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The hip is a ball-and-socket joint allowing a wide range of motion in all directions. Active movements (flexion, extension, adduction, abduction, circumduction, and medial and lateral rotations) are possible. The femoral head is nearly completely covered by the spherical acetabular socket, except for a small inferior medial aspect, the so-called acetabular notch, where there is no socket. The transverse acetabular ligament spans this deficient portion of the acetabulum. A triangularly shaped labrum rims the acetabulum. The labrum is thicker posterosuperiorly and thinner anteroinferiorly. The acetabular labrum consists of fibrocartilaginous tissue with fibrovascular bundles that are attached directly to the osseous rim of the acetabulum. It blends with the transverse ligament at the margins of the acetabular notch. Contrary to the shoulder, the acetabular labrum increases the depth of the joint rather than its diameter. Clinical and arthroscopic studies have documented the importance of the acetabular capsular labral complex as a biomechanical component of the hip joint. The joint capsule inserts onto the acetabular rim. Along the anterior and posterior joint margins, the capsule inserts directly at the base of the labrum, and a small perilabral recess is created between the labrum and joint capsule. The iliopsoas bursa, directly anterior to the hip joint, communicates with the joint in 10% to 15% of normal anatomic specimens and may be involved in patients with synovitis. The bony structures are protected by a mantle of muscles consisting of mainly short muscles. The femoral head, a region commonly involved in different diseases, is supplied by branches originating from mainly the medial and lateral femoral circumflex arteries.
Because conventional radiography, ultrasonography, CT, and conventional MRI are routine procedures everywhere, and the technique of these methods is part of basic knowledge, in this chapter, only MR arthrography and CT arthrography are discussed in more detail.
In most institutions, MR arthrography of the hip is performed as a two-step procedure. Joint puncture is usually performed under fluoroscopic guidance. The patient is supine with the leg extended and slightly internally rotated. The puncture site can be marked on the skin above the femoral neck. This point has to be lateral to the femoral artery and below the inguinal ligament. Under sterile conditions, a 20-gauge disposable needle is directed straight onto the lateral aspect of the femoral epiphysis or craniolateral part of the femoral neck. To avoid radiation exposure to the hands, a few drops of iodinated contrast agent are injected through an extension tube to confirm intraarticular location. Then the iodinated contrast material within the tube is replaced by a diluted MR contrast agent, and 10 to 20 mL of gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA) mixture is injected into the joint. This mixture consists of 0.2 mL of a standard Gd-DTPA solution (469.01 mg/mL, Magnevist, Schering AG, Germany) and 50 mL of saline, giving a 2 mmol/L of Gd-DTPA solution, which has been shown to provide an optimal contrast between the contrast medium and the intraarticular structures or abnormalities. Imaging should be performed within 30 minutes after the intraarticular injection is finished, to prevent absorption of the contrast solution and to guarantee the desired capsular distention. Gd-DTPA and iodinated contrast material can be mixed before the MRI without any release of free gadolinium and is safe for confirming the intraarticular placement of contrast material. It has been shown that intravenous administration of Gd-DTPA also leads to an enhancement effect of the joint fluid (indirect MR arthrography). This technique has been proposed as an alternative to direct MR arthrography. Intraarticular enhancement in normal joints, however, is only mild and often heterogeneous, although exercise improves both the homogeneity and amount of enhancement in the joint. The main limitation is the lack of joint distention compared with that of direct arthrography. Studies have shown that patients who have undergone MR arthrography considered discomfort less than expected. Arthrography-related discomfort was well tolerated and rated less severe than MRI-related discomfort. Although patients expressed fear of certain aspects of MR arthrