patella. The origin of the rectus femoris crosses the hip joint in knee extension and in hip flexion. Distal musculotendinous junction injuries are more likely to occur at the knee level, whereas proximal rectus femoris strains occur at the deep musculotendinous junction in the thigh.
Pathologic findings in the musculotendinous junction include an intrasubstance tear at the muscle-tendon junction involving the indirect head leading to fibrosis and pseudocyst formation, a hemorrhagic response, changes consistent with muscle fiber necrosis, edema and macrophages, and inflammatory cells and fibroblastic activity.
Hasselman et al.154,155 have described three chronic strain injuries involving the mid-muscle belly of the rectus femoris. The most common rectus femoris injury involves minimally disruptive trauma with pain at the site of injury. Partial or complete disruption of the MTU is frequently associated with rupture of distal muscle fibers from the posterior tendon insertion, with associated proximal muscle retraction (Fig. 3.125).154,155 Another type of acute strain occurs in the mid-muscle belly with disruption of the muscle-tendon junction of the deep intramuscular tendon of the indirect head, with distal retraction of muscle fibers. This injury is associated with local hemorrhage and edema. A chronic pseudocyst within the deep intramuscular tendon of the indirect head of the rectus may develop as the hematoma organizes.
Clinical presentation usually includes:
  • Groin or anterior thigh pain, tender to palpation
  • Localized swelling
  • Loss of knee extension
  • An anterior thigh soft tissue mass (in midsubstance strains)
  • Intramuscular fibrosis and recurrent hemorrhage (in chronic midsubstance strains)
  • Thigh asymmetry (in partial or complete tears)
  • Palpable defect with a retracted mass (in complete rupture)
Rectus femoris injuries have been classified according to the severity and degree of muscle damage:
  • Grade 1: Grade 1 or first-degree strains are characterized by a small area of muscle involvement without loss of function (Figs. 3.126 and 3.127). There may be interstitial edema and hemorrhage at the musculotendinous junction with disruption of the endomysium (the connective tissue surrounding individual muscle fibers) and the perimysium (the connective tissue enveloping bundles of muscle fibers).
  • Grade 2: In grade 2 or second-degree strains there is a partial tear of the MTU, and a mass, hematoma, or intramuscular fluid (Fig. 3.128) may be found. There is no retraction. The presence of extramuscular fluid is





    associated with tear of the epimysium (the connective tissue sheath surrounding the muscle).

  • Grade 3: In grade 3 or third-degree injuries there is a complete tear at the MTU, with or without a mass or palpable defect. There may or may not be retraction of the mass or detached muscle segment (Fig. 3.129).
FIGURE 3.124 ● Fatty infiltration and atrophy as sequelae of exertional muscle injury. A 48-year-old man with phosphofructokinase deficiency (an inherited defect in glycogenolysis) and recurrent subclinical rhabdomyolysis had MR imaging of the thighs performed as a screening test for muscle abnormalities. A T1-weighted spin-echo image demonstrates fatty deposition and focal diminution of the adductor magnus (AM) bilaterally. The case suggests that severe muscle necrosis may lead to atrophy and fatty replacement. (TR/TE, 500/30 msec) (Reprinted with permission from

Fleckenstein JL. Magnetic resonance imaging of muscle injury and atrophy in glycolytic myopathies. Muscle Nerve 1989;12: 849.


FIGURE 3.125 ● (A) Proximal mid- and distal muscle cross-sections of the thigh. Distal rectus femoris injuries involve the distal musculotendinous junction and are associated with retraction of the rectus contribution to the quadriceps tendon.(B) Sagittal FS PD FSE image showing a distal musculotendinous grade 3 rupture of the rectus femoris proximal to the knee joint. (C) Axial FS PD FSE image depicting both the indirect head, within the muscle belly of the distal rectus, and more posteriorly the thickened/retracted rectus contribution to the quadriceps tendon. Although this is a distal injury, there is still muscle edema surrounding the indirect head.
FIGURE 3.126 ● Coronal (A) and axial (B) FS PD FSE images depicting an acute grade 1 strain of the deep proximal indirect head of the rectus femoris in a football player. There is a mild fluid collection adjacent to the deep musculotendinous junction. The direct head remains anterior as it courses distally in the thigh. (C) The proximal-to-distal course of the rectus femoris indirect head as it rotates from a horizontal to a relatively vertical orientation deep within the muscle belly. The direct head courses in an anterior location and merges with the anterior fascia of the mid-thigh.
MR Appearance
Fibrous encasement of the deep tendon (Fig. 3.130), with scar tissue formation, is hypointense on T2-weighted images and may be mistaken for a soft tissue neoplasm. A small low-signal-intensity lesion with a surrounding hyperemic rim deep within the mid-muscle belly may also be seen. A tumor, however, would not present with the typical cylindrical shape corresponding to the tendon of the indirect head of the rectus femoris. Gradient-echo images may demonstrate susceptibility artifact in the area of hemorrhage. If the differential diagnosis includes a neoplastic process, such as a malignant fibrous histiocytoma or a synovial sarcoma, intravenous gadolinium should be administered. A distinct hyperintense (on FS PD FSE) pseudocyst (Fig. 3.131) may form at the site of chronic fibrous encasement. The pseudocyst is produced by serous fluid in the hematoma. Muscle atrophy and fatty replacement of change adjacent to the indirect head may coexist with the fibrous encasement of the deep tendon.
Additional changes seen on T1- or PD-weighted images include:
  • Low- to intermediate-signal-intensity hemorrhage (signal may be hyperintense in subacute hemorrhage)
  • Peripheral hypointense hemosiderin
  • Loss of normal muscle/fat striations
Features on FS T1-weighted contrast-enhanced images include:
  • Variable synovial and peripheral enhancement of a hemorrhagic focus or muscle disruption
  • A “bull—s-eye lesion” consisting of the peripherally enhancing muscular component of a midsubstance strain





On FS PD FSE images additional expected findings include:
  • Hyperintense edema in the affected muscle
  • A midsubstance mass of inhomogeneous signal intensity
  • A more organized central component of hematoma that demonstrates hypointense to intermediate signal
  • Hyperintense edema and atrophy in subacute injury
  • Adjacent hyperintense fluid signal
  • A cylindrical shape of the tendon of the indirect head
FIGURE 3.127 ● Subacute bilateral grade 1 strains of the deep musculotendinous junction of the rectus femoris are visualized as a hyperintense ring around the hypointense indirect head on coronal (A) and axial (B) FS PD FSE images.
FIGURE 3.128 ● (A) Coronal color illustration of a grade 2 rectus femoris strain. (B) Axial cross-section color illustration of an acute muscle strain involving the deep tendon of the indirect head. Coronal (C) and axial (D) FS PD FSE images of an acute grade 2 rectus femoris strain with hemorrhage and fluid around the deep musculotendinous junction of the indirect head. The rectus involvement is bilateral and the vastus lateralis is affected on the right.
FIGURE 3.129 ● Soccer-related disruption of the proximal rectus femoris involving both the direct and reflected heads.
FIGURE 3.130 ● Fibrous encasement of the deep indirect tendon head. (A) Coronal PD FSE image. (B) Axial FS PD FSE image. (C) Axial color cross-section illustration.
FIGURE 3.131 ● Pseudocyst formation adjacent to fibrous encasement of the deep indirect head of the rectus femoris. (A) Coronal FS PD FSE image. (B) Axial FS PD FSE image. Pseudocyst formation adjacent to fibrous encasement of the deep indirect head of the rectus femoris. (C) Axial PD DSE image.
In the majority of cases there is improvement with conservative treatment, but surgery is indicated for compartment syndrome (which may occur with severe strains and partial- or full-thickness tears), chronic strains, and complete tears. Full-thickness tendon ruptures are associated with renal failure, diabetes, and rheumatoid arthritis.
Conservative treatment consists of the RICE protocol (rest, ice, compression, elevation), physical therapy (stretching and strengthening exercises), nonsteroidal anti-inflammatory agents, and a gradual return to activity. Surgical decompression may be necessary for compartment syndrome. Other surgical interventions include hematoma evacuation, repair of a complete rupture, and resection of fibrosis in chronic injuries.
Hamstring Tendinosis and Muscle Injuries
Injuries to the hamstring muscles (the semimembranosus, semitendinosus, and biceps femoris) have a variable appearance over time that can be characterized using MR imaging.156 Distinctive findings are seen in acute, subacute, and chronic hamstring tendinosis and muscle injuries.157,158,159,160
Diagnosis, Etiology, and Clinical Features
The hamstring muscles and tendons can be injured during hip hyperflexion and knee extension. The mechanism of injury is often chronic repetitive microtrauma. The medial hamstrings are at risk during the swing segment of the recovery phase of running (i.e., follow-through, forward swing, and foot descent). The lateral hamstrings are at risk in the take-off segment of the support phase (i.e., foot strike, midsupport, and take-off). Additional factors are inadequate warm-up, inflexibility, fatigue, hamstring-to-hamstring and hamstring-to-quadriceps imbalances, and ballistic stretching. Hamstring injuries are frequently found in young athletes, especially those who participate in sports requiring bursts of speed and a repetitive hip stretching motion. Football, soccer, or basketball players and sprinters, rowers, and kick-boxers are all at risk. Injuries occur somewhat more frequently in males, probably as a result of selection of sports activity. Hamstring tendinosis may also occur with intrinsic tendon weakening from systemic conditions including gout, diabetes, hyperparathyroidism, and collagen vascular diseases.
Several anatomic features are important in the consideration of injury of the hamstrings. Except for the short head of the biceps femoris, all muscles of the hamstring group cross the hip and knee joints. The hamstrings originate at the ischial tuberosity and insert on the proximal tibia. The short head of the biceps femoris originates from the linea aspera and the posterior femur. The musculotendinous junction of the biceps femoris extends along the entire length of the muscle, causing overlap. The short head is innervated by the peroneal branch sciatic nerve; the tibial branch innervates the other muscles in the hamstring group.
Corresponding pathologic and histologic changes include partial disruption of the musculotendinous junction, partial or


complete tears, avulsion fractures, thickening of the proximal tendon and degenerative changes at the origin, collagenous degeneration, increased intratendon ground substance, and proliferation of fibroblasts and myofibroblasts. There is an absence of inflammatory signs.

Signs at clinical presentation include:
  • Gluteal pain and point tenderness
  • Pain and tightness with a forward kicking motion or dynamic hamstring stretch
  • Painful static stretch of the hamstring group
  • Feeling of an impending “pull” of the muscle
  • Ecchymosis or a palpable knot is uncommon in proximal tendinosis.
A three-stage grading system has been devised based on the severity of the injury:
  • Grade I: Small disruptions of the musculotendinous junction (Fig. 3.132)
  • Grade II: Partial tears (Fig. 3.133)
  • Grade IIIA: Complete rupture (Fig. 3.134)
  • Grade IIIB: An avulsion fracture at the origin or insertion of the tendon
FIGURE 3.132 ● (A) Superficial and deep muscle groups of the posterior thigh. Since the hamstring tendons overlap the muscle bellies, hamstring injuries can occur in any location. (B) Grade I biceps femoris muscle strain with subtle muscle hyperintensity. Coronal FS PD FSE image.
MR Appearance
In acute trauma, MR imaging depicts conjoined tendon injuries (Fig. 3.135) (the hamstring muscle originates in a conjoined tendon from the posterolateral aspect of the ischial tuberosity), with associated muscle edema, hemorrhage, and partial tearing of the musculotendinous junction. Asymmetric involvement of hamstring tendons is a common finding. Intratendinous signal heterogeneity and reactive edema of the ischial tuberosity can also be identified. Proximal injuries, the most frequent to affect the hamstring muscle group, demonstrate an abnormal increased signal intensity that is contained by muscle fascia. Increased signal intensity on T2-weighted images or STIR sequences is secondary to hemorrhage or edema. Musculotendinous junction injuries with


edema or hemorrhage may display a feather-like area of high signal intensity on T2, FS T2-weighted FSE, or STIR images. Subacute injuries may demonstrate increased signal intensity on T1-weighted images. Exertional muscle injuries show a more diffuse pattern of hyperintensity on T2 or STIR sequences. A subacute ischial avulsion may be mistaken for osteomyelitis or neoplasia with an aggressive pattern on corresponding radiographs. MR imaging may show associated edema on fat-suppressed or STIR images. Chronic injuries frequently demonstrate atrophy and fatty replacement of muscles.

FIGURE 3.133 ● Proximal biceps femoris and distal semimembranosus grade II strains. Multiple hamstring muscle strains are not infrequent. Dual involvement of the biceps femoris and semitendinosus is the most frequent combination. (A) Coronal FS PD FSE image. (B, C) Axial FS PD FSE images.
Specific findings on T1- or PD-weighted FSE images are:
  • Intermediate signal intensity in thickened hypointense tendon
  • Partial detachment of the hamstring tendon from the ischial tuberosity
  • Small osseous avulsion plus hypointense edema ischial tuberosity
  • Complete avulsion with distal retraction of the common hamstring tendon
On FS PD FSE images, characteristic findings include:
  • Intermediate to hyperintense signal within a thickened proximal hamstring tendon
  • Soft tissue hyperintensity parallel to the medial and lateral margins of the common hamstring tendon
  • Localized hyperintense fluid adjacent to tendon degeneration and in the area of a partial tear
  • Adjacent hyperintense subchondral edema of the ischial tuberosity
MR findings can be correlated to the different grades of hamstring injury:
  • Grade I: Feathery MR edema
  • Grade II: Partial tear, with hyperintense hematoma at the musculotendinous junction and intramuscular and extramuscular laminar fluid collections
  • Grade III: Hyperintense fluid gap in a torn and retracted MTU


After contrast administration there is synovial enhancement and partial enhancement of degenerative foci within the proximal hamstring tendons.
FIGURE 3.134 ● (A) The musculotendinous junctions of the biceps femoris muscle overlap and effectively extend over the entire longitudinal axis of the muscle as potential sites of injury. Unlike the rest of the hamstring group, including the biceps long head, the short head of the biceps does not cross the hip joint and receives its innervation from the peroneal branch of the sciatic nerve and not the tibial branch. (B) Grade III rupture of the hamstring tendons. Coronal FS PD FSE image.
Improvement usually occurs with conservative treatment, although the recovery process may be lengthy, lasting up to 6 months. Conservative treatment include the RICE protocol (rest, ice, compression, elevation), reduction of inflammation, and gradual, progressive muscle strengthening and stretching. The use of steroid injections is controversial and may result in tendon weakening and tearing. Untreated advanced tendinosis leads to tendon tears. Surgery has a limited role in tendinosis but may be used for débridement of involved tissue and to treat tendon tears and avulsion. It does not promote collagen synthesis.
Avulsion Fractures
FIGURE 3.135 ● (A) Color coronal illustration showing the conjoined biceps femoris semitendinosus tendon. This tendon is identified on coronal images through the posterior-most aspect of the ischial tuberosity. Directly anterior to the conjoined tendon is the origin of the semimembranosus tendon. Common hamstring tendon degeneration is illustrated. (B) Coronal FS PD FSE image of the common hamstring tendinosis with partial tearing of the origin of the semimembranosus tendon. (C) Coronal FS PD FSE image of the posterior and medial origins of the conjoined tendon of the biceps femoris and semitendinosus. Note tendinosis of the conjoined tendon. (D) Corresponding axial FS PD FSE image demonstrates preferential tearing of the semimembranosus origin.
Avulsion fractures, also known as tug injuries or tug lesions and pelvic avulsions, result from bony or cartilaginous failure resulting in a fracture.
Diagnosis, Etiology, and Clinical Features
Avulsion injuries, which are becoming more common, frequently occur in adolescents or young adults participating in athletics, perhaps associated with traction on the unfused apophysis. Fractures are most commonly secondary to forceful concentric or eccentric muscle contraction applied by a musculotendinous unit.161 Extreme passive stretch (as seen in dancers and gymnasts, for example) is another mechanism of injury, as is avulsion secondary to chronic repetitive microtrauma, although the latter is less common. Adductor and lesser trochanter insertion tears at the superior pubic ramus are also classified as avulsion injuries. Approximately 13% of pelvic fractures in children are avulsion fractures.
It is important to evaluate the contralateral side as well as the injured side in these cases, because they occur through secondary centers of ossification and because what appears to be a fracture may simply be an anatomic variant.
The structures in the hip region most prone to avulsion injury are:161
  • Iliac crest
  • Anterior superior iliac spine (ASIS)
  • Anterior inferior iliac spine (AIIS)
  • Lesser and greater trochanters
  • Ischial tuberosity
  • Acetabular rim
  • Adductor insertion at the symphysis pubis
It is also important to recognize origin and insertion relationships of the affected structures. The origin of the sartorius is the ASIS and the upper half of the iliac notch. It inserts on the medial surface of the proximal tibia. The origin of the rectus femoris is the straight head of the AIIS and the reflected head of the upper acetabular rim. The rectus femoris inserts on the superior patella and the patellar tendon inserts on the tibial tuberosity. The biceps femoris and the semitendinosus and semimembranosus attach to the ischial tuberosity, and the iliopsoas attaches to the lesser trochanter. The anterior iliac crest is the attachment site for the tensor fascia lata, the gluteus medius, the transverse abdominis, and the external oblique abdominis. The posterior iliac crest is the attachment site for the gluteus maximus and the latissimus dorsi.
Pathologic and histologic examination in avulsion fractures reveals displacement of the ASIS (limited by the fascia lata and the lateral inguinal ligament), displacement of AIIS (limited by the dual insertion of the straight and reflected heads of the rectus femoris), and displacement of the ischial apophysis (limited by sacrotuberous ligament). There may also be evidence of hematoma, revascularization and resorption of devascularized bone fragments, callus, and fibrous scar tissue.
Clinically the patient presents with local pain and weakness, especially when the involved muscle is placed under stress; swelling after activity; limitation of activity; point tenderness; discoloration (secondary to hematoma); and altered gait. If there is no history of trauma, it is important to exclude infection and tumor as causes of the clinical symptoms in the younger patient, and metastatic disease or metabolic bone disease as causes in the adult. Iliac crest avulsion, with or without right lower quadrant pain, may mimic appendicitis.
FIGURE 3.136 ● Avulsion of the iliac crest apophysis related to angulation of the hip in one direction combined with a sudden contraction of the muscles inserting at the iliac crest in the opposite direction. This fracture is at the attachment of the abdominal oblique muscles. Coronal FS PD FSE image.


Iliac Crest Avulsion Injuries
The iliac crest apophysis appears at approximately 12 to 15 years of age and the average age of closure is 18 to 21 years. Avulsion injuries of the iliac crest apophysis are rare162 and usually related to indirect trauma (Fig. 3.136). Activities that pull the oblique abdominis may cause anterior iliac apophysitis and fracture.
ASIS Avulsion
As mentioned, the ASIS is the attachment site for the sartorius (Fig. 3.137) and some fibers of the tensor fasciae latae. The ASIS apophysis appears at 13 to 15 years of age and fuses with the ilium between 21 and 25 years of age. The mechanism of injury involves forceful pull of the sartorius with the hip in extension and the knee in flexion. ASIS avulsions occur in sprinters, hurdlers, and other running athletes.
FIGURE 3.137 ● Sartorius avulsion. (A) Sartorius avulsion occurs with the hip in extension and the knee flexed, as occurs in sports involving kicking and running. Coronal (B) and axial (C) FS PD FSE images depicting avulsion fracture of the anterior superior iliac spine at the origin of the sartorius. These injuries occur with either a sudden violent muscular contraction or excessive muscle stretch across an open apophysis. Avulsion fractures are most common in adolescent athletes between 14 and 17 years of age.


AIIS Avulsion
The AIIS is the site of attachment of the direct or straight head of the rectus femoris (Fig. 3.138). The secondary ossification center appears at 13 to 14 years of age and typically fuses between 16 to 18 years of age. AIIS avulsion, the sprinter—s fracture, is less common than avulsion of the ASIS and occurs as a result of overpull of the straight head of the rectus femoris. AIIS avulsion is also associated with sports such as soccer and football that involve kicking when the hip is hyperextended and the knee flexed. The direct head is more likely to avulse than the indirect head. Both ASIS and AIIS avulsions are treated in the same manner. A few days of bed rest for pain relief, followed by protected weight-bearing until comfort is achieved, is usually adequate.163
FIGURE 3.138 ● (A) Coronal color illustration of avulsion of the direct and reflected head origins of the rectus femoris. Sagittal (B) and axial (C) images of complete avulsion of the rectus femoris attachment to both the anterior inferior iliac spine (AIIS) and superior acetabular ridge. Avulsion of the direct head is more common than avulsion of the indirect head because the direct head is taut in the beginning of hip flexion. In increased flexion the indirect head is taut and the direct head becomes lax.


Lesser Trochanter Avulsion
The iliopsoas muscle attaches to the lesser trochanter.164 The lesser trochanter apophysis appears at 8 to 12 years of age and fuses to the femoral diaphysis at 16 to 18 years of age. Avulsion occurances are not common and result from violent muscular contraction, as seen in sprinters, jumpers, or young athletes participating in kicking sports (Fig. 3.139).
Greater Trochanter Avulsion
The greater trochanteric apophysis is the attachment site for the gluteus medius, the gluteus minimus, the obturators, and the gemelli.
FIGURE 3.139 ● Iliopsoas tendon avulsion injury in a 14-year-old football player. Sudden traction of the iliopsoas muscle on its tendinous insertion occurs during forceful adduction and flexion of the hip against a fixed or extended thigh. Laxity of the iliopsoas tendon is seen medial to the lesser trochanter and hemorrhage dissects anterior to the iliopsoas, as demonstrated on sagittal images. (A) Coronal FS PD FSE image. (B) Coronal FS PD FSE image. (C) Sagittal FS PD FSE image.
The ossific nucleus of the greater trochanter appears at about 4 years of age and fuses at 16 to 18 years of age. Avulsion is relatively rare and occurs secondary to a forceful muscular contraction of the hip abductors, as occurs in cutting while running.
Ischial Tuberosity Avulsion
The ischial tuberosity is a common site for avulsion fracture in the young athlete (Fig. 3.140). The ischial apophysis appears at 14 to 16 years and usually fuses between 18 and 21 years. The hamstring muscles take origin from the ischial tuberosity. The mechanism


of injury involves a sudden, forceful eccentric contraction of the hamstring muscles with the knee in the position of extension and the hip in flexion. Overpull of the hamstrings in this position elicits pain on physical examination, as does a rectal examination. Athletes who run hurdles, long jumpers, gymnasts, cheerleaders who perform the splits, and martial arts participants are at risk. Milch also describes seeing this injury in a dancer doing splits.165 Older patients may also avulse the ischial tuberosity in association with degenerative tendon disease (Fig. 3.141). Treatment is a short period of bed rest followed by protected weight-bearing. Although the fracture invariably heals, exuberant callus formation can occur, causing chronic pain.166 This callus formation may be confused with malignancy, leading to biopsy. Excision may be required for pain relief.

FIGURE 3.140 ● (A) Posterior thigh musculature. The hamstring muscle group includes the semitendinosus, semimembranosus, and biceps femoris. The gluteus maximus and hamstring muscles represent the primary hip joint extensors. (B) Ischial apophysis avulsion in a 14-year-old. Coronal FS PD FSE image.
Acetabular Rim Avulsion
The origin of the reflected head is at the shallow concavity above the anterolateral rim of the acetabulum. Avulsion is rare (Fig. 3.142). Sprain or partial tear of the reflected head can occur in association with an intact direct head.
Adductor Avulsion at the Symphysis Pubis
The symphysis pubis and pubic ramus are the sites of origin of the adductor longus (Fig. 3.143), the adductor brevis (Fig. 3.144), and the gracilis. Adductor avulsions commonly occur in sprinters, typically young male athletes, or in gymnasts who may cause injury doing the splits. Osseous fragments may be subtle in these injuries (Fig. 3.145). Adductor magnus strains are more common than avulsions, which require violent or sudden trauma (see Fig. 3.145).
FIGURE 3.141 ● Ischial avulsion of the hamstring tendons in a 15-year-old. The proximal tendon of the semimembranosus is lateral and anterior to the conjoined tendon of the biceps femoris and semitendinosus. (A) Coronal PD FSE image. (B) Sagittal FS PD FSE image. (C) Coronal color illustration of avulsion injury sites with correlation of ischial tuberosity avulsion side.
FIGURE 3.142 ● Partial tear of the reflected head of the rectus femoris in association with a proximal MTU injury. (A) Axial FS PD FSE image. (B) Coronal FS PD FSE image. (C) Coronal FS PD FSE image.
FIGURE 3.143 ● Avulsed and retracted adductor longus tendon. (A) Coronal FS PD FSE image. (B) Axial FS PD FSE image.
FIGURE 3.144 ● (A) Adductor muscles. The obturator externus also contributes to adduction. (B) Avulsion of the adductor brevis in an 18-year-old. There is an associated MTU strain of the proximal adductor longus. Coronal FS PD image.
FIGURE 3.145 ● (A) The primary function of the ischiocondyle part of the adductor magnus is as a hip extensor, and it assists the gluteus maximus and hamstring muscles in hip extension. The anterior part of the adductor magnus functions as a hip adductor. (B) Coronal FS PD FSE image depicts avulsion of the adductor magnus origin at the inferior pubic ramus. The adductor magnus originates at the inferior pubic ramus, the ischial ramus, and the inferolateral ischial tuberosity. Note the associated sprain of the obturator externus. (C) Deep muscles of the posterior thigh. (D) Edema and hemorrhage in proximity to the sciatic nerve may be associated with transient sciatica in grade II to III hamstring or deep posterior thigh trauma. Coronal FS PD image.








MR Appearance
MR evaluation of avulsion fractures should follow an initial evaluation with conventional film radiography or bone scintigraphy. FS PD FSE, T2-weighted, or STIR images are usually necessary to identify areas of edema or hemorrhage associated with avulsion fractures. Avulsed cortical bone is hypointense and may be indistinguishable from adjacent tendons or ligaments. The contralateral side should be evaluated in these patients to distinguish an avulsed fragment from a normal, open apophysis. Features and findings in MR imaging are summarized below.
On T1-weighted or PD FSE images osseous avulsion may be difficult to visualize in a bed of soft tissue and hematoma. Characteristic findings include:
  • The involved tendon is often lax with redundant morphology.
  • In ASIS avulsion there is mild displacement with or without hypointense edema of adjacent marrow and fluid adjacent to sartorius origin.
  • In AIIS avulsion there is distal fragment displacement and laxity of the straight head of the rectus femoris.
  • In ischial apophysis avulsion there is a displaced fragment with hypointense edema at the donor site.
On FS PD FSE images there is:
  • Hyperintense marrow edema at the donor site
  • Hyperintense fluid, soft tissue edema, and hemorrhage at the site of avulsion
  • Hyperintense signal on FS PD FSE or STIR in associated muscle strain
  • Hyperintense edema of the iliopsoas adjacent to the lesser trochanter
Most avulsion injuries heal with conservative treatment, although recovery is slow (an average of 4 to 8 weeks up to 4 months). Conservative approaches include initial bed rest, non-weight-bearing, and use of crutches, ice, and anti-inflammatory agents. Physical therapy, with gradual strengthening and progressive weight-bearing, is important in a successful outcome. Surgical reattachment of a severely displaced avulsed fragment may be necessary. Poor healing may lead to chronic pain secondary to repetitive micromotion. In this event resection of a weak bony union and surgical reattachment may be helpful.
Hip Abductor (Gluteus Muscle) Injuries and Trochanteric Bursitis
Gluteus medius and gluteus minimus muscle strains, also referred to as a “charley horse” or the greater trochanter pain syndrome, represent an indirect injury secondary to overuse, repetitive microtrauma, excessive force, or muscle fiber stretch.167,168 The term “greater trochanteric pain syndrome” includes pathology of the gluteal abductors and of their related bursae.167
Diagnosis, Etiology, and Clinical Features
Iliotibial band tension leads to frictional trauma and tendon impingement. Occasionally these injuries are seen in athletes, usually football or hockey players, swimmers, runners, or individuals who do step aerobics. They are a subset of muscular and musculotendinous injuries, and MTU injuries are the most frequent sports-related condition of the hip and pelvis.
The abductor tendons and their relationship to the greater trochanter are analogous to the relationship between the rotator cuff tendons and the greater tuberosity in the shoulder. The term “rotator cuff tears of the hip” thus refers to abductor tendon pathology at the tendon insertion to the greater trochanter. Both the gluteus medius and minimus tendons attach to the greater trochanter,167 and an understanding of the facet anatomy of the greater trochanter (Fig. 3.146) is helpful in evaluation of these lesions. There are four facets on the surface of the greater trochanter. The oval anterior facet is located on the anterolateral aspect of the greater trochanter. The lateral facet (shaped like an inverted triangle) corresponds to the greater trochanter prominence on physical examination and lies between the anterior and posterior facets. The superoposterior facet represents an area that extends medially, adjacent to the posterosuperior aspect of the lateral facet, and is located at the most superior aspect of the greater trochanter. The posterior facet occupies the posterior aspect of the greater trochanter. The tendon attachments (insertions) to the facets of the greater trochanter thus extend from anterior to posterior. The gluteus muscle and tendon attachments to the various facets are as follows:
  • The anterior facet-gluteus minimus attachment (Fig. 3.147): the gluteus minimus is visualized anteriorly on sagittal images through the greater trochanter.
  • The lateral facet-gluteus medius muscle attachment (see Fig. 3.146)
  • The superoposterior facet-gluteus medius tendon attachment (Fig. 3.148): the gluteus medius tendon attachment is posterior to the minimus attachment anteriorly and the muscular fibers of the medius attachment as viewed on sagittal images through the greater trochanter.
  • The posterior facet has no tendon attachments and is covered by the trochanteric bursa (see below).
FIGURE 3.146 ● (A) Greater trochanter facet anatomy. AF, anterior facet; LF, lateral facet; SPF, superoposterior facet; PF, posterior facet. (B) Osseous attachment sites of the gluteus medius and gluteus minimus tendons to the greater trochanter facets. GMin, gluteus minimus tendon attachment to the anterior facet; GMed, gluteus medius lateral tendon attachment to the lateral facet and main tendon attachment to the superoposterior facet. (C) Sagittal T1-weighted image showing gluteus minimus and medius attachments to the greater trochanter. The minimus tendon attaches to the anterior facet and the medius tendon attaches to the superoposterior facet.
FIGURE 3.147 ● T1-weighted MR arthrograms showing the attachment of the gluteus minimus tendon to the anterior facet in the axial (A) and coronal (B) planes.




In addition, there are three bursae167 (Fig. 3.149) in proximity to the greater trochanter,165 which may become inflamed and cause hip pain:
  • The trochanteric bursa (Fig. 3.150) is also referred to as the subgluteus maximus bursa. The largest of the three bursal structures, it covers the posterior facet and partially covers the lateral facet. It is found deep to the gluteus maximus and iliotibial tract and can be visualized anterior to the gluteus maximus on sagittal or axial MR images. It parallels the linear contour (see Fig. 3.150) of the posterior facet. Sometimes two trochanteric bursae are present, a superficial bursa deep to the fascia lata and a deep bursa located medial to the superficial bursa.
  • The subgluteus medius bursa (Fig. 3.151) is located deep to the lateral aspect of the gluteus medius muscles and tendons. It covers the superior aspect of the lateral facet but is difficult to visualize unless distended with fluid. The superior border of this bursa is at the tip of the greater trochanter.
  • The subgluteus minimus bursa (Fig. 3.152) is deep to the gluteus minimus tendon and medial and superior to its insertion. It can be seen extending anterior and medial to the minimus tendon on sagittal images through the greater trochanter.
FIGURE 3.148 ● Coronal (A) and axial (B) T1-weighted images depicting the gluteus medius attachment to the superoposterior facet on posterior coronal and axial images. The medius and minimus attachments are shown on the axial image (B).
The iliopsoas bursa, which lies deep to the iliopsoas muscle, occasionally causes hip pain as well (see discussion on Iliopsoas Bursitis below).
Gluteus Muscle Injuries
Gluteus muscle injuries, which most frequently occur in elderly women, are also sometimes found in high-level athletes. They are characterized by pain (lateral hip pain that may radiate to the groin, pain at the greater trochanter, pain with resisted extension or external rotation, and tenderness to palpation), trochanteric bursitis (see below), altered gait, edema, swelling, and muscle enlargement. In complete tears there is a palpable mass with or without retraction.
Gluteus minimus and medius lesions can be classified as tendinosis (Figs. 3.153 and 3.154), partial tears (Fig. 3.155), or full-thickness tears (Fig. 3.156) with or without tendon retraction (Fig. 3.157). Avulsion tears may have a fleck of bone attached to the retracted tendon. Bursitis is found in 40% or more of patients with abductor tendon pathology (Fig. 3.158). Some abductor avulsions have occurred as complications of total hip arthroplasty. The abductor tendons may also be involved by hydroxyapatite deposition (Fig. 3.159), either within the gluteus tendons or in the periarticular soft tissues.
Trochanteric Bursitis
As mentioned, trochanteric bursitis is part of the greater trochanteric pain syndrome. It is most common in middle-aged women and is associated with gluteal tendon pathology at the insertion sites (Fig. 3.160). The trochanteric (subgluteus maximus) bursa becomes inflamed with repetitive irritation of the tensor fasciae latae sliding over the greater trochanter. Infection may incite a thickened and even nodular reaction within the bursa. The condition is also common in runners and those who play racquet sports, causing pain in the lateral aspect of the thigh. Inflammation of the deep gluteal bursa causes pain deep in the buttock and can be confused with referred pain







from the lower back. In both cases, it is important to differentiate between bursitis and lumbar disease. Rheumatoid arthritis is also associated with trochanteric bursitis. Treatment consists of activity modification, physical therapy, and nonsteroidal anti-inflammatory drugs. Occasionally, local steroid injection and, less commonly, surgical intervention play a role.

FIGURE 3.149 ● Location of the three greater trochanter bursae (the trochanteric or subgluteus maximus bursa, the subgluteus medius bursa, and the subgluteus minimus bursa). (A) 3D color illustration. (B) Coronal color section.
FIGURE 3.150 ● (A) Arthroscopic view of the trochanteric or subgluteus bursa. The trochanteric bursa has a contour parallel to the posterior facet. (B) Coronal FS PD FSE image showing the linear contour of greater trochanteric bursa in a patient with associated tendinosis of the gluteus minimus tendon.
FIGURE 3.151 ● Subgluteus medius bursa involvement in a patient with avulsion of the minimus and partial tear of the medius tendons. (A) Sagittal FS PD FSE image. (B) Coronal FS PD FSE image.
FIGURE 3.152 ● Subgluteus minimus bursal inflammation associated with tendinosis and partial tear of the gluteus minimus tendon. (A) Coronal FS PD FSE image. (B) Sagittal FS PD FSE image.
FIGURE 3.153 ● Gluteus medius tendinosis with intermediate-signal-intensity degeneration within the normally hypointense tendon. Sagittal PD-weighted image.
FIGURE 3.154 ● Tendinosis of gluteus minimus associated with subgluteus minimus bursitis. Coronal FS PD FSE image.
FIGURE 3.155 ● (A) Axial FS PD FSE image showing a partial tear of the posterior gluteus medius in comparison to a full-thickness fluid-filled tendinous defect in the anterior gluteus minimus. (B) Posterolateral coronal color illustration of a partial gluteus medius tendon tear.
FIGURE 3.156 ● Complete full-thickness tear of the gluteus minimus tendon. The gluteus medius is intact. (A) Coronal FS PD FSE image. (B) Sagittal FS PD FSE image. (C) Posterior coronal illustration.
FIGURE 3.157 ● Full-thickness tear with proximal retraction of the gluteus minimus. Coronal FS PD FSE image.
FIGURE 3.158 ● Prominent gluteus medius bursitis associated with partial tearing of the gluteus medius tendon and hyperintensity of the subgluteus bursa. Coronal FS PD FSE image.
MR Appearance
The MR appearance varies depending on the specific type of gluteus injury:
FIGURE 3.159 ● Hydroxyapatite deposition adjacent to the minimus tendon. Calcific tendinosis (tendinitis) may involve the gluteus maximus, minimus, or medius attachments. (A) Coronal FS PD FSE image. (B) Coronal T2* gradient echo image.
  • In gluteus minimus and medius tendinosis the tendons may appear either thickened or attenuated. There is increased signal on FS PD FSE images. Non-fat-suppressed T2-weighted images demonstrate intermediate-signal-intensity tendinosis and no tearing.
  • In partial tears there is hyperintensity with abnormal morphology of torn tendon fibers on both FS PD FSE and T2 FSE images. Interstitial tears (Fig. 3.161) show hyperintense signal without tendon contour abnormalities. Gluteal tendon injuries may be associated with grade 1 or 2 muscle strains (Fig. 3.162).
  • In full-thickness tears or with granulation tissue and synovitis, there is a fluid-filled gap with discontinuity




    of the retracted or torn tendon. Fatty atrophy (Fig. 3.163) can sometimes be appreciated on T1- or PD-weighted images and should be noted. Fatty atrophy is defined as a 25% or greater decrease in muscle volume compared to the contralateral side. Hyperintensity superior to the greater trochanter and gluteus medius tendon elongation (retraction of the musculotendinous junction) may also be associated with full-thickness tears.

FIGURE 3.160 ● (A) Greater trochanteric bursa superficial to the posterior facet of the greater trochanter. (B and C) Greater trochanteric bursitis associated with a tear of the gluteus minimus tendon. The greater trochanteric bursa is identified between the gluteus maximus muscle and the iliotibial tract. (B) Coronal FS PD FSE image. (C) Axial FS PD FSE image.
FIGURE 3.161 ● Intratendinous signal intensity in an interstitial tear of the gluteus minimus. Coronal FS PD FSE image.
FIGURE 3.162 ● Gluteus medius and maximus grade 2 muscle strains with intramuscular and extramuscular hemorrhagic fluid collections. Associated adductor muscle group strains are also present. (A) Coronal FS PD FSE image. (B) Sagittal FS PD FSE image.
FIGURE 3.163 ● Gluteus medius atrophy associated with chronic tear. Coronal T1-weighted image.
Most patients show improvement with conservative treatment including the RICE protocol (rest, ice, compression, elevation), physical therapy, and steroid injections. Surgery may be needed for hematoma evacuation, primary repair of a complete rupture, or reattachment of an avulsed tendon.
Piriformis Syndrome
The piriformis syndrome, also known as pseudosciatica, wallet sciatica, hip socket neuropathy, deep gluteal syndrome, or neuritis of the proximal sciatic nerve, is secondary to nerve irritation or compression by the piriformis muscle. It is seen in patients from 18 to 55 years of age (an age range that overlaps with that for low back pain), and has a female-to-male ratio of 6:1. Up to 6% of sciatica cases are caused by the piriformis syndrome.
Diagnosis, Etiology, and Clinical Features
Several anatomic features of the piriformis muscle (Fig. 3.164) are important in understanding and evaluating this syndrome.


The origin of the piriformis is anterior to the S2 to S4 vertebrae, the sacrotuberous ligament, and the upper margin of the greater sciatic foramen. It then passes through the greater sciatic notch to insert on the superior aspect of the greater trochanter. Its primary functions are external rotation with the hip in extension and abduction with the hip in flexion. It is innervated by the nerve roots of L5, S1, and S2. When assessing the piriformis it is necessary to remember that there are several developmental variations in the anatomic relationship between the sciatic nerve and piriformis.

FIGURE 3.164 ● Obturator internus and piriformis as viewed from the pelvis.
Trauma to the gluteal region is the most common cause of the piriformis syndrome (Fig. 3.165). Overuse, especially in high-performance athletes, may also be a factor. Additional conditions include compensatory contraction of hip external rotators in foot instability (secondary to Morton—s foot with a prominent second metatarsal head), spinal stenosis, anatomic variations (such as a division of the sciatic nerve splitting the piriformis and predisposing to nerve compression), and irritation of the piriformis by sacroiliitis. Some cases of bilateral piriformis syndrome are brought about by prolonged sitting.
FIGURE 3.165 ● (A) Entrapment of the sciatic nerve as it courses through the sciatic notch. Trauma to the posterior thigh may result in irritation, inflammation, spasm, adhesion, and hypertrophy of the piriformis muscle and secondary dysfunction of the sciatic nerve. (B) Enlargement of left sciatic nerve with inflammation. Axial FS PD FSE image.


Pathologic and histologic findings include:
  • Hypertrophy of the piriformis (Fig. 3.166), due to increased strain on the hip abductors, repetitive exercise-induced trauma, chronic low-energy trauma (e.g., sitting on a hard surface for prolonged periods), and bipartite and accessory muscle fibers
  • Sciatic nerve compression
  • Myositis ossificans
  • Associated mass lesion causing compression/entrapment (tumor, abscess, or hematoma) (Fig. 3.167)
  • Piriformis split by sciatic nerve
  • Inflammation
  • Interstitial myofibrositis, with extravasation of blood; release of serotonin, prostaglandin E, bradykinin, and histamine; neuritis; and fibrosis
Clinically, there is chronic gluteal pain that radiates into the lower extremity, similar to L5-S1 radiculopathy. The pain is triggered or exacerbated by hip adduction and internal rotation. The piriformis demonstrates tenderness on digital rectal examination and external palpation. Additional clues to the diagnosis include:
  • Pain elicited by passive hip flexion and internal rotation, known as Frielberg—s sign
  • Pain elicited by resisted abduction and external rotation, known as Pace—s sign
  • Lasègue sign (pain at the greater sciatic notch in knee extension and hip flexion)
  • Pain at the sacroiliac joint, gluteal muscle, or greater sciatic notch
  • Pain with the Valsalva maneuver
  • Dyspareunia or pain radiating to the genitals
  • Appearance of the piriformis as a sausage-shaped mass
  • Chronic gluteal atrophy
  • History of trauma
  • An increase in pain with lifting the extremity and a decrease in pain with traction
FIGURE 3.166 ● Piriformis syndrome with accessory fibers of a hypertrophied left piriformis muscle in a fighter pilot who carried his money in his left back pocket. Piriformis syndrome is also known as wallet sciatica. (A) Color illustration coronal section. (B) Coronal T1-weighted coronal oblique image.
MR Appearance
MR findings correspond to the pathologic and clinical features. T1-weighted and PD FSE images demonstrate piriformis


hypertrophy and effacement of fat in the greater sciatic foramen with muscle signal intensity. There is loss of muscle striations and a mass effect resulting in displacement of the muscle from anterior to posterior. Diffuse muscle edema is hyperintense on T2-weighted images. FS PD FSE images display edema associated with tumor, abscess, or hematoma. The gluteus minimus and medius and tensor fascia lata are normal, and there may or may not be signal changes within the gluteus maximus. On fat-suppressed or STIR images, gluteal atrophy may be visualized.

FIGURE 3.167 ● Lymphoma compressing the right piriformis muscle and displacing the sciatic nerve posteriorly. Axial FS PD FSE image.
Without treatment, progression is likely. However, most patients improve with conservative treatment, such as rest, physical therapy, and stretching exercises, and surgery is required only for refractory cases. Functional biomechanical deficits associated with the piriformis syndrome, such as a tight piriformis muscle, contraction and tightness of the external rotators and adductors, lumbosacral spine dysfunction, or sacroiliac joint hypomobility, may also need to be addressed.
FIGURE 3.168 ● Distention and communication of the iliopsoas bursa with the hip joint. (A) Transverse section color illustration. (B) Axial FS PD FSE image.
Iliopsoas Bursitis
Diagnosis, Etiology, and Clinical Features
The iliopsoas bursa is the largest bursa of the hip. It is bordered by the iliopsoas muscle and the AIIS. The iliopsoas tendon crosses the inferior aspect of the hip joint capsule. The psoas major (which originates on the T12 to L5 transverse processes and bodies) and the iliacus (which originates on the iliac wing) form the iliopsoas, which inserts on the lesser trochanter of the femur. In 15% of individuals with hip pathology, there is iliopsoas bursal communication with the hip.
Iliopsoas bursitis, which is common in young active adults and occurs slightly more often in females than in males, may be caused by overuse, such as occurs with repetitive strenuous hip flexion and extension, trauma, or degeneration with an inflammatory component. In addition to the snapping hip syndrome, it may also be associated with rheumatoid arthritis and synovial proliferation, tendonitis/tenosynovitis, or intra-articular


pathology such as AVN. In inflammatory and infectious disorders (Fig. 3.169), MR imaging demonstrates heterogeneity of the bursal fluid signal.

FIGURE 3.169 ● (A) Inflammation of the iliopsoas bursa anterior to the hip joint. Coronal color illustration, anterior view. (B) Infected iliopsoas bursa with irregular margins and hyperintense heterogeneity. Axial FS PD FSE image.
There is a discrete soft tissue cystic mass adjacent to femoral neurovascular bundle. Other pathologic and histologic evidence may include hemorrhage, communication with the hip joint, inflamed and hypertrophied synovial cells, fibrosis, and fibrin deposition.
Clinically the patient usually presents with a groin mass that is tender to palpation in the femoral triangle and may or may not be pulsatile secondary to adjacent femoral vessels. Occasionally the patient presents with a pelvic mass, resulting from cephalad extension and compression of intrapelvic contents (e.g., colon, bladder). The pain may radiate distally to the anterior thigh and knee and is exacerbated by flexion, abduction, and external rotation. Initially the pain may occur only with activity, but it usually progresses to pain at rest. Delays in diagnosis are not uncommon.
MR Appearance
Axial MR images with T2 weighting are useful in demonstrating iliopsoas bursal collections adjacent to the iliopsoas tendon in patients presenting with clicking of the hip during range-of-motion activities with internal and external rotation. Identification of bursal fluid correlates with snapping or clicking of the hip on clinical examination. The bursal fluid volume is greater than hip joint fluid and should not be mistaken for a malignant soft tissue neoplasm such as synovial sarcoma, which has similar imaging characteristics (i.e., low signal intensity on T1-weighted and bright signal on T2-weighted images). Specific findings on T1-weighted and PD FSE images include a hypointense to intermediate-signal-intensity mass and lateral displacement of the adjacent iliopsoas tendon. On FS PD FSE images, MR displays hyperintensity with bursal distention. The increased signal intensity is usually uniform, although hemorrhage or proteinaceous debris may produce a heterogeneous signal. Axial images are used to show direct communication with the hip through a tail-like extension that tapers medial to the iliopsoas tendon. The mass has well-marginated borders, and its long axis is oriented superior to inferior on coronal images. After contrast administration FS T1-weighted images show peripheral enhancement of the bursal lining. Fluid does not show enhancement unless complicated by synovial proliferation.
Treatment is initially conservative, and most patients improve with measures such as anti-inflammatory agents, hip abduction and external rotation stretching exercises, deep heat, ultrasound therapy, and steroid injections. If pain and snapping persist, the prominence on the iliopectineal eminence can be resected along with a partial release of the iliopsoas tendon. However, surgical intervention is rarely required.


Snapping Hip Syndrome
FIGURE 3.170 ● Snapping of the iliotibial band occurs as it displaces or subluxes posteriorly over the greater trochanter in internal rotation. (A) The iliotibial band in a neutral position. (B) Subluxation of the iliotibial band in internal rotation. (C) Axial FS PD FSE image showing edema and fluid deep to the iliotibial band at the level of the greater trochanter associated with a snapping tendon.
As the name indicates, the snapping hip syndrome, or coxa saltans, is characterized by a snapping or clicking sensation that occurs with movement of the hip. Three types or categories have been identified:170
  • External: External snapping hip (Fig. 3.170), the most common type, is related to friction from the posterior aspect of the iliotibial band as it slides over the greater trochanter as the hip extends from a flexed position. Friction from the anterior edge of the gluteus maximus may also contribute.
  • Internal: Internal snapping hip (Fig. 3.171) is caused by snapping of the iliopsoas tendon over the iliopectineal eminence, femoral head, or anterior capsule.
  • P.206


  • Intra-articular: Intra-articular snapping is caused by an abnormality in the joint itself, such as a labral tear or loose bodies (labral or chondral fragments) (see discussions below on Loose Bodies and Labral Tears).
FIGURE 3.171 ● Snapping of the iliopsoas tendon over the pectineal eminence occurs with hip extension. This anterior view color illustration shows the iliopsoas tendon in (A) hip flexion and (B) hip extension with iliopsoas contact over the pectineal eminence. (C) Coronal FS PD FSE image of snapping hip with edema of the iliopsoas MTU. (D) Proximity of the iliopectineal eminence to the iliopsoas bursa.
FIGURE 3.172 ● Snapping iliopsoas with eroded anterior medial capsule in the presence of a total hip prosthetic head.
Diagnosis, Etiology, and Clinical Features
The snapping hip syndrome occurs most commonly in young adults, 15 to 40 years of age. There is a slight predilection for females, depending in part on the kinds of activity they participate in. There is usually no history of trauma, but overuse may contribute, and in the external and internal types dancers and other athletes may be at risk. The snapping hip syndrome is frequently found in association with iliopsoas bursitis and has also been associated with the iliotibial band syndrome (external snapping hip syndrome) with irritation of the greater trochanteric bursa by the iliotibial band.171 Rare cases of snapping hip syndrome may be caused by snapping of the iliofemoral ligaments over the femoral head and the long head of the biceps femoris over the ischial tuberosity.
Pathologic findings vary, depending on the type and cause of the snapping. In external snapping hip there is a tight or thickened iliotibial band and bursitis or tendinitis, with the gluteus maximus as a causative structure. In internal causes of snapping hip the iliopsoas is tight or impinged (Fig. 3.172), with associated bursitis/tendinitis. In intra-articular snapping hip there may be loose bodies, labral tears, and chondral lesions.
Clinically, snapping hip syndrome is characterized by a palpable and sometimes audible snap during hip flexion and extension. In intra-articular snapping syndrome a click, not a snap, is more common. In external snapping hip, pressure applied to the greater trochanter will stop the snapping, since pressure reduces the iliotibial band posterior to the trochanter. In internal etiologies, pressure applied over the iliopsoas tendon at the level of the femoral head will eliminate the snapping. The hip may be painful, especially in intra-articular disease.
MR Appearance
MR features also vary depending on the type or cause of the snapping:
  • In external snapping syndrome FS PD FSE images show a hypointense to hyperintense iliotibial band and anterior border gluteus maximus and a hyperintense greater trochanteric bursa.
  • In internal snapping syndrome FS PD FSE images display hyperintense iliopsoas bursa fluid (Fig. 3.173).
  • Intra-articular snapping syndrome is characterized by hypointense to intermediate-signal-intensity loose bodies adjacent to hyperintense joint fluid. MR arthrography is used to identify labral tears and other intra-articular lesions.
Most patients are only mildly symptomatic and improve with conservative measures such as activity modification, anti-inflammatory medications, steroid injections, and physical therapy. Patients with intra-articular disorders may show continued progression of symptoms and pathology (e.g., chondral degeneration). Surgery, if needed, usually consists of partial tendon and bursa resection, tendon lengthening procedures, and arthroscopy for intra-articular lesions (e.g., loose body removal, débridement of chondral lesions).
Femoroacetabular Impingement
FIGURE 3.173 ● (A) Sagittal color illustration and (B) sagittal FS PD FSE image showing longitudinal extension of iliopsoas bursal fluid deep to the muscle and MTU as a cause of snapping hip syndrome. (C) Sagittal FS PD FSE image depicting dissection of the iliopsoas bursa and tendinosis of the iliopsoas tendon. (D) Coronal FS PD FSE image in a separate case of tendinosis in a runner. The distal iliopsoas tendon is associated with a distal lesser trochanteric bursa. This less commonly distended bursa should not be confused with the more proximal iliopsoas bursa.
Femoroacetabular impingement (FAI) is a relatively recently recognized and described disorder that causes a progressive degenerative process leading to early OA of the hip.172,173,174 FAI is a distinct pathologic entity that results from abnormal abutment between the proximal femur and acetabular rim and is associated with morphologic abnormalities that affect the proximal femur, the acetabulum, or both. Repetitive microtrauma from impingement of the femoral head against the acetabulum causes degeneration of the acetabular labrum and articular cartilage. This occurs most commonly during flexion and internal rotation, when the femoral head is in contact with the acetabular rim, which is then subject to abnormal stress. Degeneration and tearing of the labrum as well as progressive damage to the adjacent acetabular cartilage are precursors of OA (Fig. 3.174).172,173,175,176,177,178
FIGURE 3.174 ● Advanced changes of FAI resulting in osteoarthritis. (A) Coronal T1-weighted image. (B) Coronal FS PD FSE image. (C) Axial FS PD FSE image.
Patients with FAI are usually young and physically active and present with slow onset of hip or groin pain (often after minor trauma or without preceding trauma), restricted flexion and internal rotation, and a positive impingement test (pain with flexion and internal rotation). The pain gradually increases over time and is activity-dependent. Sports activities, such as soccer, kickboxing, tennis, baseball, football, or volleyball, that require hip flexion with variable torque or axial loading may aggravate symptoms and are often associated with FAI.172,179,180,181
Radiographs in patients with FAI often appear normal, and no treatment is initiated. On closer review, however, subtle abnormalities may be visible, including bony prominence of the anterolateral femoral head-neck junction, reduced offset of the femoral head-neck junction, synovial herniation pits, and changes of the acetabulum, such as an os acetabuli, ossification of the acetabular rim, or the “crossover” or “posterior wall” signs seen in acetabular retroversion.172,175,178,181,182,183,184 MR imaging and MR arthrography are the modalities of choice to evaluate the acetabular labrum and articular cartilage. Low offset of the femoral head, subchondral cysts, and ossifica-tion of the acetabular rim as well as labral tears and chondral injuries can be seen on MR imaging in patients with


FAI.176,177,180,181,185,186,187 Acetabular rim lesions on MR imaging have been shown to correlate with results of the impingement test.188 The recognition of FAI and its relation to early OA of the hip requires early diagnosis and treatment to prevent or delay degeneration of the hip.

Etiology and Pathogenesis
OA is associated with abnormal axial loading that exceeds the tolerance level of the articular cartilage and subchondral bone. Joint damage is therefore expected first in the weight-bearing area of the acetabulum, femoral head, or both.185,189 Several studies have shown damage to the acetabular rim in the anterosuperior quadrant in hips without apparent abnormalities,175,177,185,190 suggesting FAI as the trigger for OA in these hips.188
FAI is a well-recognized complication of total hip arthroplasty. It is also known to occur in patients with abnormal hip anatomy. The anatomic configuration of the femoral head and neck and acetabulum allows joint clearance during hip movement. FAI may be caused by any variation in proximal femoral and acetabular anatomy that leads to loss of the femoral head-neck offset or to excessive acetabular coverage (Fig. 3.175).172,173,191 Such variations result in decreased joint clearance between the femoral neck and acetabulum and impingement of the femoral neck against the acetabulum and labrum during terminal motion of the hip, leading eventually to lesions of the acetabular labrum or adjacent articular cartilage.173,188,190,192 Hip disorders known to be associated with FAI include DDH, SCFE, LCP, and posttraumatic deformity with a mismatch between the femoral head-neck junction and the acetabulum.178,185,192,193,194,195,196,197 FAI in patients without preexisting hip disease may be related to variations in normal anatomy or to unrecognized developmental anomalies. The detection of subtle anatomic abnormalities of the femoral head-neck junction and acetabulum is important for surgical planning because arthroscopic labral or chondral débridement alone addresses the secondary damage attributable to FAI but does not alter the underlying cause. This can lead to progression of the early labral and chondral lesions to OA.172,175,178,180,188,190,198,199
FIGURE 3.175 ● (A) Normal morphology of the femur and acetabulum with normal clearance of the hip. (B) Combination of reduced head-neck offset (cam mechanism) and excessive anterior overcoverage (pincer mechanism). Mixed cam-pincer impingement is the most common mechanism of FAI. (See text for further explanation of FAI impingement mechanisms.)
In FAI there is mechanical contact between the femoral head-neck junction and the acetabular opening and rim. As the nonspherical femoral head is forced into the acetabulum, mechanical forces may abrade the articular cartilage near the rim. As the cartilage breaks down, the labrum may separate and tear away from the rim. It has been known for years that in total hip replacement poor head-neck offset of the femoral component with small head sizes may cause impingement of the polyethylene cup. Abnormal denting of the polyethylene leads to early failure of the cup, and then to failure of the entire implant.20,200,201,202,203
Similarly, the natural hip depends on appropriate head-neck offset to provide good joint clearance. With a reduced neck offset or loss of the sphericity of the femoral head, early contact or incongruence with increased loading of the acetabular rim reduces joint clearance and causes FAI. Two distinct mechanisms of FAI have been observed during surgical dislocation of the hip,175 cam impingement caused by a nonspherical head (Fig. 3.176) and pincer impingement caused by excessive acetabular coverage (Fig. 3.177). The majority of FAI cases, however, represent a combination (mixed cam-pincer) of the two mechanisms (see Figs. 3.175 and 3.177).204
Cam Impingement
Cam-type femoroacetabular impingement (see Fig. 3.176) results from an out-of-round femoral head in which there is a bony bump in the area of the anterolateral head-neck junction.205 It is more frequently seen in young athletic men.172,175 The increase in the radius of the femoral head causes a mismatch between the femoral head and the acetabulum that results in chondral changes at the anterior and anterosuperior cartilaginous labral junction of the acetabulum. Eventually the articular cartilage avulses from


the labral rim, causing a cleft-type defect seen on MR examination. In addition to the labral tear, sometimes there is a subchondral bone avulsion that may be seen at the anterior superior edge on a plain x-ray.

FIGURE 3.176 ● Cam impingement demonstrated from the sagittal perspective. During flexion the dysplastic convex or aspherical portion of the femoral head is jammed against the anterolateral acetabular roof. The acetabular articular cartilage is sheared off and there is chondrolabral separation. Internal rotation serves to further increase impingement.
Femoral causes of cam impingement (Fig. 3.178) include insufficient femoral head-neck offset, subtle displacement of the femoral epiphysis, SCFE, and postsurgical or traumatic deformities.178,185,192,193,194,195,196,197 The femoral dysplastic bump may be related to a physeal growth plate disturbance, as is seen in SCFE, or to abnormal incorporation of the proximal femoral growth centers producing a shear plane between the greater trochanter and the femoral neck. Posterior placement of the femoral head on the femoral neck, with inadequate anterior femoral head-neck offset, results in contact and impingement between the femoral neck and acetabular rim when the hip is flexed or internally rotated. This results in abnormal forces on the acetabular cartilage and subchondral bone in the anterosuperior rim area, leading to damage to the acetabular labrum and articular cartilage.172,173,177,178,179,192,193,195,199,206
Decreased offset of the femoral head-neck junction can be seen on MR imaging or radiographs as a prominent lateral extension of the femoral head at the step-off to the adjacent femoral neck.177,185 The offset refers to the difference between the widest diameter of the femoral head and the most prominent part of the femoral neck. On cross-table lateral radiographs of the hip, a deficient anterior head-neck offset is present if the anterior head-neck junction extends beyond a circle around the femoral head.175 Loss of femoral head-neck offset results in decreased clearance between the femoral neck and acetabulum during terminal motion.173 A congruent but nonspherical head, a short neck, and a small head-to-neck ratio, especially when located anteriorly, are morphologic features of FAI that can be detected on MR images.
A bump-osteophyte complex (Fig. 3.179) is observed when the femoral bump is anterior to the buttressing osteophyte as assessed on coronal images. A separate medial or traction osteophyte is frequently observed at the medial femoral head-neck junction.
Stuhlberg et al.197 described the presence of a pistol-grip deformity in 40% of patients who develop OA of the hip (Fig. 3.180). The term “pistol-grip deformity” refers to a flattened femoral head-neck junction, depicted on radiographs or MR images as flattening of the usually concave surface of the femoral head, a bump on the anterolateral aspect of the femoral neck, or failure of the femoral head to be centered over the femoral neck.108,173 Jager et al.178 noted an osseous bump at the anterolateral femoral head-neck junction in patients with FAI. Tanzer and Noiseux173 described a pistol-grip deformity as a cause of FAI in 100% of patients with idiopathic arthritis of the hip. In a study by Leunig et al.,185 80% of hips with FAI had a lack of anterolateral head-neck offset. Other contributing factors may be delayed separation of the common femoral head and greater trochanteric physis or eccentric closure of the femoral head epiphysis. These conditions usually affect the anterosuperior aspect of the femoral head-neck junction, suggesting an epiphyseal growth abnormality as the underlying cause for the decreased femoral head-neck junction.199,207
Several methods have been devised to quantify the concavity of the femoral head-neck junction. Murray183 calculated the “femoral head ratio” on anteroposterior (AP) radiographs, constructing an axis of the femoral neck using the midpoint between the trochanters and the narrowest portion of the femoral neck and dividing the width of the femoral head above the axis by that below.180,183 Notzli et al.180 described a method using MR imaging in which the anterior extent of




the concavity of the femoral neck was defined as a point where the distance from the cortex to the center of the femoral head exceeds the radius of the cartilage-covered femoral head. Widening of the femoral neck anterior to this line reduces the concavity of the neck. The angle formed between the axis of the neck and a line connecting the center of the head and neck at its narrowest point (the alpha angle) was found to be larger in patients with FAI compared with a control group (Fig. 3.181). The alpha angle measured 74.0° ± 5.4° in patients with FAI and 42° ± 2.2° in the normal control group.180 All causes of impingement attributable to the shape of the femoral head-neck junction, such as a wide femoral neck, osteophyte formation, or posterior displacement of the femoral head, result in an increased alpha angle.180 In the study by Notzli et al.,180 all patients with a positive impingement test result demonstrated abnormalities on MR imaging, such as degeneration of the labrum or labral tears, and in 85% of the patients there was associated damage to the anterolateral acetabular cartilage.

FIGURE 3.177 ● (A) Pincer impingement from the sagittal perspective. During flexion the labrum is damaged since it functions as the buffer between the femoral neck and the acetabulum, which has excessive anterior coverage. A contrecoup posteroinferior acetabular chondral lesion results as the femoral head subluxes posteriorly, creating increased pressure between the posteromedial femoral head and posteroinferior acetabulum. (B) Mixed cam-pincer impingement with anterosuperior and posteroinferior acetabular subchondral and chondral degeneration. Sagittal PD FSE image.
FIGURE 3.178 ● Reduced femoral head-neck offset with dysplastic convex femoral bump.
FIGURE 3.179 ● (A) Anterolateral dysplastic bump lateral to the physeal scar. This produces a nonspherical head that can damage the anterosuperior acetabular cartilage and result in separation between the labrum and adjacent cartilage. Coronal T1-weighted (B) and FS PD FSE (C) images of a femoral bump anterior to a femoral osteophyte in cam impingement. There is associated acetabular sclerosis and a labral tear.
FIGURE 3.180 ● MR appearance of the pistol-grip deformity with loss of femoral head-neck concavity associated with a dysplastic anterolateral femoral bump. Coronal FS PD FSE image.
FIGURE 3.181 ● (A) Normal alpha angle used to evaluate the femoral head-neck junction in a spherical femoral head. (B) Increased alpha angle in a nonspherical femoral head with a dysplastic femoral bump.
The goal of surgical treatment of cam impingement is to allow a sufficient impingement-free range of motion during flexion and internal rotation. Procedures involve removal of the nonspherical portions of the femoral head and bony prominence of the extra-articular femoral head, thereby improving the femoral head-neck offset (Fig. 3.182). Surgical treatment also includes arthroscopic débridement of labral tears and removal of loose bodies. Cartilage defects are often not repaired, because it has been shown that cartilage repair procedures, such as microfracture, have a low success rate in the hip.172,175,178,190 A more detailed discussion of treatment is provided below.
Pincer Impingement
Pincer-type FAI (see Fig. 3.177) occurs with direct contact on the acetabular rim by the head-neck junction. It usually occurs from overcoverage by the acetabulum, as is seen in coxa profunda or acetabular retroversion. The recurrent abutment against the labrum causes labral degeneration and ossification. The ossification gives an appearance of a deepened acetabulum. Continued abutment against the ossified aspect causes development of a spur in this region. Lavigne et al. believed that pincer-type chondral lesions were limited to a small area of the acetabular rim and were more benign than the cam types: they found that pincer-type impingement was seen more frequently in middle-aged women participating in athletic activities requiring a great deal of motion, compared to the cam type, which is seen in young athletic men.190
FIGURE 3.182 ● (A) FAI with a dysplastic femoral bump on an FS PD FSE arthrogram. (B, C) Color illustrations of femoral bump resection osteoplasty to restore the normal concave contour of the femoral neck. (D) Arthroscopic view of femoral head-neck bump. (E) Arthroscopic view after resection osteoplasty of the dysplastic femoral bump.



In some patients with FAI the morphology of the femoral head is normal and the abnormal abutment between the femoral head and acetabulum is the result of acetabular abnormalities. The acetabular rim syndrome, a precursor of OA, has been described in patients with DDH. In dysplastic hips with a shallow acetabulum and insufficient acetabular coverage of the femoral head, the acetabular surface is reduced, leading to increased load and pressure on the acetabulum. This leads to labral tears, chondral lesions, intraosseous cysts in the acetabular roof, and bony fragmentation (os acetabuli). Acetabular rim syndrome in DDH is characterized by similar MR imaging findings in an identical location as FAI.188,194
Acetabular retroversion (Fig. 3.183), coxa profunda, and protrusio acetabuli result in overcoverage of the femoral head by increasing the relative depth of the acetabulum.172,175,181 Abutment of the femoral head against the acetabulum results in degeneration of the labrum with ganglion formation or ossification of the acetabular rim, which then further deepens the acetabulum, leading to worsening of the overcoverage.172,181,184 Persistent anterior abutment of the femoral head against the acetabulum can result in chondral injury of the femoral head in the “contre-coup” area of the posteroinferior acetabulum. Chondral lesions are often limited to a small area of the acetabular rim and are often more benign than the deep chondral lesions and extensive labral tears seen in cam impingement.172,175 As mentioned, pincer impingement is more frequently seen in middle-aged athletic women.172,175
In the normal hip the acetabular opening is anteverted from the sagittal plane. Retroversion of the acetabulum has been described as a posteriorly oriented acetabulum with reference to the sagittal plane.181,184 Acetabular retroversion can occur as part of a complex acetabular developmental deformity, as result of posttraumatic dysplasia, or as an isolated deformity, which is considered a precursor to OA.184,191,199,208,209 In retroversion the anterior acetabular roof edge lies lateral to the posterior edge. As the acetabular opening spirals downward, it becomes more anteverted; however, the anterior edge of the acetabulum is located in a more lateral position compared to the normal position, and the posterior edge is more medially located.
Acetabular retroversion can be diagnosed on AP radiographs on the basis of two distinctive features: the crossover or “figure of eight” sign and the posterior wall sign.181,184 The crossover sign (Fig. 3.184) is created when the anterosuperior aspect of the acetabular rim is more laterally located than the posterior aspect of the acetabulum. The anterior aspect of the acetabular rim is directed more horizontally and medially, thereby crossing over the more straight and vertical posterior aspect of the acetabular rim.181,184 The posterior wall sign is the outline of the posterior edge of the posterior wall of the acetabulum. In the normal acetabulum, the line descends through the center point of the femoral head or lateral to it. In the retroverted acetabulum, this line is medial to the center point, indicating relatively less posterior coverage.181,184
On axial MR or CT images a retroverted acetabulum appears as increased coverage of the anterior femoral head.184 The prominent anterolateral edge of the acetabulum predisposes to impingement during flexion and internal rotation, resulting in labral degeneration and/or tears of adjacent cartilage. Labral tears predispose to extraosseous ganglia formation with splitting of the labrum and acetabular cartilage. This allows penetration of synovial fluid into subchondral bone, leading to subchondral cyst formation.181,184 In later stages of FAI there may be evidence of damage from impingement and even fragmentation of the bony margin of the prominent anterior acetabular edge. In a study by Reynolds et al.,184 retroversion was found to be bilateral and symmetric in all patients.
Surgical treatment of pincer impingement includes arthroscopic débridement of labral lesions and reduction of anterior acetabular overcoverage by excising the bony prominence at the acetabular rim. The goal is to allow sufficient impingement-free range of motion during flexion and internal rotation.175,181,184,190 Acetabular retroversion has been successfully treated with reverse periacetabular osteotomy.181 A more detailed discussion of treatment is provided below.
MR Appearance
MR imaging is an excellent modality for the early detection of FAI because it can demonstrate acetabular labral disease and adjacent cartilage damage, subchondral cysts, and underlying subtle anatomic variations of the femoral head-neck junction and acetabulum associated with FAI. Findings vary depending on both the imaging parameters used and the specific location being imaged.
Specific findings on T1- or PD-weighted images include:
  • Hypointense edema and sclerosis of the lateral acetabular subchondral bone
  • Hypointense to intermediate-signal-intensity acetabular subchondral cysts
  • Abnormal (blunted) contour of the acetabular labrum
  • A femoral “dysplastic bump” lateral to physeal scar with or without loss of anterior femoral offset
On FS PD FSE images, imaging findings include:
  • Laterally located hyperintense subchondral marrow edema
  • Intermediate-signal labral degeneration
  • Labral tears with hyperintense linear or diffuse signal intensity
  • Absence of labral tissue
  • Inhomogeneous to hyperintense signal in acetabular subchondral cysts
  • A defect, attenuation, or fissure in the normally intermediate-signal-intensity articular cartilage
  • A femoral “dysplastic bump” with normal marrow fat signal or a hyperintense signal and small hyperintense femoral head/neck cysts
  • A hypointense thickened hip capsule (iliofemoral ligament)
There are also specific femoral and acetabular MR findings in FAI. Femoral findings include:
  • A decreased femoral head-neck offset
  • A dysplastic femoral bump at or adjacent to the lateral physeal scar femoral head-neck junction (Fig. 3.185)
  • P.217





  • A bump-osteophyte complex (Fig. 3.186) where the dysplastic femoral bump is anterior to the lateral to posterolateral osteophyte as visualized on coronal MR images, and the osteophyte may demonstrate hyperintense edema on FS PD FSE sequences
  • Fibrocystic change (Fig. 3.187) (herniation pits), which commonly occurs either anterior to the dysplastic bump (bump-cyst concordance) or anterior to the dysplastic bump (bump-cyst discordance) and is the result of flexion-induced pressure and not normal invagination of synovium210
  • Femoral cysts with fluid, synovial/fibrous, or fat signal intensity (Fig. 3.188), which may be associated with reactive subchondral edema (Fig. 3.189)
  • P.222


  • A femoral head chondral crease (Fig. 3.190) in DDH with labral hypertrophy. The femoral head articular crease is medial to the dysplastic bump. The bump and crease are characteristically proximal to the physeal scar, in comparison to non-DDH cam impingement.
  • Chondral fissures or defects, joint space narrowing, and femoral head edema, seen in the advanced stages of FAI
  • Thickening of the iliofemoral ligament and synovitis adjacent to the capsule and proximal femur
  • Resection of a dysplastic femoral bump and fibrocystic lesion may extend proximal to the physis.(see Fig. 3.190)
  • Heterotopic bone formation along the course of the iliofemoral ligament (Fig. 3.191) as a postoperative complication
FIGURE 3.183 ● (A) Acetabular anterior overcoverage is associated with acetabular retroversion and is a main cause of pincer-type impingement. Coxa profunda is considered the prototype for a deep hip socket in pincer impingement. Acetabular protrusion or retroversion, labral ossification, and a negative acetabular index angle also contribute to pincer-type impingement. (B) Acetabular retroversion (mild) in pincer-type FAI. (C) Femoral anteversion of the femoral neck with the knee directed anteriorly. Femoral anteversion and retroversion (which are associated with toeing in or toeing out) are separate from and should not be confused with acetabular anteversion and retroversion. (D) Cross-section showing normal acetabular anteversion. (E) Retroversion of the normal acetabulum effectively results in anterior overcoverage as the anterior lip extends more laterally compared with normal.
FIGURE 3.184 ● Crossover sign in acetabular retroversion. (A) The normal acetabulum. (B) The crossover sign in which the anterior rim crosses over the posterior acetabular rim (transparent red line).
FIGURE 3.185 ● Cam impingement with dysplastic (aspherical) femoral head-neck junction and fibrocystic change located lateral to the physeal scar. (A) Coronal color illustration of femoral bump-cyst complex. (B) Coronal T1-weighted image with femoral head-neck convexity and fibrocystic change. Note marrow fat reparative signal intensity in acetabular rim. (C) Corresponding coronal FS PD FSE image demonstrating a full-thickness sheared defect in the acetabular cartilage and hyperintense fibrocystic changes in the lateral femoral head-neck junction. (D) Arthroscopic view of a femoral dysplastic bump overlying the subchondral fibrocystic change. (E) Arthroscopic shaver removing the contents of the femoral fibrocystic lesion after resection of the overlying bump.
FIGURE 3.186 ● Femoral head-neck osteophyte located posterior to the femoral bump. The femoral bump and lateral osteophyte are referred to as the bump-osteophyte complex. (A) Coronal color illustration. (B) Coronal T1-weighted image. (C, D) Arthroscopic views of the femoral bump resected at the level of the physeal scar. Normal articular cartilage is preserved medial to the bump.
FIGURE 3.187 ● (A) Concordance of the femoral fibrocystic lesion and the femoral bump. (B, C) Coronal FS PD FSE images showing discordance with a femoral fibrocystic lesion anterior to femoral bump. Note the chondrolabral separation characteristic of cam impingement.
FIGURE 3.188 ● (A) Femoral cyst after bump osteoplasty. (B) Fibrous or synovial signal in a cyst lateral to the physeal scar, hyperintense on coronal FS PD FSE image. (C) Fat, fibrous, and fluid signal intensities are demonstrated on a coronal T1-weighted image. (D) Corresponding sagittal FS PD FSE image showing fibrous and fluid signal in a typical band-like distribution of anterolateral femoral cysts.
FIGURE 3.189 ● Hyperintense edema associated with a femoral fibrocystic lesion in a symptomatic golfer with FAI. Hyperintense edema in both the femur and acetabulum correlates with increased clinical symptoms of hip or groin pain. Acetabular chondral erosions have a high association with hip pain. (A) Coronal FS PD FSE image. (B) Axial FS PD FSE image.
Acetabular findings include:
  • Acetabular retroversion
  • Acetabular rim osteophytes contributing to pincer or mixed cam-pincer impingement (Fig. 3.192)
  • Os acetabuli, usually in combination with a femoral dysplastic bump (Fig. 3.193)
  • Subchondral sclerosis (Fig. 3.194), edema (Fig. 3.195), or cysts (Fig. 3.196) of the lateral acetabular rim
  • Acetabular subchondral changes, which occur anterolaterally and progress posteriorly. Posterior acetabular changes are associated with the pincer mechanism (see Fig. 3.196).
  • Acetabular cysts of fluid, fibrous/synovial, or fat signal intensity (Fig. 3.197)
  • Chondral fissures or defects in the superior or superolateral acetabulum. Chondral lesions show a progression (Fig. 3.198) from blister (see Fig. 3.198) to delamination (see Fig. 3.198) to peel-off (Fig. 3.199).
  • Postoperative acetabular lesions (Fig. 3.200) with fluid-filled defect
  • Regrowth of articular cartilage (occurring within 1 year)
  • Labral tears (Fig. 3.201) and paralabral cysts
  • Calcified/ossified labrum (Fig. 3.202) and os acetabuli associated with pincer impingement
  • Joint space narrowing with progression to OA (Fig. 3.203)
Key MR imaging findings include hypointense edema and sclerosis of the lateral acetabular rim on T1-weighted images, hyperintense subchondral edema on FS PD FSE images, and hyperintense acute subchondral acetabular cysts on FS PD FSE images. Intermediate-signal-intensity synovial or granulation tissue is associated with maturation of subchondral cysts. In younger patients, conversion of the cyst to fat signal intensity indicates an attempt at healing.211
The articular cartilage is hyperintense in areas of chondral softening. This softening progresses from articular cartilage fissures to frank chondral fragmentation resulting in a full-thickness chondral defect in the superior portion on the acetabular roof. Subchondral sclerosis is visualized on coronal



and sagittal images and is associated with chondral involvement. Chondral lesions are frequently associated with joint space narrowing and represent a later stage of FAI, usually less responsive to impingement surgery.187,211

FIGURE 3.190 ● (A) Coronal color section depicting DDH with hypertrophic labrum and femoral head crease between the bump and medial femoral head. (B) Coronal T1-weighted image of DDH with femoral bump proximal to the physis. The femoral crease is medial to the femoral bump. (C) Coronal color section showing resection of the bump extending proximal to the physis. (D) Coronal FS PD FSE image depicting hyperintense fluid in a femoral bump osteoplasty proximal and distal to the physis.
FIGURE 3.191 ● Coronal T1-weighted (A) and FS PD FSE (B) images showing heterotopic bone forming along the lateral capsule after osteoplasty for FAI. A full-thickness acetabular chondral defect is shown.
The acetabular labrum appears as a triangular low-signal-intensity structure with sharp margins. A recess is seen between the outer margin of the labrum and the joint capsule. With degeneration of the labrum there is increased signal on FSE PD FSE images. Labral tears usually present as a fluid-filled cleft at the base of the labrum adjacent to the acetabular cartilage. Complete detachment of the labrum can be seen in advanced tears. Paralabral cysts that are hyperintense on FS PD FSE images may be present within the adjacent bone or in an extra-articular location.188,211,212
The dysplastic femoral bump is located lateral (directly lateral, superolateral, or inferolateral) to the physeal scar of the femoral head-neck junction. This bump is a discrete contour convexity that may be associated with subchondral edema and cystic change. The finding of a femoral-sided subchondral cyst represents the point of impingement on the femur and is not a normal variation of synovial herniation.178,211 T2* GRE coronal images increase the conspicuity of the convex contour associated with the dysplastic femoral bump at the head-neck junction. GRE also improves the visualization of altered trabecular bone in the area of impingement because of increased sensitivity to altered trabecular architecture.211 A reduced femoral head-neck junction can be assessed on oblique axial images obtained perpendicular to the femoral neck to visualize the head-neck junction and the femoral bump on a single image.
Thickening of the joint capsule (Fig. 3.204), often with synovitis, and thickening of the iliofemoral ligament laterally are associated with the inflammatory changes of FAI. Treatment includes arthroscopic division of the iliofemoral ligament to allow the outflow of small loose bodies and debris not removed during the initial arthroscopic treatment. Sectioning of this ligament also provides pain relief secondary to capsular contraction.211
The acetabular contour (slope) as visualized on anterior coronal images is a sensitive indicator of acetabular dysplasia in DDH associated with FAI. In addition, the MR findings in the acetabular rim syndrome, originally described in DDH, are similar to findings in an identical location in FAI.188,194 Leunig et al.188 described hypertrophy of the acetabular labrum and an increased incidence of paralabral cysts in patients with DDH compared to patients with FAI. An enlarged or hypertrophied labrum and paralabral cysts may also be seen in patients with FAI without DDH or with mild DDH.
Anterior overcoverage of the acetabulum with a retroverted acetabulum is common in patients with pincer-type FAI.181 MR imaging has not been used routinely to evaluate acetabular overcoverage and retroversion; however, a retroverted acetabulum can be assessed on axial plane images.181,184
If unrecognized and untreated, FAI can lead to severe OA requiring total hip replacement. Although activity modification


may stabilize symptoms with synovialization of subchondral cysts, full-thickness chondral lesions of the acetabulum accelerate progression of joint space narrowing. Conservative treatment includes short-term non-weight-bearing, anti-inflammatory medications, muscle strengthening to relieve hip joint stress, and emphasis on nonloading activities such as bicycle riding or elliptical exercisers to exercise the hip joint and stimulate articular cartilage healing. Surgical options include arthroscopic débridement of labral tears, femoroacetabular débridement and femoral reshaping (resection of the dysplastic “bump”), and periacetabular osteotomy. As mentioned, advanced cases may require total hip replacement.

FIGURE 3.192 ● Coronal (A) and axial (B) FS PD FSE images showing mixed cam-pincer impingement with an acetabular rim osteophyte and a convex aspherical femoral head-neck bump. Coronal FS PD FSE image (C) and arthroscopic view (D) of a prominent acetabular rim osteophyte in a separate case.
Surgical Dislocation for Femoroacetabular Impingement
The Bern hip group175 developed a joint-preserving surgical approach for reshaping the femoral head-neck junction or the acetabular rim. The goal of this surgery is to eliminate pain and the pathologic cause of early degenerative


joint disease, and findings indicate that surgical dislocation with correction of FAI yields good results in patients with early degenerative changes. The procedure was not beneficial to those with advanced degenerative changes or extensive articular cartilage damage.175

FIGURE 3.193 ● Os acetabuli contributing to the pincer component of mixed cam-pincer impingement. The femoral bump is demonstrated lateral to the physeal scar.
The operation is performed through a lateral approach to the hip with the patient in the lateral decubitus position. A trochanteric osteotomy (trochanteric flap) and anterior dislocation of the hip allows a 360° view of the femoral head and neck and an adequate view into the acetabulum. Labral tears may be treated with partial resection or repair, and acetabular rim osteophytes are removed. The head and neck may be reshaped and contoured using osteotomes. It was found that if the lateral and epiphyseal branches of the medial femoral circumflex artery are preserved, other capsular arteries can be compromised without causing AVN.213 Postoperatively, patients are kept on two crutches, non-weight-bearing until the trochanteric osteotomy has healed.
FIGURE 3.194 ● Hypointense acetabular rim sclerosis and anterolateral femoral fibrocystic lesion in FAI. Coronal T1-weighted image.
Arthroscopic Treatment
Arthroscopy has been used for débridement of labral tears in the management of FAI, and recently it has also been used to perform surgical dislocation of the hip.214,215 Typical labral lesions in FAI include fraying or tearing of the labrum anteriorly and laterally. There may also be articular cartilage damage, ranging from a blister, to a delamination lesion, to a peel-off lesion.
The labral lesions are débrided with a shaver or radiothermal device and the articular cartilage is débrided or smoothed. Delamination defects must be débrided back to stable cartilage. Suture anchors (for chondrolabral tears) or sutures (for intrasubstance splits of the labrum) are used to restore function of the labrum.215 Microfracture technique may also be used to stimulate cartilage production in acetabular roof chondral lesions (Fig. 3.205).
Exposure of the entire bony bump or osteophyte is accomplished with an anterior capsulectomy, and a cleft or demarcation at the osseous cartilaginous junction to the femoral head-neck junction and the base of the neck is often identified. The area of resection is outlined and then contoured with a bur. If there is an acetabular rim osteophyte, this may be resected in the same fashion behind the intact labrum. Occasionally the labrum must be excised.
Labral Tears
Labral tears, including avulsions, are secondary to traumatic injury or degeneration of the labrum. They are found most commonly in patients 20 to 50 years of age, although they have been seen in patients as young as 18 and as old as 75. In young athletes the mechanism of injury is usually trauma, ranging from twisting injuries to hip dislocation. Acute, traumatic tears are common in sports requiring extreme hip rotation and flexion, such as soccer, hockey, golf, gymnastics, dancing, and kick-boxing. In middle-aged patients (under 50 years of age) FAI is a frequent contributing factor. In older patients degenerative tears associated with degenerative disease of the hip are most commonly seen. Labral


tears are more common in individuals who participate in sports that increase the risk of FAI. Patients with prior hip dislocations and those with DDH are also at increased risk. Labral abnormalities (including labral degeneration) have been found in 28% of asymptomatic individuals, and labral tears have been found in 20% of symptomatic patients with DDH.

FIGURE 3.195 ● Coronal (A) and sagittal (B) FS PD FSE images showing subchondral acetabular roof edema associated with a longitudinal labral tear. (C) Coronal FS PD FSE image in a separate case showing acetabular roof edema associated with a hypertrophied labrum without associated findings of DDH. Enlargement (hypertrophy) of the labrum is more frequent, however, in DDH.
Diagnosis and Clinical Features
The acetabular labrum is a fibrocartilaginous rim that deepens the acetabulum and attaches to the osseous acetabular rim and transverse acetabular ligament. It is not important in load transmission. MR examination with a surface coil allows definition of important anatomic features of the acetabular labrum.3 The normal labrum, variably triangular in cross-section (Fig. 3.206), is seen on coronal planar images as a low-signal-intensity triangle located between the lateral acetabulum and the femoral head. The labrum covers the hyaline cartilage at the lateral peripheral margin of the acetabulum (Fig. 3.207).12 The labrum is most substantial in its posterior superior extent; it is thinner anteroinferiorly. It is usually inverted but may be everted and may also be mobile, as determined arthroscopically. Except for the synovium in the perilabral sulcus, the labrum is nonvascularized and without associated synovial tissue. It may not be continuous with the transverse ligament at the margins of the acetabular fossa. A







demarcation or groove of acetabular articular cartilage separates the labrum and transverse ligament. The capsule of the hip attaches to the osseous acetabulum laterally, creating the perilabral sulcus, a normal finding between the capsule and labrum on coronal images peripheral to the lateral rim of the acetabulum (Fig. 3.208).

FIGURE 3.196 ● Coronal images showing acetabular cysts in FAI. Cysts are hypointense on T1-weighted images (A) and hyperintense on FS PD FSE images (B). Posterior acetabular roof progression of the cysts is demonstrated on these posterior coronal images.
FIGURE 3.197 ● (A) Coronal section depicting types of acetabular roof cysts seen in FAI. Fat signal intensity represents a quiescent stage indicative of reparative maturation of the cyst. Fluid or fibrous/synovial signal intensity is associated with ongoing symptoms of hip pain. (B) Coronal T1-weighted image showing fat signal intensity lateral to hypointense/intermediate-signal-intensity acetabular roof changes. (C) Corresponding coronal FS PD FSE image with fat suppression in the lateral rim of the acetabulum and fluid/fibrous signal more medially.
FIGURE 3.198 ● Progression from blister to delamination of acetabular articular cartilage. (A) Lateral illustration of acetabular roof blister lesion. (B) Arthroscopic view of a chondral blister. (C) Lateral illustration of superior acetabular delamination lesion. (D) Corresponding coronal FS PD FSE image showing chondral erosion with delamination of articular cartilage. (E) Arthroscopic probing of a delamination lesion.
FIGURE 3.199 ● (A) Lateral view illustration of a peel-off chondral lesion. (BD) Multiple fissures with resultant fragmentation of the acetabular chondral roof producing an unstable chondral surface and peel-off lesion of the articular surface. At arthroscopy, loose bodies may be observed as leg traction is applied and the peel-off lesion is probed. (B) Coronal FS PD FSE image. (C) Coronal color illustration showing fragmentation of acetabular roof articular cartilage (appreciated on arthroscopy). (D) Arthroscopic view of a peel-off lesion probed.
FIGURE 3.200 ● (A) Postresection osteoplasty of the acetabular bump. (B) Arthroscopic surgical division of the lateral hip capsule and bump-cyst resection 2 weeks after resection osteoplasty. Coronal FS PD FSE image. (C) Regrowth of acetabular chondral surface and reconstitution of iliofemoral ligament reimaged after 2 years. Coronal FS PD FSE image.
FIGURE 3.201 ● (A) Coronal color section of persistent chondrolabral tear with lateral labral avulsion. (B) Coronal FS PD FSE image with symptomatic labral detachment after osteoplasty for cam impingement.
FIGURE 3.202 ● (A) Axial FS PD FSE image of calcified anterior and lateral labrum. (B) Arthroscopic view with calcified labrum along the acetabular rim.
FIGURE 3.203 ● MR findings in advanced FAI including joint space narrowing and subchondral erosions involving both the femoral head and acetabulum. Coronal FS PD FSE image.
FIGURE 3.204 ● Thickened joint capsule in association with FAI. Synovitis and thickening of the iliofemoral ligaments are frequently seen in the spectrum of the inflammatory response to FAI changes. Coronal FS PD FSE image.
FIGURE 3.205 ● Post-microfracture of the acetabular roof used to stimulate fibrocartilage growth. Coronal T1-weighted image.
Most labral tears are anteroposterior or posterosuperior (more common in the younger population) and run along the base of the labrum or along the long axis (longitudinal tears). A spectrum of labral lesions, including fibrillation and radial and longitudinal morphology (Fig. 3.209), may be seen, as well as chondrolabral separation (Fig. 3.210). Other pathologic and histologic findings include a reciprocal injury to the femoral head chondral surface; associated paralabral cysts (see discussion below) and subchondral acetabular cystic changes; intra-articular displacement of the labrum; and eosinophilic, mucoid, or vascular degeneration. There may also by local, cystic cavitation and separation from the underlying bone interface. Avascular regions preclude healing.
Clinically, the patient usually presents with hip pain, decreased range of motion, snapping or clicking, and locking. Episodes of sharp pain are associated with pivoting or twisting. Anterior labral tears produce clicking with manipulation of the hip from flexion, external rotation, and abduction into extension, internal rotation, and adduction. The symptoms of posterior labral tears are elicited by full flexion and by adduction and internal rotation to extension and abduction and external rotation. Labral tears are frequently associated with acetabular



dysplasia, FAI (Fig. 3.211), LCP, SCFE, and degenerative hip disease (Fig. 3.212). Traumatic tears may occur along the inner free margin (a radial flap, the most common type) (Fig. 3.213), or they may be unstable and displaced (longitudinal tears) (Fig. 3.214).

FIGURE 3.206 ● Anterior view with both coronal and sagittal perspective of the capsule, labrum, and articular cartilage. The acetabular fossa and fat pad are shown. The transverse acetabular ligament that spans the acetabular notch is cut.
FIGURE 3.207 ● Acetabulum with crescent-shaped (lunate) surface covered with articular cartilage.
FIGURE 3.208 ● Perilabral sulcus between the capsule and lateral surface at the labrum. Coronal FS PD FSE image.
FIGURE 3.209 ● Spectrum of labral lesions with fibrillation and radial and longitudinal morphology.
Several classification schemes have been devised for acetabular labral tears. The Czerny classification, based on MR arthrography, divides tears into three general stages and has a sensitivity of 91% and a specificity of 71%:216
FIGURE 3.210 ● Hyperintense signal at area of chondrolabral separation. Coronal FS PD FSE image.
  • Stage IA: There is hyperintense signal with no communication to the articular surface, and the perilabral sulcus can be visualized.
  • Stage IB: Similar to stage IA, but there is no perilabral sulcus
  • Stage IIA: There is contrast extension into the articular surface, and the perilabral sulcus can be visualized.
  • Stage IIB: Similar to stage IIA, but there is no perilabral sulcus
  • Stage IIIA: There is labral detachment, but the normal triangular shape is maintained and the perilabral sulcus can be visualized.
  • Stage IIIB: There is labral detachment. The labrum appears thickened and is hyperintense, and the perilabral sulcus cannot be seen.
In the arthroscopic classification,215 injuries are described as either labral detachment from bone (which requires suture anchor stabilization for repair) or intrasubstance splits (which are repairable with monofilament suture if the labrum is fixed to the acetabulum with a stable outer rim). Philippon217 has defined five types of labral pathology:
  • A primary labral tear
  • Primary capsular laxity with minor labral pathology
  • Capsular laxity with pronounced labral involvement
  • FAI with an associated labral tear
  • Articular cartilage degeneration with an associated labral tear



MR Appearance
Neither conventional radiographs nor arthrography allows accurate identification of labral defects, but MR evaluation of labral tears shows potential. In patients with persistent pain and clicking with hip flexion and rotation, the chondrolabral junction of the labrum is examined to identify tears involving detachment of the labrum from the articular cartilage in the zone of transition between the fibrocartilaginous labrum and the lateral acetabular roof articular cartilage (Fig. 3.215). Labral lesions may also present as tears along one or more cleavage planes within the substance of the labrum (Fig. 3.216). Intralabral tears exist with either a perpendicular or parallel component relative to the labral surface. Labral tears extending to the subchondral bone are associated with tidemark reduplication and endochondral ossification. These labral tears can be confirmed at hip arthroscopy. Abutment of acetabular labral cartilage along the medial aspect of the fibrous labrum should not be mistaken for a partial labral tear or detachment. Subchondral degeneration within the lateral acetabular roof may be associated with chronic labral disruptions. Anterior coronal images are best for assessment of associated acetabular dysplasia.
FIGURE 3.211 ● FAI with femoral fibrocystic change lateral to the physeal scar and a torn anterior labrum. (A) Coronal FS PD FSE image. (B) Axial FS PD image.
FIGURE 3.212 ● Degenerative hip in an 85-year-old with complete absence of the lateral and anterior labrum. (A) Coronal FS PD FSE image. (B) Sagittal FS PD FSE image.
FIGURE 3.213 ● Arthroscopic view of an acetabular labral radial tear.
T1-weighted or PD FSE images may display a normal labrum, which is hypointense and covers the hyaline articular cartilage at the lateral peripheral margin of the acetabulum, or a spectrum of pathologic changes, including:
  • Intermediate linear or diffuse abnormal signal
  • Intralabral degeneration
  • Separation of the labrum at its base
  • A diastasis between the acetabular articular cartilage and the labral attachment
FS PD FSE images are also used to evaluate labral tears. Radial images, perpendicular to the tear plane, are particularly useful. Typical MR findings include:
  • Linear hyperintensity within the hypointense labrum (seen on FS PD FSE or STIR images)
  • A hyperintense paralabral cyst with septations or lobulations (on FS PD, T2 FSE, or STIR images)
  • Surface irregularities associated with the base of the degenerated labrum
  • FAI (which is associated with labral tears, acetabular chondral erosions, and subchondral acetabular hyperintensity)
  • A hyperintense macerated to absent labrum in OA
  • Labral displacement or bucket-handle tears
  • Loss of triangular morphology
  • A hyperintense joint effusion
MR arthrography demonstrates excellent accuracy in the detection and staging of acetabular labral lesions compared to conventional MR imaging.216 With MR arthrography, intra-articular contrast fills the tear, promoting uplifting or separation of the torn labrum from acetabular articular cartilage. Overall visualization of the labral complex is improved, and it is possible to visualize surface irregularities and abnormalities near the labral base.218 As mentioned above, the Czerny classification is based on MR arthrography.
Although MR correlation with histology of degeneration is poor compared with the ability to define labral morphology, some characteristic changes are found on conventional MR scans. Histology at the labral base has shown an irregular interface between the labral fibrocartilage and subchondral bone. Although acetabular roof hyaline cartilage does not extend beneath the labral base, connective tissue and degeneration can be seen in the transitional zone between acetabular roof hyaline cartilage and labral fibrocartilage.
On MR scans, intrasubstance degeneration of the labrum is intermediate to hyperintense on FS PD FSE images and does not extend to the labral surface (Fig. 3.217). The chondrolabral junction should be devoid of fluid signal intensity between the labrum and articular cartilage (Fig. 3.218). MR is used to correlate anterior labral tears on sagittal, axial, and coronal images (Figs. 3.219 and 3.220) and lateral labral tears on coronal and sagittal images (Fig. 3.221). Anterior labral tears are evaluated in three zones, the lateral, middle, and medial thirds of the femoral head (Fig. 3.222). On medial images adjacent to the transverse ligaments, anterior labral tears may be seen to be associated with adjacent capsular pathology. A tear appreciated in the coronal plane can be demonstrated in





its entire anterior-to-posterior extent on a single sagittal image (Fig. 3.223). A bucket-handle tear (Fig. 3.224), which may be seen more commonly in a hypertrophied labrum in mild DDH, is characterized by fluid cleavage separating the longitudinal tear into two separate fragments. A degenerative labrum may be associated with abnormal morphology or absence of the fibrocartilage (see Fig. 3.212). Increased signal intensity can also be seen through the labral base on gradient-echo sequences, including spoiled gradient recalled acquisition in steady state (SPGR), and is attributed to cartilage degeneration, transitional zone fissures (between the labrum and subchondral bone), and partial labral detachment. Labral surface irregularities (hyperintensity) may be associated with labral base degeneration. The limitations of MR imaging in the diagnosis of intrasubstance degeneration may be related to the presence of fibrovascular bundles or an irregular labral insertion producing signal intensity changes without corresponding degeneration.

FIGURE 3.214 ● Arthroscopic view of a longitudinal labral tear.
FIGURE 3.215 ● (A) Chondrolabral tear perpendicular to the long axis of the labrum. Coronal color section. (B) Fluid signal intensity at chondrolabral tear site. Coronal FS PD FSE image. (C) Progression of chondral labral tear to separation. Coronal color section. (D) Complete detachment of labrum from lateral acetabulum trapped between the acetabulum and femoral head. Coronal FS PD FSE image.
FIGURE 3.216 ● (A) A cleavage tear parallel to the long axis of the labrum and a labral tear perpendicular to the labrum and lateral to the chondrolabral junction. Coronal color section. (B) Cleavage tear of the anterolateral acetabular labrum. Coronal FS PD FSE image. (C) Corresponding labral peripheral cleavage tear on sagittal FS PD FSE image.
FIGURE 3.217 ● Degeneration of the acetabular labrum. (A) 3D color illustration with coronal inset. (B) Coronal FS PD FSE image with hyperintense labral degeneration associated with labral tearing and adjacent chondrolabral injury. (C) Arthroscopic view of a frayed anterior labral tear.
FIGURE 3.218 ● Mild hyperintense chondral degeneration adjacent to and at the base of the labrum without chondrolabral separation. Coronal FS PD FSE image.
FIGURE 3.219 ● Correlation of a far anterior labral tear location on sagittal (A) and axial (B) FS PD FSE images.
Untreated labral tears typically progress, and eventual development of OA is especially common in the tears seen as part of FAI. Conservative treatment measures include activity modification (limiting flexion and internal rotation), anti-inflammatory medications, and intra-articular steroid injection during acute episodes of pain. Surgical procedures include débridement and a modified Bankart repair. A modified Bankart-type repair is useful for treatment of recurrent dislocation of the hip with an associated labral lesion.219 Stability of the hip is thought to be associated with reconstruction of the labrum and reduction in capsular laxity.
Paralabral Cysts
Paralabral cysts are juxta-articular cysts usually formed secondary to a labral tear, either traumatic or degenerative.220 These cysts, also referred to as ganglion cysts or synovial cysts, are commonly located lateral to the anterosuperior or posterosuperior labrum and may communicate with a labral tear in any location, including anteroinferior or posteroinferior. Anterosuperior cysts (Fig. 3.225) are the most frequent, followed by posterosuperior and inferiorly located cysts. Labral tears are most often seen in individuals 20 to 50 years of age, and the spectrum ranges from 18 to 75 years. Paralabral cysts may range in size from 1 mm to more than 1 cm and are septated and lobulated. Development is related to an increased or abnormal load on the lateral aspect of the acetabular roof, which may be caused by FAI, OA, DDH, or femoral dysplasia, especially of the lateral aspect of the femoral head.



They may also occur secondary to the transformation of an intraosseous ganglion cyst to a soft tissue ganglion. Other etiologic factors include increased intra-articular pressure forcing synovial fluid through a labral tear and trauma. Subchondral acetabular cystic changes (Fig. 3.226) may be found, as well as chondral erosions. As with labral tears, they are commonly seen in individuals participating in sports requiring hip rotation and flexion, such as golf, hockey, soccer, gymnastics, and ballet. In middle-aged adults they are more frequently seen secondary to degenerative labral tears in FAI. They are seen more often in males, as a function of the sports-related risk of FAI.

FIGURE 3.220 ● Correlation of an anterior labral tear on coronal and sagittal images. (A) Lateral color illustration. (B) Coronal FS PD FSE image. (C) Sagittal FS PD FSE image.
FIGURE 3.221 ● Correlation of a longitudinal (bucket-handle type) tear of the lateral acetabular labrum on coronal (A) and sagittal (B) FS PD FSE images.
Histologically, ganglion cysts are lined with connective tissue and contain mucinous material, and synovial cysts are lined with synovial cells and contain synovial fluid. Either type may or may not communicate with the joint (Fig. 3.227). There may be associated labral tears and/or eosinophilic, mucoid, or vacuolar degeneration. Labral abnormalities (including labral degeneration) have been found in 28% of asymptomatic individuals, and labral tears have been found in 20% of symptomatic patients with DDH.
The patient usually presents with hip pain, a picture similar to that seen in labral tears. Pain is frequently sudden and sharp and accompanied by clicking, popping, and snapping. Sometimes there is locking of the joint as well. There may also be deep anterior groin pain with lateral hip and gluteal radiation. The symptoms correlate more with the underlying labral tear than with the cyst. If the cyst is large, however, there may be symptoms of local mass effect.
MR Appearance
The best diagnostic clue to the presence of a paralabral cyst is the appearance of a hyperintense mass adjacent to the labrum on coronal FS PD or T2 FSE images. The cyst may or may not be septated and lobulated. Characteristic findings on T1- or PD-weighted images include:
  • Hypointense to intermediate signal intensity
  • Well-defined margins without reactive soft tissue edema
  • Increased signal intensity in cysts with mucin contents
  • Sometimes, associated hyperintense intraosseous ganglion cysts of the acetabular roof or lateral rim
  • Associated intermediate signal in labral tear or separation of the labrum at its base
FS PD FSE images typically depict the following:
  • A hyperintense juxta-articular mass
  • Longitudinal extension, usually superior to inferior (Fig. 3.228) and anterior to posterior along the labral margin (Fig. 3.229)
  • Hypointense septations (Fig. 3.230)
  • Intermediate-signal synovial thickening
  • A linear hyperintense tear or detachment of adjacent labrum
  • FAI
  • Hyperintense edema progressing to cyst formation in the acetabular roof
  • P.245



  • Acetabular roof chondral erosions
  • A dysplastic lateral femoral osseous bump lateral to the physeal scar
  • Hyperintense intraosseous ganglion and labral tear
  • Associated acetabular dysplasia with a shallow acetabulum on anterior coronal images
FIGURE 3.222 ● Technique of evaluating the anterior labrum in the medial (A), superior (B), and lateral (C) locations. Tears are evaluated in the sagittal plane and cross-referenced with coronal images of the femoral head. Associated extension of the tear is shown in the lateral labrum on a sagittal image (D). (A) Sagittal FS PD FSE image medial to the center plane of the femoral head prescribed from a coronal image. (B) Sagittal FS PD FSE image directly superior to the femoral head. (C) Sagittal FS PD FSE image lateral to the midline of the femoral head. (D) Peripheral sagittal FS PD FSE image demonstrating lateral continuation of the anterior acetabular labral tear.
FIGURE 3.223 ● Anterior-to-posterior extent of an acetabular labral tear. (A) Coronal FS PD FSE image. (B) Sagittal FS PD FSE image.
FIGURE 3.224 ● Bucket-handle acetabular labral tear. (A) Color coronal section showing a longitudinal tear of the lateral labrum. (B) Separation of displaced longitudinal labral surfaces in a bucket-handle longitudinal tear pattern.
FIGURE 3.225 ● Anterosuperior-based (A) versus posterosuperior-based (B) paralabral cysts on color anterolateral views of the acetabular fossa and labrum.
After administration of intravenous contrast there is peripheral enhancement of the cyst. After intra-articular contrast there is variable demonstration of paralabral cysts. FS PD FSE images are required to visualize cysts without joint communication (see Fig. 3.227).
Paralabral cysts do not spontaneously resolve, and although conservative treatment such as anti-inflammatory medications, intra-articular steroids, and percutaneous aspiration may provide temporary pain relief, the underlying labral tear or abnormality (e.g., FAI) must be addressed or the cyst will recur. Surgical, including arthroscopic, options in management include repair and/or débridement and resection of the labrum, débridement and microfracture of the acetabular roof, and femoral resurfacing and/or acetabular osteotomy in FAI.
FIGURE 3.226 ● Subchondral acetabular cyst associated with an adjacent acetabular labral tear. Coronal FS PD FSE image.
Joint Effusions
The volume of joint fluid in the normal hip is small, and it does not generate sufficient signal for detection. Joint effusions, however, demonstrate low signal intensity on T1-weighted images and increased signal intensity on T2-weighted images. On coronal images, small collections of joint fluid first accumulate superiorly in the recess bordered by the labrum of the acetabulum and inferomedially by the transverse ligament. With larger effusions, the medial and lateral joint capsule is distended and has convex margins. Joint effusions are also easily identified on axial and sagittal images.



Osteoarthritis (OA), also referred to as degenerative joint disease (DJD) and end-stage FAI, is characterized by articular cartilage degenerative change with hip joint space narrowing. It is by far the most common form of articular cartilage degeneration. In general incidence increases with age, and most cases occur in individuals over 55 years of age. The hip is more frequently involved in males and the knees in females.
FIGURE 3.227 ● Noncommunicating paralabral cyst extending into the iliopsoas bursa between the iliofemoral and the pubofemoral ligaments. (A) Axial FS T1-weighted MR arthrogram with contrast extension into the anterior paralabral cyst. (B) Sagittal FS PD FSE image depicting the hyperintense paralabral cyst with an anterior labral tear origin. (C) Coronal FS PD FSE image showing anterior extension of the paralabral cyst into the iliopsoas bursa.
Diagnosis, Etiology, and Clinical Features
Although the etiology remains unclear, two mechanical theories predominate: (1) excessive stress on normal tissue and (2) abnormal response to normal forces. In addition, the biologic response resulting in inflammation undoubtedly contributes to cartilage degeneration. Many cases of OA in the hip are thought to be secondary to an underlying condition such as an old SCFE, dysplasia, LCP in childhood, DDH, or anatomic variants such as an intra-acetabular labrum.
In the normal hip hyaline cartilage is elastic and resists mechanical stress, but the subchondral plate and calcified cartilage are less compressible than articular cartilage. Synovial fluid is produced by synoviocytes in the synovial membrane and provides nutrients, viscosity, and elasticity for shock absorption. In OA, the articular cartilage undergoes fibrillation, fragmentation, and pressure erosion, resulting in joint space narrowing of the weight-bearing zones (Fig. 3.231). As OA progresses, there is development of subchondral cysts (Fig. 3.232), sclerosis (Fig. 3.233), osteophytes, and labral tears. Eventually there is end-stage ankylosis, osteonecrosis of subchondral bone, hypervascularity, osteoblastic activity, and trabecular thickening. Subchondral (detritic) cysts contain myxoid material, proteoglycans, articular cartilage fragments, and metaplastic cartilage. Chondrocyte replication and a decreased concentration of hyaluronic acid are additional histologic changes found in OA. The changes of OA affect the acetabular roof, the chondral surfaces of the acetabulum, and the femoral head articular surface. Involvement may be unilateral or bilateral, with varying morphology based on the extent of cartilage loss. Active OA is characterized by an extensive inflammatory reaction, osteophytes, subchondral cysts, and sclerosis.
Most patients present with joint pain and loss of internal rotation, insidious-onset groin and thigh pain, and sometimes gluteal radiation. Stiffness and limitations in the ability to sit, stand, or walk are common complaints. Symptoms are worse in the morning and are exacerbated by axial loading or weight-bearing activity.
Grading and Classification
Four grades of OA have been described, based on the MR extent of disease:
  • Grade 1: chondral inhomogeneity
  • Grade 2: inhomogeneity and discontinuity of the chondral surface, with hypointensity of the femoral head and neck on T1-weighted images
  • Grade 3: grade II disease plus irregular cortical morphology of the femoral head and acetabulum, cystic changes, and an indistinct zone between the femoral head and acetabulum
  • Grade 4: grade III disease plus femoral head deformity
MR Appearance
T1-weighted or fat-suppressed PD-weighted FSE sequences of the hip are used to detect the early changes of OA. Articular cartilage attenuation is best demonstrated on either sagittal or coronal fat-suppressed PD-weighted FSE images, but separation of acetabular and femoral head articular cartilage is better displayed in the sagittal plane. Stress-thickened trabeculae show low signal intensity on T1- and T2-weighted images, before there is evidence of subchondral sclerosis on conventional radiographs. Characteristic MR findings in OA of the hip parallel the findings seen on conventional radiographs and include:
  • Joint space narrowing with loss of superior joint space articular cartilage on both the acetabular and femoral sides
  • Hypointense subchondral sclerosis of the acetabulum and subsequently the femoral head associated with loss of joint space
  • Osteophytes with marginal or peripheral distribution in association with progressive FAI
  • Subchondral cysts larger than the cysts described in FAI
On T1-weighted and PD FSE images typical findings are:
  • An attenuated or denuded chondral surface
  • Hypointense sclerosis of the acetabular roof and the opposing surface femoral head
  • A hypointense effusion and paralabral cysts
  • Marrow fat signal in osteophytes
  • Relative preservation of medial joint space relative to narrowed superior joint space
  • Single versus multiple load-bearing zone subchondral cysts that demonstrate hypointense to intermediate signal intensity
FS PD FSE images demonstrate:
  • Linear hyperintensity in chondral fissures
  • Subchondral hyperintensity in the lateral acetabular roof and femoral head superior surface
  • Subchondral cysts, which may be multiple and variable in size
  • Hyperintense paralabral cysts adjacent to acetabular labral tears
  • Hyperintense femoral head and neck edema in active OA
  • Hyperintense fluid and inhomogeneity of synovium in the active inflammatory form of OA
Intravenous contrast is used to enhance the synovium, and MR arthrography is used in FAI.
A less common form of OA demonstrates more medial (Fig. 3.234) (superomedial) joint space narrowing. The femoral head may migrate in a superolateral direction (most common) or a medial direction or may demonstrate an axial pattern. Subchondral marrow edema is related to both subchondral cysts (Fig. 3.235) and increased load across the weight-bearing segment of the hip, which is no longer buffered by articular cartilage (Fig. 3.236). Destructive arthrosis of the hip, which also demonstrates reactive subchondral




edema, is seen in Postel coxarthropathy.221 This form of destructive OA is associated with rapid chondrolysis and hip joint destruction with minimal osteophytic response. As seen in FAI, there may be an accentuated convexity of the femoral head-neck contour laterally (Fig. 3.237), but chondral loss affects both the acetabulum and the femoral head.

FIGURE 3.228 ● Superior and inferior extension of a lateral paralabral cyst. Coronal FS PD FSE image.
FIGURE 3.229 ● Anteroposterior extension of a lateral paralabral cyst on axial (A) and coronal (B) FS PD FSE images.
FIGURE 3.230 ● Hyperintense paralabral cyst with secondary osseous extension septations that are hypointense. Sagittal FS PD FSE image.
FIGURE 3.231 ● Superior joint space narrowing in osteoarthritis in a 50-year-old. Coronal T1-weighted MR arthrogram.
FIGURE 3.232 ● Eggers cyst of the acetabulum associated with superior joint space narrowing. (A) Coronal T1-weighted image. (B) Sagittal FS PD FSE image.
FIGURE 3.233 ● OA superimposed on osteonecrosis of the femoral head (secondary OA). Coronal T1-weighted image.
FIGURE 3.234 ● Medial joint space narrowing in osteoarthritis variant on coronal (A) and axial (B) FS PD FSE images.
FIGURE 3.235 ● Coronal T1-weighed (A) and FS PD FSE (B) images of subchondral marrow edema associated with OA affecting both the acetabular and femoral sides of the joint. The femoral head edema is associated with a subchondral cyst.
Labral tears, paralabral cysts (Fig. 3.238), and synovitis (intermediate signal on FS PD FSE) are associated with OA. Synovitis is seen in association with an inflammatory component of OA. This is distinct from processes where degenerative arthritis may develop as a complication of an inflammatory process such as rheumatoid arthritis. Synovium-filled degenerative cysts about the hip are identified with low signal intensity on T1-weighted images and with uniform high signal intensity on T2-weighted or T2*-weighted images. When these cysts present within the subchondral bone of the acetabulum they are referred to as Egger—s cysts.222
OA may also be associated with or superimposed on osteonecrosis of the femoral head. In osteonecrosis, there is greater involvement of the femoral head prior to joint space narrowing and reciprocal changes within the acetabulum.
In selected cases, MR arthrography may be required to identify small posttraumatic or degenerative chondral lesions. FS PD-weighted FSE sequences will additionally demonstrate signal abnormalities within the articular cartilage surface.
The first line of treatment involves activity modification and support (e.g., a cane) and nonsteroidal anti-inflammatory medications. When these modalities are no longer effective, surgery may be considered. The most common surgical procedure is total joint replacement, but osteotomies and arthrodesis remain viable options in appropriately selected patients. If FAI is detected prior to the progression to advanced OA, treatment options should also include arthroscopic intervention.
Loose Bodies
Loose bodies, also referred to as free fragments or joint mice, include free-floating or adherent intra-articular fragments. They are most frequently located in the acetabular fossa (Fig. 3.239) but may also be seen in other capsular locations (Fig. 3.240), including the anterior joint capsule, recesses around the zona orbicularis, and the perilabral sulcus. Loose bodies vary in size from small chondral fragments to larger osteochondral fragments and are round to oval or elongated.




They occur more commonly in older adults, due to associated OA, and in males slightly more often than in females. Their development may be related to the inelasticity of the fibrous capsule of the hip, which is reinforced by the iliofemoral, pubofemoral, and ischiofemoral ligaments. In addition, there is no articular cartilage surface for the fovea capitis of the femoral head. Loose bodies may be associated with trauma (commonly secondary to posterior dislocation and acetabular fracture), OA, pigmented villonodular synovitis (PVNS), and synovial chrondromatosis/osteochondromatosis. Crystal-induced arthropathies, such as gout and calcium pyrophosphate dihydrate deposition (CPPD), as well as rheumatoid arthritis, infection or septic arthritis, AVN, and LCP, may all predispose to the formation of loose bodies. OA, however, remains the most common source of chondral debris.

FIGURE 3.236 ● Advanced OA with osteophytosis, joint space narrowing, and denuded chondral surfaces. (A) Coronal color illustration of OA. (B) Coronal T1-weighted image. (C) Eggers cyst in acetabular roof with enhancing reactive edema and adjacent microacetabular insufficiency fracture. Sagittal enhanced T1-weighted image. (D) Destructive Postel coxarthropathy associated with chondrolysis without osteophytes shown for comparison. Coronal T1-weighted image.
FIGURE 3.237 ● Coronal T1-weighted (A) and FS PD FSE (B) images of femoral head remodeling in advanced OA with joint space loss.
FIGURE 3.238 ● Paralabral cyst associated with OA. The cyst has intermediate-signal-intensity synovial thickening. Coronal FS PD FSE image.
FIGURE 3.239 ● Acetabular fossa loose bodies related to calcified chondromatosis fragments. Coronal T1-weighted image.
Pathologic and histologic changes include the finding of osseous fracture fragments, acetabular fractures, osteochondral fractures, chondral fractures, traumatic labral tears and free-floating labral fragments, chondral degeneration and sloughing, synovial proliferations, and proteinaceous debris in the setting of infection. The microscopic appearance is laminated, with identification of proliferation of concentric layers of new cartilage and bone, and cartilaginous metaplasia can be seen in osteochondromatosis.
Patients usually present with locking or catching of the hip and pain secondary to retained material in the acetabular fossa. Additional signs and symptoms are clicking, snapping, and popping. Symptoms are aggravated by activity.
Radiographic Appearance
Initial investigation by plain films, usually using AP and frog-leg views, is often insensitive, even for bony or calcified bodies. Chondral loose bodies (non-radiopaque) and particulate matter and debris typically cannot be visualized. Predisposing conditions, such as fractures (acetabular, osteochondral, or femoral head), OA, AVN, or LCP, can frequently be identified, as can the donor site.
MR Appearance
Surface coil imaging of the hips has improved the identification of intra-articular loose bodies, which may be missed on images acquired with body coils and larger FOVs. On axial images, interruption of the low-signal-intensity space between the femoral head and the acetabulum is interposed with cartilaginous or osteocartilaginous tissue. A cartilaginous loose body demonstrates low to intermediate signal intensity and is not detectable on corresponding radiographs. The haversian fat pad or pulvinar in the acetabular fossa should not be confused with a loose body when viewing a T2*-weighted contrast image.
On T1- and PD-weighted images expected findings include hypointense to intermediate-signal-intensity fragments or, less commonly, osteochondral fragments with marrow fat signal and a hypointense sclerotic border. On FS PD FSE or STIR images the fragments are hypointense to intermediate in signal intensity, with hyperintense adjacent synovial fluid. They may be free-floating or adherent to synovium. Evaluation of the donor site reveals a defect in the chondral surface of the femoral head or acetabulum.
On MR arthrograms osseous, calcified, chondral, or osteochondral bodies can be visualized, as can particulate matter and debris. The donor site is also well displayed (Fig. 3.241), although MR arthrography is less sensitive to subchondral changes or basal chondral degeneration.
Unless surgically removed, most loose bodies remain in the joint and may enlarge over time. Rarely they are resorbed. Loose bodies secondary to an underlying joint disorder, synovitis, and particulate debris are treated conservatively and improve when the underlying pathology is corrected. Infection is treated with antibiotics to avoid joint destruction. Most loose bodies (i.e., osseous fracture fragments, ossified or calcified loose bodies), however, are removed arthroscopically. Chondral and osteochondral fragments may be reattached to the donor site or removed. Loose bodies associated with chondromatosis/osteochondromatosis or PVNS and free-floating labral fragments are removed arthroscopically.
Synovial Chondromatosis
The hip is commonly involved in synovial chondromatosis (osteochondromatosis), a monarticular synovium-based cartilage metaplasia (Fig. 3.242).223 Development of intra-articular loose bodies may result in destruction of the hyaline cartilage and progress to OA. On FS PD FSE MR images, multiple ossified loose bodies are seen as foci of intermediate signal intensity, bathed in the surrounding joint effusion, which is bright in signal intensity. These nodules may demonstrate the high-signal-intensity characteristics of fatty marrow on T1- and T2-weighted images. The metaplastic cartilaginous nodules may progress from a uniform small size to larger detached cartilaginous bodies. Calcification may be seen within the cartilaginous hypointensity on MR.
Rheumatoid Arthritis
Rheumatoid arthritis is a systemic autoimmune inflammatory disorder of unknown etiology primarily affecting the synovial membranes and articular surfaces of the small joints of the hands and feet. It is found in 1% of the population. Adults 25 to 60 years of age are most commonly affected, with a peak incidence from 40 to 60 years of age. Females are affected three times more often than males.
Diagnosis, Etiology, and Clinical Features
Rheumatoid arthritis is an inflammatory condition of synovial tissue with bilateral, symmetric joint involvement. The hip joints are not usually involved until late in the disease process. Although the cause remains unknown, the disorder is associated with HLA-DR4 and has been classified as an autoimmune


disease. There appears to be a genetic predisposition to inheritance of the HLA-D antigen. Immune complexes can be found in the articular cartilage in this disease, but these complexes have not been shown to stimulate inflammatory reactions in peripheral blood lymphocytes or monocytes in vitro.224 An infectious etiology has also been postulated, and arthrotropic parvoviruses and lentiviruses have come under suspicion. These viruses are thought to induce T4 helper cells and cytokine-mediated oligoclonal B-cell responses producing IgG and IgM rheumatoid factors.

FIGURE 3.240 ● (A) Color axial section showing anterior capsule loose body. (B) Coronal T1-weighted image depicting perilabral sulcus loose body in a former ballet dancer with FAI.
The criteria for the diagnosis of rheumatoid arthritis were established in 1958 and modified in 1987.225 These criteria include:
  • Morning stiffness
  • Arthritis affecting three or more joints
  • Involvement of the joints of the hand
  • Symmetric joint involvement
  • Rheumatoid nodules
  • Presence of rheumatoid factor in the serum
  • Radiographic changes
Although rheumatoid factor is estimated to be positive in approximately 75% of rheumatoid arthritis cases, the presence of rheumatoid factor alone is not sufficient for a diagnosis of rheumatoid arthritis. Conversely, the diagnosis can be made in a patient who tests negative for rheumatoid factor if other criteria are met.
In the hip, the most commonly affected locations are the femoral head, the acetabulum, and the joint capsule. There is usually diffuse involvement of the femoral head, and the entire joint is at risk. Morphologically there is concentric loss of joint space and a protrusio deformity (medial displacement of femoral head).
Pathologically and histologically the disease is characterized by synovial inflammation; pannus; tendon tears and ruptures; articular cartilage erosions; superior and medial protrusion of the hip into the pelvis; subchondral synovial cysts; hyperplasia of synovial cells, redundant synovial folds, villae, and masses; lymphocyte and plasma cell infiltration of the synovial membrane; and fibrinous exudates.
Clinically, there is an insidious onset of hip pain and stiffness, and four of the seven criteria for diagnosis must be present. Malaise, weakness, weight loss, myalgias, and fever are not uncommon constitutional symptoms, and they are accompanied by joint swelling, tenderness to palpation, and pain with active and passive range of motion. Autoimmune antibodies, including rheumatoid factor (serum IgM antibody in 70% of cases and antibodies directed against the Fc fragment of IgG) and serum antinuclear antibodies (ANA) in 30% of cases, are a prominent laboratory feature.
Radiographic Appearance
Approximately 50% of patients with rheumatoid arthritis have radiographic evidence of hip disease, although plain film radiographs may be negative early in the disease.226,227 Radiographic changes in the hip are usually bilateral, although unilateral lesions have been described and may confuse the initial diagnosis.228 The earliest radiographic findings are symmetric loss of joint space, reflecting cartilage loss and periarticular osteopenia. There may also be juxta-articular osteoporosis, soft tissue swelling, and loss of the subchondral plate. Associated subchondral cysts are usually less than 1 cm in diameter. With progressive worsening


and eventual complete loss of joint space, bony erosion can occur, resulting in bare areas at capsular insertions and protrusio acetabuli (migration of the medial femoral head cortex medial to the ilioischial line) or axial migration of the femoral head. Protrusio acetabuli may also be associated with steroid therapy.

FIGURE 3.241 ● (A) Chondral flap lesion of the femoral head (FH). (B) A focal chondral lesion (arrow) can be seen superior to the fovea on a coronal FS T2-weighted FSE MR arthrogram.
MR Appearance
MR examination of the hip joint in patients with juvenile chronic arthritis (JCA), formerly known as juvenile rheumatoid arthritis (JRA), demonstrates irregularities of the femoral capital epiphysis and growth plate, as well as osseous erosions that may be underestimated on conventional radiographs.229,230 Thinning of the hyaline articular cartilage can be identified on coronal and sagittal images before there is radiographic evidence of joint space narrowing (Fig. 3.243). Low- to intermediate-signal-intensity synovial hypertrophy is seen in both the juvenile and adult forms of disease, and concentric joint space narrowing and marginal erosions adjacent to thickened pannus are seen in adult rheumatoid arthritis (Fig. 3.244). MR imaging is also useful for evaluating acute episodes of pain in rheumatoid arthritis patients on corticosteroid therapy who are at risk for osteonecrosis. Hip protrusio secondary to rheumatoid arthritis is more common than idiopathic protrusio acetabuli.
The following findings are seen on T1-weighted and PD FSE images:
  • Hypointense joint effusions
  • Hypointense subchondral erosions
  • A hypointense mass (fluid in iliopsoas bursa)
  • Hypointense acetabular and femoral head edema
FS PD FSE images show:
  • Hyperintense joint effusions
  • Joint capsule distention
  • Demineralization (juxta-articular bone loss) with marrow hyperintensity (on FS PD FSE or STIR images)
  • Attenuation or loss of the normally hypointense subchondral plate
  • Intermediate to hyperintense subchondral cysts without a sclerotic reactive interface
  • Femoral and acetabular erosions not confined to any specific quadrant (as would be expected in OA)
  • Hyperintense marrow edema
  • Inhomogeneity of effusions, synovium, and debris relative to hyperintense fluid
Intravenous contrast administration is used to enhance pannus tissue and to map the extent and distribution of synovial involvement.
Rheumatoid arthritis is a slowly progressive disease with intermittent flare-ups. Although it may follow an indolent course, the eventual result is cartilaginous destruction and joint obliteration. Other complications include joint effusions with capsular distention and pain, large synovial cysts, tendinous tears or disruptions, osseous destruction, fibrous or bony ankylosis, and AVN (secondary to steroid use).
The initial approach to treatment is conservative, with efforts directed at decreasing inflammation to delay joint destruction and preserve function. Drug therapy is useful in decreasing symptoms but has not been proven to alter the natural history of the disease. When drug therapy fails to control synovitis, synovectomy is an option. However, if there is radiographic evidence of significant joint destruction synovectomy is less likely to be beneficial, and the precise role of synovectomy in the hip has not been established. When medical management fails to control symptoms, surgical options include reattachment of severely displaced avulsed fragments and resection of weak bony unions and surgical reattachment. Total hip replacement provides good pain relief.
Ankylosing Spondylitis
Ankylosing spondylitis is an autoimmune disorder associated with HLA-B27. Although its presence is not diagnostic, approximately 90% of Caucasian patients with ankylosing spondylitis




are HLA-B27 positive. Unlike rheumatoid arthritis, which predominantly affects small joints, ankylosing spondylitis involves the spine and larger joints. The hip is frequently affected and may be the initial site of involvement. Overall, 17% to 35% of patients with ankylosing spondylitis have hip disease.231 Hip disease is most commonly found in patients with adolescent onset of disease. The role of MR imaging in ankylosing spondylitis has not been defined, and initial assessment with conventional radiography is the standard for diagnostic evaluation.

FIGURE 3.242 ● Spectrum of synovial chondromatosis (osteochondromatosis). (A) Small cartilage-signal-intensity posterior intra-articular bodies on a sagittal FS PD FSE image. (B) Characteristic cartilaginous nodules on gross examination. (C) Large detached cartilaginous bodies in the acetabular fossa and inferior capsule. (D) Sclerotic hypointense calcified cartilaginous bodies in the anterior hip capsule. Coronal PD FSE image.
FIGURE 3.243 ● Early juvenile chronic arthritis. (A) T1-weighted coronal images of normal, age-matched control hips in a 9-year-old child with intact, intermediate-signal-intensity articular cartilage (large arrow). Normal low-signal-intensity fovea are present (small arrows). (B) In the early stages of juvenile chronic arthritis, T1-weighted coronal image shows attenuated articular cartilage (arrow).
FIGURE 3.244 ● Rheumatoid arthritis with hypertrophic synovium, concentric joint space narrowing, and reactive subchondral edema. (A) Coronal color illustration of rheumatoid arthritis in adult. (B, C) Hypertrophic inflammatory synovium on axial FS PD FSE images. (D) Arthroscopic view of synovitis.
FIGURE 3.245 ● PVNS with hemosiderin-laden synovium eroding the medial femoral head-neck junction. (A) Coronal color illustration with subchondral erosion adjacent to proliferation of the synovium. (B) Coronal FS PD FSE image. (C) Arthroscopic view illustrated with insets of chondrosis and PVNS tissue. (D) Direct arthroscopic view of PVNS lesion above inferior capsule.
Pigmented Villonodular Synovitis
Pigmented villonodular synovitis (PVNS) results from an abnormal proliferation of synovial cells (Fig. 3.245). The etiology is unknown, and although similar lesions can be induced experimentally in animals by repeated intra-articular injections of blood, patients usually deny significant trauma in the clinical situation. Histologically, there is a hyperplastic layer of synovial cells with large numbers of histiocytes and giant cells containing hemosiderin, which causes the pigmentation.
The disease usually presents in the third to fifth decade of life, with clinical complaints of joint pain aggravated by activity. Although the knee is the joint most commonly affected, the hip joint may also be involved. The diagnosis can be difficult, and delay in diagnosis is common. In a study by Chung and Janes, the delay in diagnosis ranged from 2.5 to 11 years after the onset of symptoms.232
Early in the disease, radiographic findings are often negative. Later, multiple cystic areas can be seen in the acetabulum and femoral head and neck. Unlike the cysts in OA, cysts


in ankylosing spondylitis are often located away from the areas of maximum weight-bearing. Arthrography can be very helpful diagnostically. The arthrogram usually demonstrates a large joint space with many irregularities. On aspiration, blood-stained yellow joint fluid is noted.

FIGURE 3.246 ● (A) Large cystic erosions of the femoral neck as seen on an AP radiograph in a patient on chronic renal dialysis (arrows). (B) T1-weighted coronal image shows intermediate-signal-intensity amyloid deposits in the femoral head and neck (arrow). (C) Axial CT shows multiple cystic erosions of the femoral head (arrows).
FIGURE 3.247 ● Amyloid arthropathy with diffuse hypointense amyloid deposits in areas of capsular thickening. Axial FS PD FSE image.
MR examination using FS PD FSE images and especially T2*-weighted sequences is sensitive to the presence of hemosiderin in a hemorrhagic effusion or in PVNS of the hip.3,233 It may be difficult, however, to differentiate hemorrhagic effusion or hemorrhagic synovium from the repeated bouts of hemosiderin deposition that occur in PVNS. The MR characteristics of PVNS reflect the proportions of hemorrhage, hemosiderin, fibrous tissue, inflamed synovium, and effusion. Thus, low- to intermediate-signal-intensity areas may be defined on T2-weighted, T2*-weighted, or STIR images.
Synovectomy is the treatment of choice for PVNS. Radiation is now used sparingly and reserved for recurrent lesions or incomplete resections.234 Eventually, articular cartilage damage may necessitate a salvage procedure. Arthrodesis and total joint replacement are viable alternatives, depending on the patient—s clinical status.
Amyloid Hip
Patients receiving long-term hemodialysis are at risk for an osteoarthropathy that affects the hand, wrist, and less commonly the spine.3,235 Large cystic erosions (Fig. 3.246) have also been observed in the hip. These lesions are thought to represent a spectrum of amyloid (i.e., beta-microglobulin) deposition occurring in synovium, tendons, and cysts. In a chronic hemodialysis patient with amyloid of the hips, MR examination reveals intermediate-signal-intensity masses in the femoral head and neck on T1-weighted images.


There is only a minimal increase in signal intensity on T2-weighted images. MR examination also reveals an associated soft tissue component not evident on plain radiographs. Although amyloid deposits may mimic the imaging characteristics of PVNS, including hypointense deposits (Fig. 3.247), the more diffuse capsular thickening and bilateral involvement indicate amyloid arthropathy, given the history of dialysis.

Calcium Pyrophosphate Dihydrate Crystal Deposition (CPPD) Disease
CPPD targets middle-aged and older men and women equally. In its asymptomatic presentation chondrocalcinosis may be the initial finding. The term pseudogout is used when symptomatic presentation occurs. Calcium pyrophosphate arthropathy is associated with CPPD crystal deposition and structural chondral damage and results in eventual joint space narrowing, subchondral sclerosis, and osteophytosis. MR identification of CPPD crystals requires the use of gradient echo imaging to produce local susceptibility artifact surrounding the affected articular cartilage (Fig. 3.248).
Stellate Lesion and Plica
The stellate lesion, more prominent in young adults but also evident in older patients, is a normal process located superior to the acetabular fossa within the acetabular roof. On MR examination in younger patients (adolescents), this lesion or crease may be mistaken for a traumatic articular lesion with an osteochondritis-like morphology (Fig. 3.249). At arthroscopy (Fig. 3.250), the lesion is viewed as an area of chondral thinning, similar to that seen in chondromalacia. It has not, however, been shown to contribute to symptoms of hip pain. The stellate lesion may be associated with a plica (Fig. 3.251) or fibrous cord that extends from the crease and is attached to the medial aspect of the affected chondral/subchondral surface of the acetabular roof and is directed toward the acetabular fossa.
The MR appearance is characteristic on coronal and sagittal images, on which it is depicted as a defect with discontinuity of the acetabular roof articular cartilage. A prominent subchondral osseous fragment may be present within the stellate lesion. The hypointense plica, which varies in thickness, is attached to the medial aspect of the fragment, which is either fully incorporated or hinged medially.
Separate from the stellate lesion, a physeal scar (Fig. 3.252) may be identified at arthroscopy demarcating the remnants of the triradiate cartilage. This physeal scar has a linear



morphology and is located in the medial aspect of the acetabulum with either anterior or posterior extension relative to the fossa. The physeal scar is not a fracture and should not be confused with the more superior stellate lesion.

FIGURE 3.248 ● CPPD crystal deposition disease with hypointense crystal deposits throughout the chondral surfaces. (A) Color coronal section. (B) Coronal T2* gradient-echo image with susceptibility artifact induced by the crystal deposition.
FIGURE 3.249 ● Stellate lesion in a 15-year-old associated with a thick plica. The plica is attached to the medial aspect of the stellate lesion and courses toward the pulvinar and acetabular fossa. (A) Coronal color section. (B) Coronal FS PD FSE image. (C) Lateral color illustration. (D) Sagittal FS PD FSE image.
FIGURE 3.250 ● Arthroscopic view of a stellate lesion with associated attenuated chondral surface and plica.
FIGURE 3.251 ● Stellate lesion in a teenager with superior acetabular irregularity and adherent plica cord adjacent to the medial aspect of the lesion and directed toward the acetabular fossa. (A) Coronal FS PD FSE image. (B) Sagittal FS PD FSE image. (C) Corresponding arthroscopic view demonstrating attached plica. (D) Arthroscopic view after a plical resection.
Fractures of the Proximal Femur and Acetabulum
Fractures about the hip may be associated with significant morbidity, especially when diagnosis and treatment are delayed.236,237,238 Femoral fractures are classified as either intracapsular or extracapsular. Intracapsular femoral neck fractures are subcapital, transcervical, or basicervical in location. The incidence of posttraumatic osteonecrosis increases as the fracture site nears the femoral head, culminating in a 30% incidence


for fractures in closest proximity to the femoral head. The less common capital fracture is an intracapsular fracture of the femoral head. Extracapsular fractures are intertrochanteric or subtrochanteric.

FIGURE 3.252 ● A physeal scar represents the remnant of the triradiate cartilage. This area is devoid of articular cartilage and may extend either posteriorly or anteriorly from the acetabular fossa.
Stress fractures of the hip most frequently involve the femoral neck. They occur in two patient populations: the young adult, in whom stress fractures result from overuse and repeated stress to normal bone (e.g., military recruits and runners); and in older patients with osteoporosis (especially women), in whom the fractures are more appropriately termed “insufficiency fractures” and may occur with normal activity or a seemingly insignificant increase in activity.239,240
Patients usually present with groin pain aggravated by weight-bearing. Passive movement is often painful, especially rotation. Radiographic findings are often normal, and symptoms can be subtle. A careful history and a high index of suspicion are necessary to avoid missing the injury.
Femoral Head Fractures
Femoral head or capital fractures are usually associated with a posterior hip dislocation. Femoral head osteochondritis dissecans or osteochondral fracture (Fig. 3.253) is a distinct lesion.
Diagnosis, Etiology, and Clinical Features
There is an oblique fracture of the femoral head relative to the long axis of the femoral neck. Fractures involving the central fossa (fovea) tend to be larger and fractures located below the central fossa are more likely to be smaller. Although relatively rare, this type of fracture is associated with acute shearing that occurs when the hip is dislocated. It is seen most often with posterior dislocation sustained in a motor vehicle accident. When associated with high-energy trauma it is usually seen in young adults (under 35 years of age), mostly males. Trauma secondary to falls is more likely to occur in patients over age 65 years.
Relevant anatomic considerations include the multiaxial, synovial ball-and-socket morphology of the femoral head and neck as well as the vascular supply that originates from the medial and lateral femoral circumflex arteries and includes the extracapsular vascular ring (cervical arteries). In adults, the ligamentum teres vascular supply to the head is insignificant.
Pathologic changes include a possible impaction fracture, possible fragmentation of surrounding osseous and cartilaginous structures, entrapment of fragments in the joint, and associated sciatic nerve compression (in posterior dislocation). In adolescents the capital femoral epiphysis may be sheared off. There may be signs of vascular disruption, hematoma, revascularization, and repair (callus and primary bone repair).
Clinically patients present with pain in the hip area, and identification of a dislocated hip is the primary concern. Immediate reduction of the dislocation is essential, since the risk of AVN increases substantially after 6 hours. No more than two or three attempts at closed reduction should be made due to the increased risk of AVN and iatrogenic injury. Associated injuries in high-energy trauma may include head, abdominal, and pelvic trauma.
Pipkin developed a four-stage classification system for femoral head fracture dislocations:
  • Type I: This fracture is located caudad to (below) the central fovea and ligamentum teres. There is disruption of the ligamentum teres but no other associated injuries.
  • Type II: This fracture is located cephalad to (above) the fovea and ligamentum teres. The ligamentum teres remains attached to the fracture fragment and there are no associated injuries.
  • Type III: This is a type I or type II fracture with an associated femoral neck fracture (sometimes caused by overly aggressive closed reduction).
  • Type IV: This is a type I or type II fracture with fracture of the superoposterior acetabular rim.
MR Appearance
Capital fractures are often radiographically occult, especially when the spherical morphology of the femoral head is maintained or when an area of impacted trabecular (subchondral) bone is involved. MR is used to determine the status of the involved fragment (as in situ or absent) and to identify extension of fluid across the chondral surface in unstable lesions. In femoral head fractures MR imaging demonstrates a circumscribed crater involving the articular cartilage and subchondral bone.241,242 Axial and sagittal images may provide better delineation of fracture morphology than coronal plane images.
FIGURE 3.253 ● Osteochondral fracture with mild subchondral plate depression. (A) Coronal T1-weighted image. (B) Sagittal FS PD FSE image. (C) Arthroscopic view of an osteochondral loose body. Donor site is not visible. Osteochondral fracture or osteochondritis dissecans with a crater morphology representing the osteocartilaginous fracture fragment. Osteochondritis dissecans occurs in response to an acute injury with shearing forces and may appear with similar characteristics as AVN.


Features seen on T1- or PD-weighted images include:
  • A hypointense fracture line (Fig. 3.254)
  • Hypointense femoral head edema, localized or diffuse
  • Hypointense to intermediate-signal-intensity hemorrhagic effusion
FS PD FSE images are used to evaluate complications and display:
  • Hyperintense femoral head edema (Fig. 3.255) and effusions
  • Hyperintense muscle strains and tears
  • Labral tears and hyperintense paralabral cysts
  • Chondral injuries, indicated by interruption of the intermediate-signal chondral surface
  • AVN
Anatomic or near-anatomic fracture alignment is essential in younger patients to preserve function and to avoid the complications of AVN and OA. The outcome depends on the type of femoral head fracture, the presence or absence of associated fractures (acetabular, femoral neck, or pelvic ring), and the length of time until reduction is achieved. The prognosis for Pipkin types I and II is better than for types III and IV.
Conservative treatment (closed reduction) is preferred for Pipkin type I fractures and a displaced inferior fragment is acceptable if it does not affect weight-bearing structures. For a Pipkin type II fracture, closed reduction can be used only if the fracture fragments are congruent.
The indications for surgery and open reduction include:
  • Failed closed reduction
  • Associated femoral neck fracture
  • Incongruent reduction
  • Intra-articular fragments
  • Fracture repair
Pipkin type II fractures are treated with open reduction and internal fixation (ORIF) for displaced or unstable fracture fragments. Pipkin type III fractures are treated with ORIF for younger patients (rigid pinning) and a hemiprosthesis for


older patients. Pipkin type IV fractures are treated with ORIF for displaced or unstable acetabular fractures in younger patients and total arthroplasty in older individuals. Impacted femoral head fractures are treated by surgical elevation and grafting. Postreduction treatment includes traction, minimal weight-bearing, and physical therapy. Common complications include AVN, posttraumatic arthritis, recurrent dislocation, and sciatic nerve injury.

FIGURE 3.254 ● (A) Capital fracture classified as an intracapsular fracture of the proximal femur. (B) Hypointense fracture line of the medial femoral head. Axial T1-weighted image.
Subchondral Femoral Head Fractures
Femoral head subchondral fractures are considered stress fractures in young patients and insufficiency fractures in older patients with abnormal bone and normal stress (Fig. 3.256). These fractures may mimic AVN or transient osteoporosis of the hip (TOH) (Fig. 3.257). Many cases previously diagnosed as TOH are in fact subchondral stress fractures. Surface coil imaging with high resolution and a small FOV is required to appreciate the subtle hypointense fracture line of the femoral head located superiorly and subjacent to the subchondral plate. This fracture line or segment remains hypointense on both T1-weighted and FS PD FSE images. There is diffuse edema, which is more hyperintense adjacent to the fracture site. Without surface coil and small FOV imaging techniques, the fracture component is overlooked and only the edema is appreciated. Subacute fractures (Fig. 3.258) demonstrate partial resolution of the femoral head/neck edema pattern. A hyperemic linear area may develop during the healing phase of the fractures. The differential diagnosis may also include rapidly destructive OA or Postel—s disease. However, joint space narrowing with chondrolysis is evident in this aggressive form of OA.
FIGURE 3.255 ● Posterolateral femoral head trabecular fracture without medial extension. (A) Coronal T1-weighted image. (B) Sagittal FS PD FSE image.


Femoral Neck Fractures
FIGURE 3.256 ● (AC) Subchondral stress fracture with subtle subarticular hypointense fracture line and edema that is most hyperintense adjacent to the involved subchondral trabecular microfracture. (A) Color coronal illustration. (B) Coronal T1-weighted image. (C) Coronal FS PD FSE image. (D) Insufficiency fracture in a 70-year-old patient. Imaging findings are the same as in a stress fracture in a younger patient.
Femoral neck fractures, also known as fractures of the proximal femur, subcapital femoral neck fractures, stress fractures,




and insufficiency fractures,161 can be subdivided into three general categories based on location (Fig. 3.259):

FIGURE 3.257 ● (A) Diffuse left femoral head and neck marrow edema that mimics transient osteoporosis of the hip on a T1-weighted large-FOV coronal image. (B) The distinct but subtle subchondral fracture is conspicuous on this coronal FS PD FSE image. (C) Metastatic disease may also produce a diffuse pattern of reactive (peritumoral) edema and should not be mistaken for transient osteoporosis. Coronal FS PD FSE image.
FIGURE 3.258 ● (A) Coronal T1-weighted images showing a subacute subchondral femoral head stress fracture. (B) Coronal FS PD FSE image of the resolution phase. The fracture line is hyperintense on the FS PD FSE image.
FIGURE 3.259 ● Fractures of the proximal femur are divided into intracapsular and extracapsular types. Subcapital fractures are common intracapsular fractures; the capital, mid- or transcervical and basicervical are uncommon.
FIGURE 3.260 ● Distraction-type transverse fracture of the superior femoral neck in a 90-year-old. The distraction fracture involves the tension side of the femoral neck and may become displaced; therefore, internal fixation is recommended. (A) Coronal T1 FSE image. (B) Coronal FS PD FSE image.
FIGURE 3.261 ● Compression-type medial fracture in the inferomedial femoral neck. These fractures are more common in the young athlete and rarely become displaced. (A) Coronal T1-weighted image. (B) Coronal FS PD FSE image. (C) Normal bony trabecular architecture of the proximal femur seen on conventional radiographs. A lack of integrity of the trabecular groups is associated with fracture comminution and decreased stability of fixation.
  • Subcapital fractures (common)
  • Transcervical fractures (uncommon)
  • Basicervical fractures (uncommon)
Diagnosis, Etiology, and Clinical Features
Transverse distraction stress fractures (Fig. 3.260) are usually insufficiency fractures involving the superior cortex of the femoral neck and occur most commonly in older patients. Compression stress fractures are more common in younger patients, with 50% occurring in individuals under 60 years of age. They range from incomplete to complete fractures traversing the femoral neck and may be limited to the medial cortex (Fig. 3.261) or may extend into the medial medullary cavity (Fig. 3.262). Subchondral edema is often more extensive than the associated fracture.
Anatomic considerations in the evaluation of femoral neck fractures include assessment of the calcar femorale (the weight-bearing bone of the femur from the inferomedial femoral neck cortex toward the lesser trochanter) (Fig. 3.263) and the blood supply to the femoral head (via the femoral neck from branches



of the circumflex arteries) (Fig. 3.264). Overall, 15% of runners develop a stress fracture (Fig. 3.265) at some time, and 5% to 10% of stress fractures involve the femoral neck.

FIGURE 3.262 ● (A) Medial femoral neck compression-type stress fracture. Fracture is hypointense on T1-weighted (B) and FS PD FSE (C) coronal images. Marrow edema is hyperintense on the FS PD FSE image.
FIGURE 3.263 ● Medial calcar stress reaction prior to the development of a stress fracture. (A) Coronal T1 FSE image. (B) Sagittal FS PD FSE image.
FIGURE 3.264 ● Vascular supply to the proximal femur with primary contribution from the circumflex femoral arteries. AVN of the femoral head is associated with intracapsular fractures. The tenuous blood supply to the femoral head derives from branches of the medial femoral circumflex artery. (A) Anterior perspective. (B) Posterior perspective.
In males femoral neck fractures have been seen in the military population in trainees with increased body mass index and poor fitness. Female athletes with an eating disorder and associated amenorrhea or premature osteoporosis are also at risk. A fall with impact on the greater trochanter and lateral rotation of the femur is a primary mechanism of injury. Cyclic loading with microfracture and torsional force may also cause femoral neck fractures. Training errors, such as improper footwear and uneven running surfaces, also predispose to stress fractures. Coxa vara also predisposes the athlete to the risk of fracture.
Pathologic and histologic changes include vascular disruption of bone, hematoma, revascularization, resorption of devascularized bone, and healing with callus versus primary bone repair.
The common clinical presentation is pain in the groin, anterior thigh, or knee that increases with weight-bearing or exertion and can be elicited by axial compression or greater trochanter percussion. There is also limitation of hip motion, particularly internal rotation.
Several classification schemes have been proposed for femoral neck fractures. The Pauwels classification243 is based on the angle the fracture line makes with the horizontal and divides fractures into three categories:



  • Pauwels I: The fracture line is 0° to 30° to horizontal.
  • Pauwels II: The fracture line is 30° to 70° to horizontal.
  • Pauwels III: The fracture line is more than 70° to horizontal.
FIGURE 3.265 ● Complete stress fracture in a 23-year-old runner extending from the medial to the lateral cortex of the femoral neck. (A) Coronal color illustration. (B) Coronal T1-weighted image. (C) Coronal FS PD FSE image.
FIGURE 3.266 ● Garden classification of femoral neck (subcapital) fractures. Stage 1 fractures are incompletely impacted fractures with valgus malalignment, stage 2 fractures are complete fractures without displacement, stage 3 fractures are complete fractures with partial displacement, and stage 4 fractures are displaced fractures with complete fracture segment diastasis. Displacement is based on the position of the medial compressive trabeculae.
FIGURE 3.267 ● Stage IV complete subcapital (femoral neck) fracture. In a complete fracture the femoral head is separated from the proximal femur but the medial trabeculae of the femoral head remain aligned with the acetabular trabeculae. (A) PD FSE image. (B) FS PD FSE image.
The Garden classification244 is the most commonly used system and divides fractures into four categories based on the degree of displacement of the fracture fragments (Fig. 3.266):
  • Garden 1: the fracture is incomplete or impacted
  • Garden 2: the fracture is complete and nondisplaced
  • Garden 3: the fracture is complete with partial displacement
  • Garden 4: the fracture is complete with total displacement (Fig. 3.267)
A separate classification for stress fractures was developed by Blickenstaff and Morris,245,246 who identified three types:
  • Type I: endosteal or periosteal callus without a fracture line
  • Type II: fracture line present
  • Type III: fracture is displaced
FIGURE 3.268 ● Femoral neck and acetabular insufficiency fracture in a 67-year-old woman. AVN is seen as a hypointense focus in the superior femoral head. (A) Coronal T1-weighted image. (B) Coronal FS PD FSE image.
MR Appearance
Radiographic signs of cortical disruption may be subtle, especially if there is either an incomplete fracture or a complete fracture without displacement of the medial trabeculae.247,248 MR examination is particularly useful in identifying nondisplaced femoral neck fractures that require surgical treatment but are not detected on routine radiography. Although bone scintigraphy is also sensitive to fractures, it is nonspecific. With MR imaging, it is possible to demonstrate the morphology of the fracture segment not detectable on bone scans. Early microtrabecular stress fracture, with intact medial and lateral cortices and a negative CT finding, can also be identified on MR images. T1-weighted coronal fat-suppressed FSE and STIR sequences are sensitive in detecting occult femoral and pelvic fractures.249,250 Associated soft tissue abnormalities, including adjacent edema and hemorrhage, are common. Contrast-enhanced MR imaging is useful for assessment of femoral head perfusion after femoral neck fracture. Intact perfusion is shown as a uniformly increased signal intensity in the proximal femoral diaphysis, femoral neck, and head.251 MR imaging can differentiate an


osteoporotic-related subcapital fracture of the femoral neck from a pathologic fracture. The radiographic appearance of a subcapital fracture may mimic a pathologic fracture secondary to rotation displacement of the fracture fragments.252 3D CT or MR rendering can display varus or valgus deformities and postoperative screw placement. In displaced fractures, complicating osteonecrosis can be excluded on an MR image, and viability of the femoral head can be assessed. Early detection of hypointense sclerosis in AVN (Fig. 3.268) is also possible. T1-weighted images provide the best contrast for the low-signal-intensity fracture segment in contrast to adjacent bright-signal-intensity marrow fat. STIR images have shown greater sensitivity than gradient-echo techniques in displaying associated hemorrhage and edema at the fracture site.

Typical findings on T1-weighted or PD FSE images include:
  • Hypointense signal in the medial femoral neck in stress fracture
  • A discrete well-defined hypointense fracture line with or without complete extension across the femoral neck
  • A microtrabecular stress fracture with intact medial and lateral cortices
  • Hypointense joint effusion/hemorrhage and synovitis
On FS PD FSE images, findings include:
  • Hyperintense marrow edema
  • Focal involvement of the medial cortex
  • Definition of fracture plane obliquity from 30° or less to over 70° (from the horizontal)
  • Differentiation of transverse from compression (medial) stress fractures
  • A hypointense fracture line
  • Marrow replacement and trabecular destruction in pathologic fractures
  • Direct visualization of associated chondral lesions in the acetabulum and femoral head
  • Possible association of a hyperintense acetabulum and edema in trabecular microfracture
  • Hyperintense adjacent soft tissue edema and hemorrhage
Extracapsular fractures, which are divided into intertrochanteric and subtrochanteric subgroups (Fig. 3.269), need to be distinguished from intracapsular femoral neck fractures. Extracapsular fractures are caused by direct injury (e.g., a fall) and affect an older population than intracapsular fractures. Intertrochanteric fractures are classified based on the number of fragments or extension of the fracture line. Subtrochanteric fractures are classified based on the relative proximal or distal level at the fracture line, fracture obliquity, and presence or absence of comminution. The risk of AVN is low because of the adequate blood supply for both intertrochanteric and subtrochanteric fractures.
Early diagnosis and aggressive treatment are usually required to minimize the development of complications such as delayed union, non-union, AVN (which occurs in 10% to 30% of cases), and secondary degenerative OA. Healing is not complete for 6 to 12 months. Conservative treatment (i.e., non-weight-bearing until the patient is pain-free and then progressive weight-bearing) may be considered for prefracture stress reaction and for nondisplaced compression (medial) stress fractures. Tension-transverse stress fractures and distraction injuries require immediate anatomic reduction and internal fixation regardless of the degree of displacement. Surgical options include Knowles pinning or endoprostheses.
Acetabular Fractures
Acetabular fractures occur secondary to significant trauma. The key finding in a fracture is interruption of the acetabular osseous column cortices. Acetabular fractures are generally seen more frequently in males.
Diagnosis, Etiology, and Clinical Features
Fractures may be located at the anterior (iliopubic/iliopectineal) column (Fig. 3.270) or the posterior (ilioischial) column (Fig. 3.271). They vary in size depending on whether they are simple or combination fractures. Simple fractures are posterior wall (Fig. 3.272), anterior wall, transverse, anterior column, or posterior column. The posterior wall fracture, the most common acetabular fracture type, is also referred to as a posterior lip or posterior rim fracture. A transverse fracture extends across both anterior and posterior acetabular columns. An anterior column fracture is usually seen in association with a posterior column or transverse fracture. Combination fractures are posterior column and posterior wall, transverse and posterior wall, complete (both anterior and posterior columns), and anterior and posterior column, and hemitransverse fractures. A transverse and posterior wall fracture represents the most common type of associated or complex acetabular fracture. Fracture of both the anterior and posterior columns is the most complex of acetabular fractures and is associated with comminution, rotation, and displacement. The spur sign, seen on axial CT images, is associated with an inferiorly directed apex of a triangular fragment of iliac bone (the spur).253
The lateral aspect of the acetabulum is formed by the anterior and posterior columns with the intervening superior dome of the acetabulum. Hip flexion and internal rotation are associated with posterior wall and column injuries.254 In posterior column fracture, hip abduction is part of the mechanism of injury, in addition to the indirect forces acting through the femur in the position of hip flexion (this is the mechanism of posterior wall fractures). Hip extension and external rotation are involved in anterior wall and column injuries.254


A T-shaped fracture is a transverse fracture with a vertical component that extends through the medial aspect of the acetabulum and divides the ischiopubic ramus. An anterior column fracture, in association with a transverse fracture, produces an anterior column and posterior hemitransverse fracture. A combination of posterior column fracture and posterior wall fracture is unusual.
FIGURE 3.269 ● (A) The modified Evans classification of intratrochanteric fractures divides them into three main types. Type I fractures are two-part fractures, classified as either type Ia (not displaced) or type Ib (displaced). Type II fractures are three-part fractures and are classified as either IIa (involving the greater trochanter) or type IIb (involving the lesser trochanter). Type III fractures involve both the greater and lesser trochanters and are unstable and difficult to reduce. Coronal T1-weighted (B) and FS PD FSE (C) images of a nondisplaced linear intertrochanteric fracture with extension across the superior aspect of the greater trochanter.
As mentioned, acetabular fractures are usually associated with significant (high-energy) trauma such as a motor vehicle accident or fall from a height. Anatomically, the acetabulum consists of contributions from the ilium, the ischium, and the pubic bone (which together form the innominate [hip bone]). The superior gluteal artery and the sciatic nerve exit the pelvis at the greater sciatic notch. In traumatic injury, femoral force is transmitted to the acetabulum and the position of the femur determines the type of acetabular fracture. In older patients osteoporosis may be associated with acetabular fractures in low-energy trauma, such as a fall directly onto the hip.
FIGURE 3.270 ● Axial FS PD FSE image of an isolated anterior (iliopubic) column fracture in a 28-year-old woman sustained in a motor vehicle accident.
FIGURE 3.271 ● Posterior (ilioischial) column fracture. An anterior force applied to the femoral head is transmitted to the posterior acetabular wall and column.
FIGURE 3.272 ● Posterior acetabular wall fracture after a posterior dislocation. A posterior acetabular wall fracture is more common than a posterior column fracture. With trauma, high-energy forces are transmitted or transferred from the femoral head to the acetabulum. The posterior wall is larger in area than the anterior wall. A posterior wall fracture occurs either in isolation or as part of a posterior column or transverse fracture. (A) Color illustration as viewed from anterolateral to posterior. (B) Sagittal FS PD FSE image.


Pathologic findings vary depending on the fracture site. The anterior column is the larger of the two columns and extends from the iliac wing to the anterior acetabulum to the superior pubic ramus. The posterior column extends from the sciatic notch to the posterior acetabulum to the ischium. The medial acetabular wall is quadrilateral plate and the posterior wall is a dome, superiorly located and the most weight-bearing surface of acetabulum. Fractures are characterized by vascular disruption, hematoma, revascularization, resorption of the devascularized bone ends, and callus versus primary bone repair.
Clinically, patients present with pain at the fracture site. In pelvic ring fractures there is often associated bladder rupture. Hip dislocations and femoral head/neck fractures may also be seen, as well as severe hemorrhage; solid organ injuries; and head, thoracic, and abdominal injuries.


Two classification systems are used for acetabular fractures. In the Judet and Letournel system255 fractures are categorized as either simple or elementary fractures with a single fracture plane or as combination fractures, with more than one elementary type. In Matta—s system classification is based on acetabular roof arcs and the force per unit area (pressure on the acetabulum). This differentiation is important, since nonoperative treatment may be adequate for fracture lines outside roof arc measurements and for fractures in which the femoral head is congruent to the roof in three projections.
FIGURE 3.273 ● A 78-year-old with acetabular insufficiency fracture that is hypointense on the coronal T1-weighted image (A) and hyperintense on the sagittal FS PD FSE image (B). CT may be needed to identify the fracture line(s). Postmenopausal and senile osteoporosis, pelvic irradiation, corticosteroid therapy, and rheumatoid arthritis are all risk factors.
Radiographic Findings
X-rays are usually the initial imaging study, but they may underestimate fracture complexity and intra-articular fragments. AP views of the pelvis and oblique (Judet) views are most helpful. The iliac oblique view is a 45° external oblique view for evaluation of the posterior column and anterior wall. The obturator oblique view is a 45° internal oblique view for evaluation of the anterior column and posterior wall. The iliopectineal or iliopubic line represents disruption and fracture of the anterior column and the ilioischial line represents disruption and fracture of the posterior column. Pelvic inlet/outlet views display pelvic ring fractures.
CT Findings
Acetabular fractures may also be assessed with thin-section CT and subsequent image reformation and 3D rendering. 3D reconstruction can be used to classify injuries of a single structural component (elementary fractures) and associated fractures representing combinations of elementary fracture types.256 Disarticulation of the femoral head on 3D CT renderings can be used to identify size, morphology, and number of osseous fragments, helpful in surgical planning. CT is superior to plain films for visualization of intra-articular fragments and associated pelvic ring and soft tissue injuries and/or hematoma. It also allows improved visualization of the weight-bearing dome of the joint (not detected on conventional radiographs). It is also used for detection of associated femoral head fractures.
MR Appearance
MR imaging in direct coronal, sagittal, and axial orthogonal planes is excellent for the evaluation of the acetabular columns and subchondral marrow.257 Retained fragments within the hip joint are usually seen on axial T1- and T2-weighted images. The association of AVN in posterior fractures (18%) can also be evaluated with MR imaging. In detecting injuries to the sciatic nerve and occult capital fractures, MR imaging is preferable to CT.257 Intra-articular fragments may be better displayed on thin-section CT, however.257
FIGURE 3.274 ● Coronal T1-weighted image demonstrating an acetabular roof insufficiency fracture with linear fracture morphology in a 90-year-old patient.


Fractures about the acetabulum and ilium (Fig. 3.273) may be associated with extension edema and demonstrate low signal intensity on T1-weighted images and high signal intensity on T2-weighted, T2*-weighted, FS PD-weighted FSE, or STIR images when there is no identifiable fracture segment.258 Thin-section, high-resolution CT or high-resolution MR (Fig. 3.274) may be necessary to achieve the precise cortical detail needed to display subtle cortical discontinuities. Metastatic disease (Fig. 3.275) involving the acetabulum should not be mistaken for an insufficiency fracture, and other sites of involvement should be assessed with both T1 and FS PD FSE images.
MR imaging affords direct visualization of cartilage prior to the appearance of ossification centers, which facilitates the identification of physeal fractures. In complex hemipelvis fracture-dislocations, MR imaging or CT can be used to assess interruptions of both the anterior and posterior pelvic ring segments and sacroiliac joint separation.
Typical findings on T1- or PD-weighted images include:
  • A hypointense fracture line and associated subchondral edema
  • Intra-articular fragments that may either demonstrate marrow fat signal or be sclerotic and appear hypointense
  • Pelvic ring fractures, best seen on coronal and axial images.
FS PD FSE images allow improved visualization of the medial wall acetabular fossa and show:
  • Hyperintense marrow edema adjacent to the fracture site
  • Associated pelvic ring and femoral head fractures
  • Hypointense free fragments
  • Disruption of the intermediate-signal-intensity chondral surfaces
  • Muscle trauma, including hyperintense edema and hemorrhage
FIGURE 3.275 ● Metastatic breast carcinoma mimicking the appearance of an acetabular insufficiency in a 34-year-old patient. Other lesions are identified on the large-FOV T1-weighted image. (A) Coronal FS PD FSE image. (B) Coronal T1-weighted image.
Most injuries are treated surgically, although some nondisplaced or minimally displaced fractures may be treated conservatively. Conservative treatment consists of bed rest, femoral traction, and non-weight-bearing with crutches. Surgical options include ORIF and total hip arthroplasty. Complications are not uncommon and include heterotopic ossification, infection, AVN, posttraumatic arthritis, deep venous thrombosis (DVT) in the deep pelvic and lower extremity veins, nerve damage (to the sciatic, superior gluteal, or femoral nerves), and the Morel-Lavallée lesion (an internal degloving injury causing local and regional hemorrhage associated with the crush or shearing component of the injury; see earlier discussion).
Hip Dislocation


Hip dislocation is a traumatic disarticulation of the femoral head from the acetabulum of the hip. Approximately 70% of all hip dislocations are secondary to motor vehicle accidents (e.g., dashboard mechanism). Normally, the iliofemoral, pubofemoral, ischiofemoral, transverse, and femoral head ligaments maintain the femur in the acetabulum, and a high level of force is required for dislocation. Associated injuries frequently include fracture of the acetabulum, the femoral head, or both.
FIGURE 3.276 ● Posterior dislocation of the hip. (A) Posterior dislocations occur when the knee and hip are flexed and a posterior force is applied at the knee. These injuries are usually the result of a motor vehicle accident or a fall from a height, which may occur in sports such as snowboarding. Axial (B) and sagittal (C) FS PD FSE images showing posterior dislocation with a posterior wall fracture and a trapped and ruptured obturator internus tendon. Associated injury to the sciatic nerve may be caused by compression or laceration from a posterior osseous acetabular fragment.
Diagnosis, Etiology, and Clinical Features
Posterior dislocations (Fig. 3.276), in which femoral internal rotation and adduction places the femoral head lateral and superior to the acetabulum, is the most common type of injury, occurring in over 90% of cases. Anterior cortical fractures of the femoral head and fractures of the acetabular rim are associated with posterior dislocations.259,260 Anterior dislocations, in which the femoral head is displaced into the obturator, pubic, or iliac regions, occur less frequently and are most commonly identified anteroinferiorly.158,261 Traumatic anterior dislocations are classified into superior and inferior types. Associated impaction fractures may lead to the development of traumatic arthritis.262 In central (medial) dislocations the femoral head protrudes into the pelvic cavity. Anterior dislocation and central fracture-dislocations account for less than 10% of hip dislocations.
The size of the dislocation varies, depending on associated osseous, cartilage, joint space, muscle, and ligament injuries. Other pathologic findings include osseous fragments and joint space widening. Posterior dislocation may be associated with sciatic nerve injury secondary to compression or laceration and local hematoma, and anterior dislocation may be associated with injury to the femoral nerve and artery.
Traumatic injuries from motor vehicle accidents and sports injuries account for most hip dislocations in patients (usually male) less than 35 years of age. In older patients, over 65 years, trauma secondary to a fall is the most common mechanism.
The clinical picture is dominated by pain and a characteristic deformity but varies depending on the location of the dislocation.
Posterior dislocations are characterized by:
  • Hip and gluteal pain
  • P.282

  • Shortening, adduction, internal rotation, and flexion of the lower extremity
  • A lack of range of motion and inability to bear weight
  • Sciatic nerve injury with loss of sensation in the posterior leg and foot and inability to dorsiflex and plantar flex
  • Hematoma and soft tissue swelling (Fig. 3.277)
  • Associated rupture of the ligamentum teres (Fig. 3.278)
FIGURE 3.277 ● Hematoma associated with a posterior dislocation is compressing the sciatic nerve. Other associated injuries include tears of the obturator externus and internus and quadratus femoris, gemelli, and gluteus minimus. Axial FS PD FSE image.
Anterior dislocations are characterized by:
  • Hip, gluteal, and groin pain
  • External rotation, adduction, and extension of the hip
  • Inability to walk and bear weight
  • Femoral nerve and femoral artery injury with pain, pallor, absence of the pulse, loss of motor function, and absent reflexes
Central dislocations are characterized by:
  • Shortening of the affected limb
  • Abduction or adduction and internal or external rotation of the hip
  • Intrapelvic soft tissue injury and hemorrhage
Hip dislocations with femoral head fractures are classified using the Pipkin system:
  • Pipkin I: fracture of the femoral head below the central fossa
  • Pipkin II: fracture of the femoral head involving the central fossa
  • Pipkin III: fracture of the femoral head and neck
  • Pipkin IV: fracture of the femoral head and superoposterior acetabular rim
Radiographic Findings
Typically, plain films are the initial diagnostic examination, and AP views are usually diagnostic. Lateral views may be necessary to evaluate the hip dislocated anterior or posterior to the acetabulum. Additional views occasionally used include oblique (Judet) views (the iliac oblique view, which is a 45° external oblique view, and the obturator oblique view, which is a 45° internal oblique view) and pelvic inlet or outlet views.
MR Appearance
Chronic arthritis and AVN may complicate dislocations and fractures of the hip, and MR imaging is helpful in their early identification. Also, axial MR images may be used to follow the course of the sciatic nerve, which is injured in 8% to 19% of posterior hip dislocations. T1- or PD-weighted images are usually used to evaluate complications such as AVN with a hypointense subchondral fracture and central marrow fat signal intensity, loose bodies with central marrow fat signal intensity, labral tears with intermediate signal, chondral injuries, and occult fractures. On FS PD FSE images there is hyperintense marrow edema of the anterior or posterior acetabular rim, and in posterior displacement an anteroinferior fragment of the femoral head may be seen as well. In one case of posterior fracture-dislocation of the hip, MR imaging revealed an impacted femoral head fracture (low signal intensity on T1-weighted images), an acetabular rim fracture (high-signal-intensity hemorrhage), and multiple intra-articular fragments that were subsequently removed through an arthroscope. At a 6-month follow-up, MR imaging showed the development of osteonecrosis at the initial fracture site. Thus, it may be difficult to predict the subsequent development of osteonecrosis in a patient sustaining a low-signal-intensity compression fracture of the femoral head.
Fracture-dislocations are considered an orthopaedic emergency and are associated with a high degree of morbidity and mortality secondary to significant trauma. Accompanying injuries frequently include severe intra-abdominal, intrapelvic, and head injuries as well as pelvic ring fractures and severe hemorrhage. The longer the hip remains dislocated, the higher the incidence of AVN; therefore, prompt reduction of the hip and treatment of any associated fractures are essential.
In uncomplicated cases closed reduction is successful in 76% to 93% of patients. Reduction is accomplished using maneuvers that re-create the deforming force and then applying longitudinal traction. For posterior dislocation this includes flexion, adduction, and internal rotation—the Stimson maneuver, which is performed with the patient in the prone position, and the Allis maneuver, which is performed with


the patient in the supine position. For anterior dislocation, abduction, external rotation, and extension are used.

FIGURE 3.278 ● Ruptured ligamentum teres associated with a posterior dislocation. (A) Coronal illustration of ruptured ligamentum teres at its foveal attachment. The discontinuity of the ligamentum teres is assessed on both coronal (B) and axial (C) FS PD FSE images. An associated femoral head contusion can be seen on the coronal image (B).
Open reduction is required for failed closed reduction, intra-articular loose bodies, interposed soft tissue, and concomitant femoral head-neck fractures. When fractures are present, the prognosis is not as good. Recurrent dislocations indicate disruption of the ligamentous support of the hip.
Common complications include AVN, OA, sciatic nerve injuries, femoral nerve or artery injuries, and DVT.
Thigh Splints


Adductor insertion avulsion syndrome (Fig. 3.279) or thigh splints involve the proximal to mid-femoral insertion of the adductor muscles.263 MR imaging demonstrates a thin rim of hyperintensity subjacent to the medial periosteum of the proximal to mid-femoral shaft. Coronal or sagittal images are used to identify the longitudinal extent (which may vary from 4 to 10 cm) of the involved femoral diaphysis. In both the medial tibial stress syndrome and the adductor insertion avulsion syndrome, the hyperintense signal changes may be restricted to the periosteum or involve the medullary bone and cortex. The pull of the adductor longus and brevis tendons is thought to produce the periosteal changes observed in thigh splints.
FIGURE 3.279 ● Thigh splint with posteromedial periosteal edema tracking along the adductor insertion. (A) Color axial cross-section through the affected periosteum. (B) Axial FS PD FSE image. (C) Sagittal FS PD FSE image.
Pubic Rami Stress Fractures and Osteitis Pubis


Pubic rami stress fractures include incomplete or complete fractures of the pubic ramus.264,265 Inferior pubic ramus stress fractures (Fig. 3.280) are most commonly seen in female runners or military recruits and involve the pubic ramus adjacent to the symphysis. The mechanism of injury in these fractures is related to the pull of the adductor magnus muscle. Insufficiency fractures represent approximately 1% of cases and are most commonly seen in women over 55 years of age. Osteitis pubis (Fig. 3.281) is a noninfectious inflammation adjacent to the pubic symphysis involving the medial aspect of the superior pubic ramus. It is associated with muscle imbalance between the abdominal and adductor muscles and abnormal vertical motion of the pubic symphysis. Four clinical types of osteitis pubis have been defined:
FIGURE 3.280 ● Color illustration of bilateral inferior pubic rami stress fractures. Inferior perspective.
  • Noninfectious
  • Infectious
  • Sports-related
  • Degenerative
Diagnosis, Etiology, and Clinical Features
Several anatomic features are relevant to the understanding of pubic rami stress fractures. The origin of the gracilis muscle is the lower half of the pubic symphysis and the upper half of the pubic arch. The origin of the pectineus is the pectineal line, the pubis between the iliopectineal eminence and the pubic tubercle. The origin of the adductor longus is the anterior pubis angle between the crest and the symphysis, and the origin of the adductor brevis is the outer surface of the inferior ramus pubis. The adductor magnus originates at the ischial tuberosity, the rami of the ischium, and the pubis. The obturator externus originates at the outer margin obturator foramen.
The most common cause of pubic rami injury is a fatigue fracture from repetitive loading of normal bone. In insufficiency fractures, which may occur in the superior pubic rami, injury is caused by normal forces applied to abnormal or weakened bone. Bone failure secondary to cyclic, repetitive muscle


contraction is related to insufficient repair time and osteoclastic resorption that outpaces osteoblastic bone formation.

FIGURE 3.281 ● Osteitis pubis directly adjacent to the pubic symphysis may occur in sports requiring excessive twisting and turning (such as soccer) or from repetitive shear stress with excessive side-to-side motion, as occurs in runners. (A) Coronal PD-weighted image. (B) Coronal FS PD FSE image. (C) Corresponding coronal color illustration illustrates parasymphyseal edema.
Specific etiologic factors include:
  • In female runners and military recruits, inferior pubic rami fractures result from the specifics of female versus male pelvic geometry, an increased stride (gait) length-to-height ratio compared with taller male recruits, and decreased muscle bulk, which subjects bones to greater forces.
  • Fractures that occur after hip arthroplasty are probably stress fractures related to increased activity with the new prosthesis.
  • Insufficiency fractures are seen most often in older women with postmenopausal osteoporosis. They may be secondary to sacral insufficiency fractures, which cause increased forces to the pubic arch.
  • Tensile stress, generated by muscle mass originating from the pubic ramus, is another mechanism of injury.
  • Malgaigne fracture (see discussion below)
Fractures may be unilateral or bilateral parasymphyseal and in athletes are usually associated with the inferior pubic ramus. Fractures of the superior pubic ramus are less frequent and are more likely to be unilateral insufficiency fractures associated with osteitis pubis (Fig. 3.282). Posttraumatic ischiopubic rami fracture associated with ipsilateral sacroiliac joint disruption may mimic a pubic rami stress fracture.
FIGURE 3.282 ● Osteitis pubis in a football player with a discrete fracture of the left medial superior pubic ramus. Stress fractures in athletes commonly occur in the inferior pubic ramus as a result of the pull of the adductor magnus muscle unrelated to the osteitis pubis. Coronal FS PD FSE image.
Callus formation, absence of a soft tissue mass, osteoclastic resorption, lamellar bone filling of osteoclastic cavities, new periosteal and endosteal bone, and a periosteal reaction are additional pathologic and histologic findings.
Pain dominates the clinical picture, usually groin pain but sometimes gluteal and thigh or inguinal, perineal, or adductor pain. There is point tenderness at the inferior pubic ramus and abduction and resisted abduction are painful, as is external hip rotation. Pain is usually relieved by rest. There may be an antalgic gait, and the standing sign (patient unable to stand unsupported on the affected leg) is positive. Athletes may provide a history of intensified training.
MR Appearance
T1- and PD-weighted images are used to identify hypointense marrow edema (on T1-weighted images) and to differentiate between unilateral and bilateral fractures. It may or may not be possible to visualize the fracture line and hypointense edema or soft tissue thickening.
FS PD FSE sequences are excellent for characterization of hyperintense marrow edema in both inferior pubic rami stress fractures and parasymphyseal osteitis pubis. Fractures may be visualized as a single fracture line perpendicular to the long axis of the superior pubic ramus, in contrast to the hyperintense changes of osteitis pubis. Adjacent fracture or resorption of medial superior pubic ramus avulsion fragments at the adductor insertion may be visualized on coronal images (Fig. 3.283). The secondary cleft sign (hyperintensity on STIR or FS PD FSE images in the symphysis pubis) is associated with dysfunction of the adductor gracilis or conjoined tendon.266 Pregnancy-related stress fractures may be unilateral and involve the superior pubic ramus (Fig. 3.284). These images


may also depict a hypointense thickened cortex or hyperintense edema parallel to the superior/inferior border of the pubic ramus.

FIGURE 3.283 ● Osteitis pubis with avulsion of the thick inferior arcuate pubic ligament. Marginal irregularity, symmetric bone resorption, sclerosis, and cortical avulsion may be seen in athletes with osteitis pubis. There is superior osseous beaking of the symphysis with mild impression on the base of the bladder. Coronal FS PD FSE image.
FIGURE 3.284 ● Left superior pubic ramus fracture that occurred during the third trimester of pregnancy. (A) Coronal T1-weighted image. (B) Coronal FS PD FSE image.
Most fractures heal with rest and cessation of training or stress-inducing activity. Improper treatment or failure to rest may result in non-union. The healing process is slow and may take 4 to 12 weeks or up to 5 months. Analgesics and physical therapy, including stretching, range-of-motion exercises, and muscle strengthening exercises, are sufficient for most patients. Surgery is rarely needed, except for non-union that does not heal with rest or a displaced fracture.
Sacral Insufficiency Fractures
Sacral insufficiency fractures (Fig. 3.285) are usually stress fractures of the sacral alar bone secondary to normal forces applied to weakened or abnormal (osteopenic) bone. They occur more often in patients, particularly women, over 55 years of age. Runners are also susceptible, as are others who participate in impact-type sports activities. Sacral fractures are frequently associated with postmenopausal osteoporosis and less commonly with rheumatoid arthritis, corticosteroid use, and pelvic irradiation or tumors.
The pelvic ring consists of the sacrum and the two innominate bones. The innominate bone is formed by the fusion of the ossification centers of the ilium, the ischium, and the pubis. The sacroiliac (SI) joints are located at the junction of the innominate bones and sacrum posteriorly. Anatomically important ligaments include the posterior SI, the sacrotuberous, the sacrospinous, and the iliolumbar. The sciatic nerve is derived from the roots of L4, L5, and S1-3 and may be compromised in sacral injury. The lumbosacral trunk of the lumbosacral plexus crosses anterior to the sacral ala.
Stress fractures of the sacrum may be associated with secondary pubic bone fractures but are less common (Fig. 3.286). Fractures of the sacral ala are often vertically oriented, parallel to the SI joints, and may or may not have a transverse fracture component. There is usually histologic evidence of osteoclastic resorption that is greater than osteoblastic activity and reduced bone mineral density.
Clinically, patients present with hip, gluteal, or groin pain with weight-bearing or ambulation and with either no history of trauma or only minimal to low-velocity trauma. There is usually point tenderness over the sacrum and, if patients are ambulatory, a gait abnormality and limited range of motion. The symptoms may be more prominent than physical signs.
MR Appearance
On T1- or PD-weighted images the sacral ala are hypointense and a hypointense fracture line may or may not be visualized. Fracture lines may be seen parallel to the SI joints, and there may be a transverse fracture component in bilateral fractures.
FIGURE 3.285 ● (A) Bilateral sacral alar insufficiency fractures with associated edema. (B) Coronal T1-weighted image identifying marrow edema and fracture morphology. (C) Coronal FS PD FSE image with characteristic linear regions of hyperintensity parallel to the sacroiliac joints.


On FS PD FSE images sacral marrow edema is hyperintense and a hypointense fracture line may be seen in unilateral fractures (Fig. 3.287). In bilateral fractures the “H” or “Honda” sign can be seen connecting the ala. There is no trabecular destruction, and there may or may not be adjacent soft tissue edema (no mass) and a concomitant pubic arch stress fracture. High-resolution images may be required to identify fractures.
The majority of sacral insufficiency fractures heal with conservative treatment, although some may progress to complete fracture. Healing is slow and may take 2 to 5 months. Complications are related to prolonged immobility and include DVT, pulmonary embolus, and decubitus ulcers. Falls related to the use of crutches and walkers may also complicate the healing process. Conservative measures include analgesics, bed rest, reduced weight-bearing, and physical therapy, including range-of-motion exercises, gait training, and muscle strengthening/ stretching. The surgical alternative is sacroplasty, an interventional radiologic technique similar to vertebroplasty consisting of percutaneous injection of polymethylmethacrylate to stabilize the fracture.
Malgaigne Fracture
The unstable Malgaigne fracture (Fig. 3.288) is usually a unilateral fracture involving the ischiopubic rami and should not be mistaken for a sacral insufficiency fracture. Careful assessment of both the superior and inferior pubic rami and ipsilateral SI joint is required to make an accurate diagnosis. Several subtypes of Malgaigne fracture have been identified:
  • Fracture with disruption of the ipsilateral SI joint
  • P.289

  • Fracture through a sacral wing
  • Fracture through the ilium
FIGURE 3.286 ● Superior pubic ramus insufficiency fracture associated with bilateral sacral alar fractures. Superior pubic ramus fractures may develop secondary to increased anterior arch strain resulting from the initial failure of the sacrum or posterior arch. (A) Coronal T1-weighted image. (B) Coronal FS PD FSE image. (C) Coronal FS PD FSE image.
In addition, the sacral nerves may be stretched in association with superior and posterior dislocation of the SI joint (Fig. 3.289).
Sacroiliitis (Fig. 3.290) can be distinguished from sacral alar insufficiency fractures by the identification of signal changes on both sides of the SI joint. It may be bilateral and symmetric or asymmetric or unilateral (Fig. 3.291). Ankylosing spondylitis (Fig. 3.292) is an example of bilateral and symmetric involvement. (A more detailed discussion of ankylosing spondylitis can be found earlier in the chapter.)
Muscle Denervation Patterns


Knowledge of the relevant distribution of the sciatic, femoral, and obturator nerves is helpful in understanding muscle denervation patterns. The sciatic nerve (Fig. 3.293) gives rise to two divisions, the tibial and peroneal. Sciatic and peroneal nerve palsies may occur following total hip arthroplasty. The femoral nerve may also be damaged after total hip arthroplasty, secondary to cement extravasation, lengthening or stretch, hematoma and pseudoaneurysm, or retractor placement. Invasive tumor about the hip may involve the lumbar plexus anterior to the sacral ala and SI joint (Fig. 3.294). The obturator nerve may be subject to entrapment neuropathy,267 which is a potential cause of hip and groin pain in the athlete. Focal nerve entrapment may be caused by fascial or vascular structures. Obturator injury has been associated with retroperitoneal hemorrhage (e.g., as occurs in pelvic fractures), an invading pelvic tumor (Fig. 3.295), endometriosis, hypogastric artery aneurysm, and obturator hernia. In some cases impingement has been attributed to fascial thickening around the vascular pedicle of the medial circumflex femoral artery. Zones of entrapment of the obturator nerve have been described and include:
  • Obturator canal
  • Interval between the pectineus and obturator externus
  • Interval between the adductor longus and brevis
  • Interval between the obturator externus and adductor magnus
  • Interval between the adductor magnus and the adductor brevis
FIGURE 3.287 ● Unilateral sacral insufficiency fracture of the left sacral alar. The majority of patients affected with pelvic insufficiency fractures are 60 years of age or older, with a female predominance. (A) Anterior perspective color illustration. (B) Coronal T1-weighted image. (C) Coronal FS PD FSE image.
Less commonly, obturator injury has been described after total hip arthroplasty.
FIGURE 3.288 ● (A) Malgaigne fracture with fracture of the superior and inferior pubic ramus and ipsilateral sacroiliac joint. (B) Coronal FS PD FSE image with left-sided sacroiliac joint disruption. (C) Corresponding anterior coronal image demonstrating left superior pubic ramus fracture.
FIGURE 3.289 ● Malgaigne fracture with superior and posterior dislocation of the sacroiliac joint and fracture of the superior and inferior pubic rami (ipsilateral). The superior shift of the hemipelvis is associated with stretching of the sacral nerves. Associated ischial spine and transverse process fractures are shown.
FIGURE 3.290 ● Bilateral sacroiliitis is hypointense on coronal T1-weighted (A) and hyperintense on coronal FS PD FSE (B) images. In ankylosing spondylitis, Reiter syndrome, and enteropathic sacroiliitis, the pattern of sacroiliac joint involvement is bilateral and symmetric. In psoriatic arthritis, rheumatoid arthritis, and juvenile chronic arthritis, it is bilateral and asymmetric.
FIGURE 3.291 ● Unilateral sacroiliitis involving the inferior aspect of the right SI joint. Unilateral involvement is seen in gout, infection, and OA. Coronal FS PD FSE image.
Osteomyelitis usually presents as acute hematogenous osteomyelitis (Fig. 3.296) in the pediatric patient and as chronic posttraumatic osteomyelitis in the adult patient (Fig. 3.297).268 Young children are most commonly affected; in adults infection is usually secondary to direct contamination (e.g., trauma, surgery). Infection may affect several different bone components—the periosteum (periostitis), the cortex (osteitis), the marrow (osteomyelitis), and the metaphysis and epiphysis. After the age of 1 year the physis acts as a barrier to epiphyseal spread, and metaphyseal capillary sinusoidal lakes and slow blood flow contribute to the development of infection. Involvement of subcutaneous fat results in cellulitis.
FIGURE 3.292 ● Ankylosing spondylitis with bilateral sacroiliitis complicated by a right sacral alar insufficiency fracture. Axial FS PD image.
Staphylococcus aureus is the most common infecting organism (80% to 90% of cases) in all age groups. Other common organisms include streptococci, Pseudomonas, Haemophilus, and Enterobacter. In adults chronic osteomyelitis and osteomyelitis secondary to trauma are most commonly seen. Hematogenous seeding via vascular metaphyseal bone is most common in children. Direct contamination is usually the mechanism in penetrating trauma and postoperative cases. Contiguous spread (Fig. 3.298) from a soft tissue infection or septic arthritis is also seen in adults. Histologically there is leukocytic infiltration of bone marrow; vascular compression; and necrosis, abscesses, and sequestra.
Patients present with pain, fever, restricted motion, and point tenderness. Laboratory tests reveal an elevation in the sedimentation rate, C-reactive protein, and white cells. There may also be soft tissue swelling with erythema and a sinus tract. Hematogenous osteomyelitis may be acute, subacute (Brodie—s abscess), or chronic (chronic recurrent multifocal osteomyelitis [CRMO]).
Radiographic Findings
Radiographs are insensitive for early osteomyelitis since changes are not seen for 10 to 14 days after onset of fever. As the disease progresses there may be evidence of soft tissue edema and swelling, a focal lucency to frank destruction of bone, a subperiosteal abscess (indicated by periosteal elevation and an underlying lucency), an intramedullary abscess (indicated by a focal lucency with or without a tract to the cortical surface), sequestration (necrotic fragments) and involucrum (periosteal bone) as parosteal ossification, and joint effusions (indicated by widening of the affected hip joint).
MR Appearance
MR, because of its sensitivity to marrow edema and soft tissue changes, is an excellent modality for early detection and overall evaluation of osteomyelitis. Contrast-enhanced images are particularly helpful. The sequestrum is hypointense on T1- and T2-weighted images and the involucrum (a periosteal reaction) is hypointense on T1- and T2-weighted images. Hyperintense adjacent soft tissue edema may also be depicted.
On T1- or PD-weighted images, findings include:
  • Hypointense marrow edema and cortical destruction (marrow edema is especially well displayed on T1-weighted images and has a high association with osteomyelitis)269
  • P.293




  • Hypointense reactive joint effusion (up to one third of patients with septic arthritis may lack an associated joint effusion)269
  • Hypointense soft tissue abscess
  • A sinus tract from the skin to the cortex
FIGURE 3.293 ● (A) Sciatic (tibial and peroneal) motor nerve distribution. (B, C) Semimembranosus and partial biceps femoris atrophy in a 45-year-old patient presenting with lower extremity involvement in facioscapulohumeral muscular dystrophy. (B) Axial T1-weighted image. (C) Axial FS PD FSE image.
FIGURE 3.294 ● (A) Femoral nerve distribution. Coronal (B) and axial (C) FS PD FSE images of invasive chondrosarcoma with proximal involvement of the posterior branches of the lumbar nerve roots.
FIGURE 3.295 ● Obturator nerve denervation associated with metastatic pelvic side wall mass. (A) Obturator nerve motor distribution. (B) Left lateral pelvic metastatic mass. (C) Adductor muscle denervation.
FIGURE 3.296 ● Septic joint complicated by osteomyelitis. In children there is separation of the blood supply to the metaphysis and epiphysis, resulting in hematogenous spread with the focus of infection in the metaphysis. Coronal FS PD FSE image.
FIGURE 3.297 ● (A) Osteomyelitis of the femoral diaphysis with sequestrum, sinus tract, and periosteal reaction. Axial T1-weighted (B) and FS PD FSE (C) images showing osteomyelitis with a hyperintense focus within the medullary cavity and hyperintense periosteal reaction in (C).
Characteristic findings on FS PD FSE images are:
  • Hyperintense marrow involvement
  • Hyperintense intraosseous abscess
  • Intermediate to hyperintense cortical destruction
  • Cloaca (periosteal opening) demonstrating focal hyperintensity in the hypointense periosteum
  • Intermediate to hyperintense sinus tract
  • Brodie—s abscess (a round abscess cavity seen in chronic pyogenic infections) with a hyperintense abscess, a hypointense sclerotic rim, and hyperintense marrow edema
  • Hypointense sequestrum
  • Associated cellulitis demonstrating reticulated subcutaneous hyperintensity
  • P.297




  • Associated myositis with muscle hyperintensity and enlargement
FIGURE 3.298 ● (A) Synovitis and femoral head nidus of infection that has extended to involve the acetabulum. In the adult, contiguous spread and direct implantation of infection from an adjacent soft tissue infection or wound are more common mechanisms. (BD) Osteomyelitis with femoral and acetabular erosions in an HIV-infected patient. The infected joint fluid is associated with intermediate-signal-intensity thickened synovium. Soft tissue inflammatory muscle edema is visualized on the large-FOV image. (B) Coronal FS PD FSE image. (C) Coronal T1-weighted image. (D) Coronal FS PD FSE image.
FIGURE 3.299 ● Tuberculous abscess associated with proximal femoral destruction (osteomyelitis). Monarticular involvement of large joints such as the hip is common. Joint infection is caused by direct extension of osteomyelitis or hematogenous dissemination. (A) Coronal FS PD FSE image. (B) Coronal T1-weighted image.
FIGURE 3.300 ● Myxoid liposarcoma of the medial thigh, which could be mistaken for an abscess. The myxoid type (40% to 50% of liposarcomas) characteristically shows a lack of fat signal on T1-weighted images and may peripherally enhance with contrast administration. The intermediate to hyperintense signal on FS PD FSE images, however, indicates a solid soft tissue sarcoma. (A) Axial T1-weighted image. (B) Axial FS PD FSE image. (C) FS T1-weighted contrast-enhanced image.
FIGURE 3.301 ● (A) Prominent veins associated with a cortical osteoid osteoma of the proximal femur. A pair of veins is frequently associated with the focus of osteoid osteoma. Coronal FS PD FSE image. (B) In a separate case, venous signal is associated with a soft tissue hemangioma about the hip. Axial FS PD FSE image.
FIGURE 3.302 ● Liposclerosing myxofibrous tumor of the proximal femur with a sclerotic hypointense border on a coronal T1-weighted image (A) and heterogeneous hyperintense signal on Sagittal FS PD FSE image (B). There is characteristic intertrochanteric involvement. Fibrous dysplasia of the proximal femur is shown with a characteristic thick sclerotic rim and intermediate-signal homogeneous matrix on coronal T1-weighted (C) and FS PD FSE (D) images. (E) Separate case demonstrating polyostotic fibrous displasia affecting both the pelvis and femur. Coronal T-1-weighted image.
FIGURE 3.303 ● Soft tissue infection with abscess formation associated with an intramedullary rod. The localized artifact does not preclude visualization of adjacent soft tissue. (A) Axial PD FSE image. (B) Axial FS PD FSE image. (C) Axial FS-enhanced TI-weighted image.
After contrast administration there is enhancement of affected areas, including:
  • Bone marrow enhancement (indicating inflammation)
  • Peripheral enhancement within the medullary canal or soft tissue (thick wall) in abscesses
  • Enhancement peripheral to a sequestrum
  • Cortical erosion and destruction may or may not show enhancement.
  • Peripheral enhancement of sinus tracts
FIGURE 3.304 ● Aggressive granulomatous reaction in a cementless total hip arthroplasty with destruction of the medial acetabulum. Coronal PD FSE image.
Initial treatment is with intravenous antibiotics. If unsuccessful, surgical débridement and placement of antibiotic-impregnated beads is attempted. The prognosis is good if the infection is recognized and treatment started promptly. Progression of the infection, however, leads to chronic infection (Fig. 3.299), intramedullary and subperiosteal abscesses, and eventual osseous destruction. Soft tissue extension (see Fig. 3.299) may also occur.
Differential Diagnosis of Infection
Up to 41% of liposarcomas involve the lower trunk, including the gluteal region and medial thigh.270 The myxoid subtype (Fig. 3.300) is sometimes mistaken for a cystic fluid-filled mass because there may be minimal to no fat signal on T1-weighted images and the enhancement pattern may be peripheral. The more differentiated the liposarcoma, the more the signal intensity approaches fat. Knowledge of liposarcoma subtypes and differential diagnosis is useful when encountering soft tissue masses about the hip.
Osteoid Osteomas
Osteoid osteomas 270 involve the metaphysis/diaphysis of long bones in 65% to 80% of cases. MR images typically show extensive bone marrow edema, often with an intermediate-signal-intensity nidus. Hyperintense veins (Fig. 3.301) may also be associated with this vascularized lesion.
Liposclerosing Myxofibrous Tumor
Liposclerosing myxofibrous tumors (Fig. 3.302)270 are fibro-osseous lesions involving the intertrochanteric region of the femur. Histologic elements include features of lipoma, fibroxanthoma, myxoma, myxofibroma, fibrous dysplasia (see Fig. 3.302), cyst formation, fat necrosis, ischemic ossification, and, rarely, cartilage. The lesion has a thin, well-defined sclerotic margin with an intermediate-signal matrix (similar to skeletal muscle on T1-weighted images). The globular mineralized matrix may demonstrate hypointensity. Malignant transformation may occur


in up to 10% of cases, and these lesions should be monitored for changes in morphology, signal intensity, or clinical symptoms such an associated pain.

Joint Prostheses
Metallic total joint prostheses or arthroplasties and hardware may produce local artifact, but it should not prevent accurate determination of component loosening or infection (Fig. 3.303).271,272 In addition, MR imaging is useful in identifying proximal and medial migration of the prosthesis into the pelvis, which complicates prosthetic revision and replacement. In such instances, proximity to neurovascular structures can be assessed without invasive angiography. Osteolysis around total hip replacement components represents a major problem in total joint arthroplasty. Osteolysis refers to particle-induced bone resorption. Because of the geometry of the pelvis and acetabular components, it is often difficult to determine the extent of these lesions. MR evaluation of osteolysis is compromised by the magnetic susceptibility artifact associated with total hip replacement components, and CT may provide more information regarding the extent of lysis. Recently, however, metal suppression techniques have increased the potential to appreciate joint reactions to fine micron-sized wear particles, which may lead to adverse tissue reactions, bone resorption, and component loosening (Fig. 3.304).
1. Conway WF, Totty WG, McEnery KW. CT and MR imaging of the hip. Radiology 1996;198(2):297-307.
2. Pitt MJ, Lund PJ, Speer DP. Imaging of the pelvis and hip. Orthop Clin North Am 1990;21(3):545-559.
3. Stoller DW, Genant HK. Magnetic resonance imaging of the knee and hip. Arthritis Rheum 1990;33(3):441-449.
4. Chatha DS, Arora R. MR imaging of the normal hip. Magn Reson Imaging Clin North Am 2005;13(4):605-615.
5. Toomayan GA, Holman WR, Major NM, et al. Sensitivity of MR arthrography in the evaluation of acetabular labral tears. AJR Am J Roentgenol 2006;186(2):449-453.
6. Berquist TH. Imaging of orthopedic trauma and surgery. Philadelphia: WB Saunders, 1986:181.
7. Gillespy T 3rd, Genant HK, Helms CA. Magnetic resonance imaging of osteonecrosis. Radiol Clin North Am 1986;24(2):193-208.
8. Porter BA. Low field STIR imaging of avascular necrosis, marrow edema, and infarction. Radiology 1987;165:83.
9. Zoga AC, Morrison WB. Technical considerations in MR imaging of the hip. Magn Reson Imaging Clin North Am 2005;13(4):617-634.
10. Wasielewski RC. Anatomy: the hip. In: Callaghan JJ, Rosenberg AG, Rubash HE, eds. The adult hip. Philadelpha: Lippincott-Raven, 1998:57-74.
11. Byrd JW. Gross anatomy. In: Byrd JW, ed. Operative hip arthroscopy, 2nd ed. New York: Springer, 2005:6-35.
12. Keene GS, Villar RN. Arthroscopic anatomy of the hip: an in vivo study. Arthroscopy 1994;10(4):392-399.
13. Bos CF, Verbout AJ, Bloem JL, et al. A correlative study of MR images and cryo-sections of the neonatal hip. Surg Radiol Anat 1990;12(1):43-51.
14. Johnson ND, Wood BP, Noh KS, et al. MR imaging anatomy of the infant hip. AJR Am J Roentgenol 1989;153(1):127-133.
15. Petersilge C. Imaging of the acetabular labrum. Magn Reson Imaging Clin North Am 2005;13(4):641-652.
16. Dinauer PA, Murphy KP, Carroll JF. Sublabral sulcus at the posteroinferior acetabulum: a potential pitfall in MR arthrography diagnosis of acetabular labral tears. AJR Am J Roentgenol 2004;183(6):1745-1753.
17. Byrd JW. The supine approach. In: Byrd JW, ed. Operative hip arthroscopy, 2nd ed. New York: Springer, 2005:145-169.
18. Byrd JW. Indications and contraindications. In: Byrd JW, ed. Operative hip arthroscopy, 2nd ed. New York: Springer, 2005:6-35.
19. Byrd JW. Hip arthroscopy in athletes. In: Byrd JW, ed. Operative hip arthroscopy, 2nd ed. New York: Springer, 2005:195-203.
20. Andrews CL. From the RSNA Refresher Courses, Radiological Society of North America. Evaluation of the marrow space in the adult hip. RadioGraphics 2000;20 Spec No:S27-42.
21. Steinberg ME. Management of avascular necrosis of the femoral head—an overview. AAOS Instr Course Lect 1988;37:41-50.
22. Jones JP, Jr. Fat embolism and osteonecrosis. Orthop Clin North Am 1985;16(4):595-633.
23. Cruess RL. Osteonecrosis of bone. Current concepts as to etiology and pathogenesis. Clin Orthop Relat Res 1986(208):30-39.
24. Gotschalk F. Indications and results of intertrochanteric osteotomy in osteonecrosis of the femoral head. Clin Orthop 1989;249:219.
25. Jacobs B. Epidemiology of traumatic and nontraumatic osteonecrosis. Clin Orthop Relat Res 1978(130):51-67.
26. Byrd JW. Physical examination. In: Byrd JW, ed. Operative hip arthroscopy, 2nd ed. New York: Springer, 2005:36-50.
27. Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg [Am] 1995;77(3):459-474.
28. Mitchell DG, Rao VM, Dalinka MK, et al. Femoral head avascular necrosis: correlation of MR imaging, radiographic staging, radionuclide imaging, and clinical findings. Radiology 1987;162(3):709-715.
29. Beltran J, Herman LJ, Burk JM, et al. Femoral head avascular necrosis: MR imaging with clinical-pathologic and radionuclide correlation. Radiology 1988;166(1 Pt 1):215-220.
30. Mitchell MD, Kundel HL, Steinberg ME, et al. Avascular necrosis of the hip: comparison of MR, CT, and scintigraphy. AJR Am J Roentgenol 1986;147(1):67-71.
31. Glickstein MF, Burk DL, Jr, Schiebler ML, et al. Avascular necrosis versus other diseases of the hip: sensitivity of MR imaging. Radiology 1988;169(1):213-215.
32. Shuman WP, Castagno AA, Baron RL, et al. MR imaging of avascular necrosis of the femoral head: value of small-field-of-view sagittal surface-coil images. AJR Am J Roentgenol 1988;150(5):1073-1078.
33. Berquist TH. Pelvis, hips, and thigh. In: Berquist TH, ed. MRI of the musculoskeletal system, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2006:203-302.
34. Ficat RP. Treatment of avascular necrosis of the femoral head in the hip. In: Proceedings of the 11th Open Scientific Meeting of the Hip Society. St Louis: CV Mosby, p. 279.
35. Ficat RP. Necrosis of the femoral head. In: Hungerford DS, ed. Ischemia and necrosis of the bone. Baltimore: Williams & Williams, 1980.
36. Jones JP. Osteonecrosis. In: McCarthy DJ, ed. Arthritis and allied conditions, 10th ed. Philadelphia: Lea & Febiger, 1985:1356.
37. Springfield DS, Enneking WF. Idiopathic aseptic necrosis. In: Bones and joints. Baltimore: Williams & Williams, 1976:61.
38. Fishman EK, Magid D, Mandelbaum BR, et al. Multiplanar (MPR) imaging of the hip. Radiographics 1986;6(1):7-54.
39. Dee R. Ischemic necrosis of the femoral head. In: Dee R, ed. Principles of orthopaedic practice. New York: McGraw-Hill, 1989:1357.
40. Markisz JA, Knowles RJ, Altchek DW, et al. Segmental patterns of avascular necrosis of the femoral heads: early detection with MR imaging. Radiology 1987;162(3):717-720.
41. Lang P. 2.0 T MR imaging of the femoral head in avascular necrosis: histologic correlation [abstract]. In: Sixth Annual Meeting and Exhibition of the Society of Magnetic Resonance in Medicine; Aug. 17, 1987; New York.
42. Stevens K, Tao C, Lee SU, et al. Subchondral fractures in osteonecrosis of the femoral head: comparison of radiography, CT, and MR imaging. AJR Am J Roentgenol 2003;180(2):363-368.
43. Vande Berg B, Malghem J, Labaisse MA, et al. Avascular necrosis of the hip: comparison of contrast-enhanced and nonenhanced MR imaging with histologic correlation. Work in progress. Radiology 1992;182(2):445-450.
44. Vande Berg BE, Malghem JJ, Labaisse MA, et al. MR imaging of avascular necrosis and transient marrow edema of the femoral head. Radiographics 1993;13(3):501-520.
45. Bluemke DA, Petri M, Zerhouni EA. Femoral head perfusion and composition: MR imaging and spectroscopic evaluation of patients with systemic lupus erythematosus and at risk for avascular necrosis. Radiology 1995;197(2):433-438.
46. Mankey M. Comparision of magnetic resonance imaging and bone scan in the early detection of osteonecrosis of femoral head. Presented to the Academy of Orthopedic Surgeons, January 1987.
47. Turner DA, Templeton AC, Selzer PM, et al. Femoral capital osteonecrosis: MR finding of diffuse marrow abnormalities without focal lesions. Radiology 1989;171(1):135-140.
48. Stulberg BN, Levine M, Bauer TW, et al. Multimodality approach to osteonecrosis of the femoral head. Clin Orthop Relat Res 1989(240):181-193.
49. Iida S, Harada Y, Shimizu K, et al. Correlation between bone marrow edema and collapse of the femoral head in steroid-induced osteonecrosis. AJR Am J Roentgenol 2000;174(3):735-743.
50. Huang GS, Chan WP, Chang YC, et al. MR imaging of bone marrow edema and joint effusion in patients with osteonecrosis of the femoral head: relationship to pain. AJR Am J Roentgenol 2003;181(2):545-549.
51. Koo KH, Ahn IO, Kim R, et al. Bone marrow edema and associated pain in early stage osteonecrosis of the femoral head: prospective study with serial MR images. Radiology 1999;213(3):715-722.
52. Genez BM, Wilson MR, Houk RW, et al. Early osteonecrosis of the femoral head: detection in high-risk patients with MR imaging. Radiology 1988;168(2):521-524.
53. Tervonen O, Mueller DM, Matteson EL, et al. Clinically occult avascular necrosis of the hip: prevalence in an asymptomatic population at risk. Radiology 1992;182(3):845-847.
54. Mulliken BD, Renfrew DL, Brand RA, et al. The prevalence and natural history of early osteonecrosis (ON) of the femoral head. Iowa Orthop J 1994;14:115-119.


55. Jiang CC, Shih TT. Epiphyseal scar of the femoral head: risk factor of osteonecrosis. Radiology 1994;191(2):409-412.
56. Coleman BG, Kressel HY, Dalinka MK, et al. Radiographically negative avascular necrosis: detection with MR imaging. Radiology 1988;168(2):525-528.
57. Lafforgue P, Dahan E, Chagnaud C, et al. Early-stage avascular necrosis of the femoral head: MR imaging for prognosis in 31 cases with at least 2 years of follow-up. Radiology 1993;187(1):199-204.
58. Steinberg MD, Hayken GD, Steinberg DR. The conservative management of avascular necrosis of the femoral head. In: Arlet J, Ficat RP, eds. Bone circulation. Baltimore: Williams & Wilkins, 1984:334.
59. Bonfiglio M, Voke M. Aseptic necrosis of femoral head and nonunion of the femoral neck. J Bone Joint Surg [Am] 1968;50:48.
60. Camp JF, Colwell CW, Jr. Core decompression of the femoral head for osteonecrosis. J Bone Joint Surg [Am] 1986;68(9):1313-1319.
61. Hungerford DS. Bone marrow pressure, venography, and core decompression in ischemic necrosis of the femoral head. In: Proceedings of the Seventh Open Scientific Meeting of the Hip Society, 1979. St. Louis: CV Mosby, 1979:218.
62. Marcus ND, Enneking WF, Massam RA. The silent hip in idiopathic aseptic necrosis. Treatment by bone-grafting. J Bone Joint Surg [Am] 1973;55(7):1351-1366.
63. Steinberg ME, Brighton CT, Corces A, et al. Osteonecrosis of the femoral head. Results of core decompression and grafting with and without electrical stimulation. Clin Orthop Relat Res 1989(249):199-208.
64. Stulberg BN, Bauer TW, Belhobek GH. Making core decompression work. Clin Orthop Relat Res 1990(261):186-195.
65. Sugioka Y. Transtrochanteric anterior rotational osteotomy of the femoral head in the treatment of osteonecrosis affecting the hip: a new osteotomy operation. Clin Orthop Relat Res 1978(130):191-201.
66. Aaron RK, Lennox D, Bunce GE, et al. The conservative treatment of osteonecrosis of the femoral head. A comparison of core decompression and pulsing electromagnetic fields. Clin Orthop Relat Res 1989(249):209-218.
67. Steinberg ME, Brighton CT, Hayken GD, et al. Early results in the treatment of avascular necrosis of the femoral head with electrical stimulation. Orthop Clin North Am 1984;15(1):163-175.
68. Smith SW, Fehring TK, Griffin WL, et al. Core decompression of the osteonecrotic femoral head. J Bone Joint Surg [Am] 1995;77(5):674-680.
69. Beltran J. Core decompression for avascular necrosis of the femoral head: correlation between long-term results and preoperative MR staging. Radiology 1990;175:553.
70. Shimizu K, Moriya H, Akita T, et al. Prediction of collapse with magnetic resonance imaging of avascular necrosis of the femoral head. J Bone Joint Surg [Am] 1994;76(2):215-223.
71. Phemister DB. Treatment of the necrotic head of the femur in adults. Dallas Burton Phemister (1882-1951). Clin Orthop Relat Res 2000(381):4-8.
72. Urbaniak J, Nunley JA, Goldner RD. Treatment of avascular necrosis of the femoral head by vascularized graft. In: Presented at 8th Combined Meeting of Orthopedic Associations of the English-Speaking World, May 3-8, 1987, Washington, DC.
73. Urbaniak JR, Coogan PG, Gunneson EB, et al. Treatment of osteonecrosis of the femoral head with free vascularized fibular grafting. A long-term follow-up study of one hundred and three hips. J Bone Joint Surg [Am] 1995;77(5):681-694.
74. Brown TD, Pedersen DR, Baker KJ, et al. Mechanical consequences of core drilling and bone-grafting on osteonecrosis of the femoral head. J Bone Joint Surg [Am] 1993;75(9):1358-1367.
75. Cabanela ME. Bipolar versus total hip arthroplasty for avascular necrosis of the femoral head. A comparison. Clin Orthop Relat Res 1990(261):59-62.
76. Catterall A, Roberts GC, Wynne-Davies R. Association of Perthes disease with congenital anomalies of genitourinary tract and inguinal region. Lancet 1971;1(7707):996-997.
77. Wynee-Davies R, Gormley J. The etiology of Perthes disease. J Bone Joint Surg [Br] 1978;60:6.
78. Catterall A. The natural history of Perthes disease. J Bone Joint Surg [Br] 1971;53(1):37-53.
79. Salter RB, Thompson GH. Legg-Calvee-Perthes disease: the prognostic significance of the subchondral fracture and two-group classification of femoral head involvement. J Bone Joint Surg [Br] 1978;60:6.
80. Herring JA, Lundeen MA, Wenger DR. Minimal Perthes disease. J Bone Joint Surg [Br] 1980;62(1):25-30.
81. Catterall A, Pringle J, Byers PD, et al. A review of the morphology of Perthes disease. J Bone Joint Surg [Br] 1982;64(3):269-275.
82. Dolman CL, Bell HM. The pathology of Legg-Calve-Perthes disease. A case report. J Bone Joint Surg [Am] 1973;55(1):184-188.
83. Green NE, Beauchamp RD, Griffin PP. Epiphyseal extrusion as a prognostic index in Legg-Calve-Perthes disease. J Bone Joint Surg [Am] 1981;63(6):900-905.
84. Easton EJ. Magnetic resonance imaging and scintigraphy in Legg-Perthes disease: diagnosis, treatment and prognosis. Radiology 1987;165:35.
85. Heuck A. Magnetic resonance imaging in the evaluation of Legg-Perthes disease. Radiology 1987;165:83.
86. Rush BH, Bramson RT, Ogden JA. Legg-Calve-Perthes disease: detection of cartilaginous and synovial change with MR imaging. Radiology 1988;167(2):473-476.
87. Jamamillo D, Kasser Jr, Villegas-Medina OL, et al. Cartilaginous abnormalities and growth disturbance in Legg-Calve-Perthes disease: evaluation with MR imaging. Radiology 1995;187:767.
88. Ranner G, Ebner F, Fotter R, et al. Magnetic resonance imaging in children with acute hip pain. Pediatr Radiol 1989;20(1-2):67-71.
89. Herring JA. The treatment of Legg-Calve-Perthes disease. A critical review of the literature. J Bone Joint Surg [Am] 1994;76(3):448-458.
90. Fitzgerald RH. Legg-Calve-Perthes. In: Orthopaedics. St. Louis: Mosby, 2002:1420-1432.
91. Thompson GH, Salter RB. Legg-Calve-Perthes disease. Current concepts and controversies. Orthop Clin North Am 1987;18(4):617-635.
92. Weinstein SL. Legg-Calve-Perthes disease. In: The Proceedings of the 13th Open Scientific Meeting of the Hip Society, 1985. St. Louis: CV Mosby, 1985:28.
93. Bloem JL. Transient osteoporosis of the hip: MR imaging. Radiology 1988;167(3):753-755.
94. Vande Berg BC, Malghem JJ, Lecouvet FE, et al. Idiopathic bone marrow edema lesions of the femoral head: predictive value of MR imaging findings. Radiology 1999;212(2):527-535.
95. Guerra JJ, Steinberg ME. Current concepts review: distinguishing transient osteoporosis from avascular necrosis of the hip. J Bone Joint Surg [Am] 1995;77:616.
96. Kerr R. Transient osteoporosis of the hip. Orthopedics 1990;13(4):485-486.
97. Pantazopoulos T, Exarchou E, Hartofilakidis GA. Idiopathic transient osteoporosis of the hip. J Bone Joint Surg [Am] 1973;55(2):315-321.
98. Imhof H, Kramer J, Hofmann S, et al. MRI of osteonecrosis: transient bone marrow edema. In: Abstract Presentation at the 1st International Symposium, Musculoskeletal Magnetic Resonance Imaging, 1996, San Francisco.
99. Dillon JE, Connolly SA, Connolly LP, et al. MR imaging of congenital/developmental and acquired disorders of the pediatric hip and pelvis. Magn Reson Imaging Clin North Am 2005;13(4):783-797.
100. Wilcox PG, Weiner DS, Leighley B. Maturation factors in slipped capital femoral epiphysis. J Pediatr Orthop 1988;8(2):196-200.
101. Gelberman RH, Cohen MS, Shaw BA, et al. The association of femoral retroversion with slipped capital femoral epiphysis. J Bone Joint Surg [Am] 1986;68(7):1000-1007.
102. Agamanolis DP, Weiner DS, Lloyd JK. Slipped capital femoral epiphysis: a pathological study. II. An ultrastructural study of 23 cases. J Pediatr Orthop 1985;5(1):47-58.
103. Johnson ND, Wood BP, Jackman KV. Complex infantile and congenital hip dislocation: assessment with MR imaging. Radiology 1988;168(1):151-156.
104. Berend K, Vail TP. Hip arthroscopy in adolescence and childhood. In: Byrd JW, ed. Operative hip arthroscopy, 2nd ed. New York: Springer, 2005:204-219.
105. Crawford AH. The role of osteotomy in the treatment of slipped capital femoral epiphysis. AAOS Instr Course Lect 1989;38:273-279.
106. Swiontkowski MF. Slipped capital femoral epiphysis: complications relative to internal fixation. Orthopaedics 1983;6:705.
107. Wiener DS. Bone graft epiphysiodesis in the treatment of slipped capital femoral epiphysis. In: Barr JS, ed. AAOS Instructional Course Lectures, 1989, Las Vegas.
108. Stuhlberg SD, Cordell LD. Unrecognized childhood hip disease: a major cause of idiopathic osteoarthritis of the hip. In: Proceedings of the Hip Society, 1975. St. Louis: CV Mosby, 1975:212.
109. Soboleski DA, Babyn P. Sonographic diagnosis of developmental dysplasia of the hip: importance of increased thickness of acetabular cartilage. AJR Am J Roentgenol 1993;161(4):839-842.
110. Atar D, Lehman WB, Grant AD. 2-D and 3-D computed tomography and magnetic resonance imaging in developmental dysplasia of the hip. Orthop Rev 1992;21(10):1189-1197.
111. Eggli KD, King SH, Boal DK, et al. Low-dose CT of developmental dysplasia of the hip after reduction: diagnostic accuracy and dosimetry. AJR Am J Roentgenol 1994;163(6):1441-1443.
112. Hubbard AM, Dormans JP. Evaluation of developmental dysplasia, Perthes disease, and neuromuscular dysplasia of the hip in children before and after surgery: an imaging update. AJR Am J Roentgenol 1995;164(5):1067-1073.
113. Lang P, Genant HK, Steiger P, et al. Three-dimensional digital displays in congenital dislocation of the hip: preliminary experience. J Pediatr Orthop 1989;9(5):532-537.
114. Lang P. Three-dimensional CT and MR imaging in congenital dislocation of the hip: technical considerations. Radiology 1987;165:279.
115. Dunn PM. The anatomy and pathology of congenital dislocation of the hip. Clin Orthop Relat Res 1976(119):23-27.
116. Hillmann JS, Mesgarzadeh M, Revesz G, et al. Proximal femoral focal deficiency: radiologic analysis of 49 cases. Radiology 1987;165(3):769-773.
117. Garrett WE, Jr. Injuries to the muscle-tendon unit. AAOS Instr Course Lect 1988;37:275-282.
118. Garrett WE, Jr. Muscle strain injuries: clinical and basic aspects. Med Sci Sports Exerc 1990;22(4):436-443.
119. Gilcreest EL. Rupture of muscles and tendon, particularly subcutaneous rupture of biceps flexor cubiti. JAMA 1925;84:1819.
120. Glick JM. Muscle strains: prevention and treatment. Physician Sports Med 1980;8:73.
121. O—Donoghue DH. Principals in the management of specific injuries. In: Treatment of injuries to athletes, 4th ed. Philadelphia: WB Saunders, 1984:51.
122. Kibler WB. Clinical aspects of muscle injury. Med Sci Sports Exerc 1990;22(4):450-452.
123. Ryan AJ. Quadriceps strain: rupture and charley horse. Med Sci Sports Exerc 1969;1:106.
124. Oakes BW. Hamstring muscle injuries. Aust Fam Physician 1984;13(8):587-591.
125. Tarsney FF. Rupture and avulsion of the triceps. Clin Orthop Relat Res 1972;83:177-183.
126. Fleckenstein JL, Weatherall PT, Parkey RW, et al. Sports-related muscle injureis: evaluation with MR imaging. Radiology 1988;172:793.


127. De Smet AA, Fisher DR, Heiner JP, et al. Magnetic resonance imaging of muscle tears. Skeletal Radiol 1990;19(4):283-286.
128. Herring SA. Rehabilitation of muscle injuries. Med Sci Sports Exerc 1990; 22(4):453-456.
129. Dooms GC, Fisher MR, Hricak H, et al. MR imaging of intramuscular hemorrhage. J Comput Assist Tomogr 1985;9(5):908-913.
130. Ehman RL, Berquist TH. Magnetic resonance imaging of musculoskeletal trauma. Radiol Clin North Am 1986;24(2):291-319.
131. Fisher MK. MRI of the normal and pathological musculoskeletal system. Magn Reson Imaging 1986;4:491.
132. Mink JH. Muscle injuries. In: Mink JH, Reicher MA, Crues JV, 3rd, et al, eds. MRI of the knee. New York: Raven Press, 1995:401.
133. Jackson DW, Feagin JA. Quadriceps contusions in young athletes. Relation of severity of injury to treatment and prognosis. J Bone Joint Surg [Am] 1973; 55(1):95-105.
134. Fleckenstein JL, Shellock FG. Exertional muscle injuries: magnetic resonance imaging evaluation. Top Magn Reson Imaging 1991;3(4):50-70.
135. Amendola MA, Glazer GM, Agha FP, et al. Myositis ossificans circumscripta: computed tomographic diagnosis. Radiology 1983;149(3):775-779.
136. Swensen SJ, Keller PL, Berquist TH, et al. Magnetic resonance imaging of hemorrhage. AJR Am J Roentgenol 1985;145(5):921-927.
137. Mellado JM, Bencardino JT. Morel-Lavallee lesion: review with emphasis on MR imaging. Magn Reson Imaging Clin North Am 2005;13(4):775-782.
138. Armstrong RB. Mechanisms of exercise-induced delayed onset muscular soreness: a brief review. Med Sci Sports Exerc 1984;16(6):529-538.
139. Abraham WM. Factors in delayed muscle soreness. Med Sci Sports 1977;9(1):11-20.
140. Evans WJ, Cannon JG. The metabolic effects of exercise-induced muscle damage. In: Holloszy JO, ed. Exercise and sport sciences reviews. Baltimore: Williams & Wilkins, 1991:99.
141. Jones DA, Newham DJ, Round JM, et al. Experimental human muscle damage: morphological changes in relation to other indices of damage. J Physiol 1986;375:435-448.
142. Newham DJ, McPhail G, Mills KR, et al. Ultrastructural changes after concentric and eccentric contractions of human muscle. J Neurol Sci 1983;61(1):109-122.
143. Clarkson PM, Tremblay I. Exercise-induced muscle damage, repair, and adaptation in humans. J Appl Physiol 1988;65(1):1-6.
144. Friden J, Sfakianos PN, Hargens AR. Muscle soreness and intramuscular fluid pressure: comparison between eccentric and concentric load. J Appl Physiol 1986;61(6):2175-2179.
145. Fleckenstein JL, Weatherall PT, Bertocci LA, et al. Locomotor system assessment by muscle magnetic resonance imaging. Magn Reson Q 1991;7(2):79-103.
146. Nurenberg P, Giddings CJ, Stray-Gundersen J, et al. MR imaging-guided muscle biopsy for correlation of increased signal intensity with ultrastructural change and delayed-onset muscle soreness after exercise. Radiology 1992;184(3):865-869.
147. Shellock FG, Fukunaga T, Day K, et al. Serial MRI and Cybex testing evaluations of exertional muscle injury: concentric vs. eccentric actions [abstr]. Med Sci Sports 1991;23:110.
148. Shellock FG, Fukunaga T, Mink J, et al. Serial MRI evaluation of exertional muscle injury: concentric vs. eccentric actions. Radiol Clin North Am 1991;179:659.
149. Fleckenstein JL, Weatherall PT, Parkey RW, et al. Sports-related muscle injuries: evaluation with MR imaging. Radiology 1988;172:793.
150. Fleckenstein JL, Peshock RM, Lewis SF, et al. Magnetic resonance imaging of muscle injury and atrophy in glycolytic myopathies. Muscle Nerve 1989; 12(10):849-855.
151. Lamminen AE, Hekali PE, Tiula E, et al. Acute rhabdomyolysis: evaluation with magnetic resonance imaging compared with computed tomography and ultrasonography. Br J Radiol 1989;62(736):326-330.
152. Amendola A, Rorabeck CH, Vellett D, et al. The use of magnetic resonance imaging in exertional compartment syndromes. Am J Sports Med 1990;18(1):29-34.
153. Bordalo-Rodrigues M, Rosenberg ZS. MR imaging of the proximal rectus femoris musculotendinous unit. Magn Reson Imaging Clin North Am 2005;13(4):717-725.
154. Hasselman CT, Best TM, Hughes C, et al. An explanation for various rectus femoris strain injuries using previously undescribed muscle architecture. Am J Sports Med 1995;23(4):439-493.
155. Hughes C, Hasselman CT, Best TM, et al. Incomplete, intrasubstance strain injuries of the rectus femoris muscle. Am J Sports Med 1995;23(4):500-506.
156. Brandser EA, el-Khoury GY, Kathol MH, et al. Hamstring injuries: radiographic, conventional tomographic, CT, and MR imaging characteristics. Radiology 1995;197(1):257-262.
157. Connell DA, Schneider-Kolsky ME, Hoving JL, et al. Longitudinal study comparing sonographic and MRI assessments of acute and healing hamstring injuries. AJR Am J Roentgenol 2004;183(4):975-984.
158. Slavotinek JP, Verrall GM, Fon GT. Hamstring injury in athletes: using MR imaging measurements to compare extent of muscle injury with amount of time lost from competition. AJR Am J Roentgenol 2002;179(6):1621-1628.
159. Bencardino JT, Mellado JM. Hamstring injuries of the hip. Magn Reson Imaging Clin North Am 2005;13(4):677-690.
160. Koulouris G, Connell D. Hamstring muscle complex: an imaging review. RadioGraphics 2005;25(3):571-586.
161. Paletta GA, Jr., Andrish JT. Injuries about the hip and pelvis in the young athlete. In: Micheli LJ, ed. Clinics in sports medicine. Philadelphia: WB Saunders, 1995:591-628.
162. Micheli LJ. The young athlete. Clin Sports Med 1995;14:3.
163. Cleaves EN. Fracture avulsion of the anterior superio iliac spine of the ilium. J Bone Joint Surg [Am] 1938;20:490.
164. Shabshin N, Rosenberg ZS, Cavalcanti CF. MR imaging of iliopsoas musculotendinous injuries. Magn Reson Imaging Clin North Am 2005;13(4):705-716.
165. Milch H. Avulsion fracture of the tuberosity of the ischium. J Bone Joint Surg [Am] 1926;8:832.
166. Rogge EA, Romano RL. Avulsion of the ischial apophysis. Clin Orthop 1957;9:239-243.
167. Cvitanic O, Henzie G, Skezas N, et al. MRI diagnosis of tears of the hip abductor tendons (gluteus medius and gluteus minimus). AJR Am J Roentgenol 2004; 182(1):137-143.
168. Dwek J, Pfirrmann C, Stanley A, et al. MR imaging of the hip abductors: normal anatomy and commonly encountered pathology at the greater trochanter. Magn Reson Imaging Clin North Am 2005;13(4):691-704.
169. Vaccaro JP, Sauser DD, Beals RK. Iliopsoas bursa imaging: efficacy in depicting abnormal iliopsoas tendon motion in patients with internal snapping hip syndrome. Radiology 1995;197(3):853-856.
170. Miller MD, Howard RF, Plancher KD. Treatment of snapping hip. In: Surgical atlas of sports medicine. Philadelphia: Saunders, 2003.
171. Paletta GA, Jr., Andrish JT. Injuries about the hip and pelvis in the young athlete. Clin Sports Med 1995;14(3):591-628.
172. Ganz R, Parvizi J, Beck M, et al. Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clin Orthop Relat Res 2003(417):112-120.
173. Tanzer M, Noiseux N. Osseous abnormalities and early osteoarthritis: the role of hip impingement. Clin Orthop Relat Res 2004(429):170-177.
174. Bredella MA, Stoller DW. MR imaging of femoroacetabular impingement. Magn Reson Imaging Clin North Am 2005;13(4):653-664.
175. Beck M, Leunig M, Parvizi J, et al. Anterior femoroacetabular impingement: part II. Midterm results of surgical treatment. Clin Orthop Relat Res 2004(418):67-73.
176. Ito K, Leunig M, Ganz R. Histopathologic features of the acetabular labrum in femoroacetabular impingement. Clin Orthop Relat Res 2004(429):262-271.
177. Ito K, Minka MA, 2nd, Leunig M, et al. Femoroacetabular impingement and the cam-effect. A MRI-based quantitative anatomical study of the femoral head-neck offset. J Bone Joint Surg [Br] 2001;83(2):171-176.
178. Jager M, Wild A, Westhoff B, et al. Femoroacetabular impingement caused by a femoral osseous head-neck bump deformity: clinical, radiological, and experimental results. J Orthop Sci 2004;9(3):256-263.
179. Murphy S, Tannast M, Kim YJ, et al. Debridement of the adult hip for femoroacetabular impingement: indications and preliminary clinical results. Clin Orthop Relat Res 2004(429):178-181.
180. Notzli HP, Wyss TF, Stoecklin CH, et al. The contour of the femoral head-neck junction as a predictor for the risk of anterior impingement. J Bone Joint Surg [Br] 2002;84(4):556-560.
181. Siebenrock KA, Schoeniger R, Ganz R. Anterior femoro-acetabular impingement due to acetabular retroversion. Treatment with periacetabular osteotomy. J Bone Joint Surg [Am] 2003;85(2):278-286.
182. Harris WH. Etiology of osteoarthritis of the hip. Clin Orthop Relat Res 1986(213):20-33.
183. Murray RO. The aetiology of primary osteoarthritis of the hip. Br J Radiol 1965;38(455):810-824.
184. Reynolds D, Lucas J, Klaue K. Retroversion of the acetabulum. A cause of hip pain. J Bone Joint Surg [Br] 1999;81(2):281-288.
185. Leunig M, Beck M, Woo A, et al. Acetabular rim degeneration: a constant finding in the aged hip. Clin Orthop Relat Res 2003(413):201-207.
186. Leunig M, Werlen S, Ungersbock A, et al. Evaluation of the acetabular labrum by MR arthrography. J Bone Joint Surg [Br] 1997;79(2):230-234.
187. Schmid MR, Notzli HP, Zanetti M, et al. Cartilage lesions in the hip: diagnostic effectiveness of MR arthrography. Radiology 2003;226(2):382-386.
188. Leunig M, Podeszwa D, Beck M, et al. Magnetic resonance arthrography of labral disorders in hips with dysplasia and impingement. Clin Orthop Relat Res 2004(418):74-80.
189. Buckwalter JA, Lohmander S. Operative treatment of osteoarthrosis. Current practice and future development. J Bone Joint Surg [Am] 1994;76(9):1405-1418.
190. Lavigne M, Parvizi J, Beck M, et al. Anterior femoroacetabular impingement: part I. Techniques of joint-preserving surgery. Clin Orthop Relat Res 2004(418): 61-66.
191. Tonnis D, Heinecke A. Acetabular and femoral anteversion: relationship with osteoarthritis of the hip. J Bone Joint Surg [Am] 1999;81(12):1747-1770.
192. Beck M, Leunig M, Clarke E, et al. Femoroacetabular impingement as a factor in the development of nonunion of the femoral neck: a report of three cases. J Orthop Trauma 2004;18(7):425-430.
193. Eijer H, Myers SR, Ganz R. Anterior femoroacetabular impingement after femoral neck fractures. J Orthop Trauma 2001;15(7):475-481.
194. Klaue K, Durnin CW, Ganz R. The acetabular rim syndrome. A clinical presentation of dysplasia of the hip. J Bone Joint Surg [Br] 1991;73(3):423-429.
195. Leunig M, Casillas MM, Hamlet M, et al. Slipped capital femoral epiphysis: early mechanical damage to the acetabular cartilage by a prominent femoral metaphysis. Acta Orthop Scand 2000;71(4):370-375.
196. Myers SR, Eijer H, Ganz R. Anterior femoroacetabular impingement after periacetabular osteotomy. Clin Orthop Relat Res 1999(363):93-99.
197. Pitto RP, Klaue K, Ganz R, et al. Acetabular rim pathology secondary to congenital hip dysplasia in the adult. A radiographic study. Chir Organi Mov 1995; 80(4):361-368.
198. Chell J, Flowers MJ. Is diagnostic arthroscopy of the hip worthwhile? J Bone Joint Surg [Br] 2000;82(2):306.


199. Siebenrock KA, Wahab KH, Werlen S, et al. Abnormal extension of the femoral head epiphysis as a cause of cam impingement. Clin Orthop Relat Res 2004(418):54-60.
200. Barrack RL, Schmalzried TP. Impingement and rim wear associated with early osteolysis after a total hip replacement: a case report. J Bone Joint Surg [Am] 2002;84(7):1218-1220.
201. Bradford L, Kurland R, Sankaran M, et al. Early failure due to osteolysis associated with contemporary highly cross-linked ultra-high molecular weight polyethylene. A case report. J Bone Joint Surg [Am] 2004;86(5):1051-1056.
202. Urquhart AG, D—Lima DD, Venn-Watson E, et al. Polyethylene wear after total hip arthroplasty: the effect of a modular femoral head with an extended flange-reinforced neck. J Bone Joint Surg [Am] 1998;80(11):1641-1647.
203. Widmer KH, Zurfluh B. Compliant positioning of total hip components for optimal range of motion. J Orthop Res 2004;22(4):815-821.
204. Beck M, Kalhor M, Leunig M, et al. Hip morphology influences the pattern of damage to the acetabular cartilage: femoroacetabular impingement as a cause of early osteoarthritis of the hip. J Bone Joint Surg [Br] 2005;87(7):1012-1018.
205. Kassarjian A, Yoon LS, Belzile E, et al. Triad of MR arthrographic findings in patients with cam-type femoroacetabular impingement. Radiology 2005;236(2):588-592.
206. Crowninshield RD, Maloney WJ, Wentz DH, et al. Biomechanics of large femoral heads: what they do and don—t do. Clin Orthop Relat Res 2004(429):102-107.
207. Morgan JD, Somerville EW. Normal and abnormal growth at the upper end of the femur. J Bone Joint Surg [Br] 1960;42:264-272.
208. Dora C, Zurbach J, Hersche O, et al. Pathomorphologic characteristics of posttraumatic acetabular dysplasia. J Orthop Trauma 2000;14(7):483-489.
209. Murphy SB, Kijewski PK, Millis MB, et al. Acetabular dysplasia in the adolescent and young adult. Clin Orthop Relat Res 1990(261):214-223.
210. Leunig M, Beck M, Kalhor M, et al. Fibrocystic changes at anterosuperior femoral neck: prevalence in hips with femoroacetabular impingement. Radiology 2005;236(1):237-246.
211. Stoller DW, Tirman PFJ, Bredella MA. Femoroacetabular impingement. In: Stoller DW, Tirman PFJ, Bredella MA, eds. Diagnositic imaging: orthopaedics. Salt Lake City: Amirsys, 2004:82-85.
212. Sadro C. Current concepts in magnetic resonance imaging of the adult hip and pelvis. Semin Roentgenol 2000;35(3):231-248.
213. Gautier E, Ganz K, Krugel N, et al. Anatomy of the medial femoral circumflex artery and its surgical implications. J Bone Joint Surg [Br] 2000;82(5):679-683.
214. Guanche CA, Bare AA. Arthroscopic treatment of femoroacetabular impingement. Arthroscopy 2006;22(1):95-106.
215. Kelly BT, Weiland DE, Schenker ML, et al. Arthroscopic labral repair in the hip: surgical technique and review of the literature. Arthroscopy 2005;21(12):1496-1504.
216. Czerny C, Hofmann S, Neuhold A, et al. Lesions of the acetabular labrum: accuracy of MR imaging and MR arthrography in detection and staging. Radiology 1996;200(1):225-230.
217. Philippon MJ, Martin RR, Kelly B. A classification system for labral tears of the hip [abstract]. Arthroscopy 2005:SS-74.
218. Hodler J, Yu JS, Goodwin D, et al. MR arthrography of the hip: improved imaging of the acetabular labrum with histologic correlation in cadavers. AJR Am J Roentgenol 1995;165(4):887-891.
219. Lieberman JR, Altchek DW, Salvati EA. Recurrent dislocation of a hip with a labral lesion: treatment with a modified Bankart-type repair. Case report. J Bone Joint Surg [Am] 1993;75(10):1524-1527.
220. Magee T, Hinson G. Association of paralabral cysts with acetabular disorders. AJR Am J Roentgenol 2000;174(5):1381-1384.
221. Boutry N, Paul C, Leroy X, et al. Rapidly destructive osteoarthritis of the hip: MR imaging findings. AJR Am J Roentgenol 2002;179(3):657-663.
222. Haller J, Resnick D, Greenway G, et al. Juxtaacetabular ganglionic (or synovial) cysts: CT and MR features. J Comput Assist Tomogr 1989;13(6):976-983.
223. Szypryt P, Twining P, Preston BJ, et al. Synovial chondromatosis of the hip joint presenting as a pathological fracture. Br J Radiol 1986;59(700):399-401.
224. Schurman DJ, Palathumpat MV, DeSilva A, et al. Biochemistry and antigenicity of osteoarthritic and rheumatoid cartilage. J Orthop Res 1986;4(3):255-262.
225. Arnett FC, Edworthy SM, Bloch DA, et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 1988;31(3):315-324.
226. Duthie RB, Harris CM. A radiographic and clinical survey of the hip joint in sero-positive rheumatoid arthritis. Acta Orthop Scand 1969;40(3):346-364.
227. Glick EN, Mason RM, Wenley WG. Rheumatoid arthritis affecting the hip joint. Ann Rheum Dis 1963;22:416-423.
228. Resnick D, Williams G, Weisman MH, et al. Rheumatoid arthritis and pseudo-rheumatoid arthritis in calcium pyrophosphate dihydrate crystal deposition disease. Radiology 1981;140(3):615-621.
229. Senac MO, Jr., Deutsch D, Bernstein BH, et al. MR imaging in juvenile rheumatoid arthritis. AJR Am J Roentgenol 1988;150(4):873-878.
230. Stoller DW. MRI in juvenile (chronic) arthritis. Presented to the Association of University Radiologists, March 22, 1987, Charleston, SC.
231. Wilkinson M, Bywaters EG. Clinical features and course of ankylosing spondylitis; as seen in a follow-up of 222 hospital referred cases. Ann Rheum Dis 1958;17(2):209-228.
232. Chung SM, Janes JM. Diffuse Pigmented villonodular synovitis of the hip joint. Review of the literature and report of four cases. J Bone Joint Surg [Am] 1965;47:293-303.
233. Jelinek JS, Kransdorf MJ, Utz JA, et al. Imaging of pigmented villonodular synovitis with emphasis on MR imaging. AJR Am J Roentgenol 1989;152(2):337-342.
234. McMaster PE. Pigmented villonodular synovitis with invasion of bone. J Bone Joint Surg [Am] 1960;42:1170.
235. Brancaccio D. Amyloid arthropathy in patients on regular dialysis: a newly discovered disease. Radiology 1987;65(P):335.
236. Fairclough J, Colhoun E, Johnston D, et al. Bone scanning for suspected hip fractures. A prospective study in elderly patients. J Bone Joint Surg [Br] 1987; 69(2):251-253.
237. Griffiths HJ. Computed tomography in the management of acetabular fractures. Radiology 1985;154:567.
238. Tile M, Kellam J, Joyce M. Fractures of the acetabulum, classification, management protocol and results of treatment. J Bone Joint Surg [Br] 1985;67:173.
239. Devas M. Stress fractures. New York: Churchill-Livingstone, 1975.
240. Gilbert RS, Johnson HA. Stress fractures in military recruits: a review of 12 years— experience. Milit Med 1966;131:716.
241. Beltran J, Opsha O. MR imaging of the hip: osseous lesions. Magn Reson Imaging Clin North Am 2005;13(4):665-676.
242. Weaver CJ, Major NM, Garrett WE, et al. Femoral head osteochondral lesions in painful hips of athletes: MR imaging findings. AJR Am J Roentgenol 2002;178(4):973-977.
243. Pauwels F. Biomechanics of the normal hip. New York: Springer-Verlag, 1976.
244. Garden RS. Reduction and fixation of subcapital fractures of the femur. Orthop Clin North Am 1974;5(4):683-712.
245. Blickenstaff LD, Morris JM. Fatigue fracture of the femoral neck. J Bone Joint Surg [Am] 1966;48(6):1031-1047.
246. Morris JM, Blickenstaff LD. In: Fatigue fractures. Springfield, IL: Charles C Thomas, 1967.
247. Berger PE, Ofstein RA, Jackson DW, et al. MRI demonstration of radiographically occult fractures: what have we been missing? RadioGraphics 1989;9(3):407-436.
248. Deutsch AL, Mink JH, Waxman AD. Occult fractures of the proximal femur: MR imaging. Radiology 1989;170(1 Pt 1):113-116.
249. Bogost GA, Lizerbram EK, Crues JV, 3rd. MR imaging in evaluation of suspected hip fracture: frequency of unsuspected bone and soft-tissue injury. Radiology 1995;197(1):263-267.
250. Quinn SF, McCarthy JL. Prospective evaluation of patients with suspected hip fracture and indeterminate radiographs: use of T1-weighted MR images. Radiology 1993;187(2):469-471.
251. Lang P, Mauz M, Schorner W, et al. Acute fracture of the femoral neck: assessment of femoral head perfusion with gadopentetate dimeglumine-enhanced MR imaging. AJR Am J Roentgenol 1993;160(2):335-341.
252. Schwappach JR, Murphey MD, Kokmeyer SF, et al. Subcapital fractures of the femoral neck: prevalence and cause of radiographic appearance simulating pathologic fracture. AJR Am J Roentgenol 1994;162(3):651-654.
253. Johnson TS. The spur sign. Radiology 2005;235(3):1023-1024.
254. Tile M. Fractures of the acetabulum. In: Steinberg ME, ed. The hip and its disorders. Philadelphia: WB Saunders, 1991:201.
255. Letournel E. Acetabulum fractures: classification and management. Clin Orthop Relat Res 1980(151):81-106.
256. Potok PS, Hopper KD, Umlauf MJ. Fractures of the acetabulum: imaging, classification, and understanding. RadioGraphics 1995;15(1):7-24.
257. Potter HG, Montgomery KD, Heise CW, et al. MR imaging of acetabular fractures: value in detecting femoral head injury, intraarticular fragments, and sciatic nerve injury. AJR Am J Roentgenol 1994;163(4):881-886.
258. May DA, Purins JL, Smith DK. MR imaging of occult traumatic fractures and muscular injuries of the hip and pelvis in elderly patients. AJR Am J Roentgenol 1996;166(5):1075-1078.
259. Richardson P, Young JW, Porter D. CT detection of cortical fracture of the femoral head associated with posterior hip dislocation. AJR Am J Roentgenol 1990;155(1):93-94.
260. Tehranzadeh J, Vanarthos W, Pais MJ. Osteochondral impaction of the femoral head associated with hip dislocation: CT study in 35 patients. AJR Am J Roentgenol 1990;155(5):1049-1052.
261. Berquist TH, Coventry MB. The pelvis and hips. In: Berquist TH, ed. Imaging of orthopaedic trauma and surgery. Philadelphia: WB Saunders, 1986:181.
262. Erb RE, Steele JR, Nance EP, Jr., et al. Traumatic anterior dislocation of the hip: spectrum of plain film and CT findings. AJR Am J Roentgenol 1995;165(5):1215-1219.
263. Hwang B, Fredericson M, Chung CB, et al. MRI findings of femoral diaphyseal stress injuries in athletes. AJR Am J Roentgenol 2005;185(1):166-173.
264. Mora SA, Mandelbaum BR, Szalai LJ, et al. Extraarticular sources of hip pain. In: Byrd JW, ed. Operative hip arthroscopy, 2nd ed. New York: Springer, 2005:70-99.
265. Nelson EN, Kassarjian A, Palmer WE. MR imaging of sports-related groin pain. Magn Reson Imaging Clin North Am 2005;13(4):727-742.
266. Brennan D, O—Connell MJ, Ryan M, et al. Secondary cleft sign as a marker of injury in athletes with groin pain: MR image appearance and interpretation. Radiology 2005;235(1):162-167.
267. Yukata K, Arai K, Yoshizumi Y, et al. Obturator neuropathy caused by an acetabular labral cyst: MRI findings. AJR Am J Roentgenol 2005;184(3 Suppl):S112-114.
268. Koulouris G, Morrison WB. MR imaging of hip infection and inflammation. Magn Reson Imaging Clin North Am 2005;13(4):743-755.
269. Karchevsky M, Schweitzer ME, Morrison WB, et al. MRI findings of septic arthritis and associated osteomyelitis in adults. AJR Am J Roentgenol 2004;182(1):119-122.
270. Bancroft LW, Peterson JJ, Kransdorf MJ. MR imaging of tumors and tumor-like lesions of the hip. Magn Reson Imaging Clin North Am 2005;13(4):757-774.
271. Feldman F. MR imaging of soft-tissue reaction to prostheses. Radiology 1987;165(P):84.
272. Laakman RW. MR imaging in patients with metallic implants. Radiology 1985;157:711.

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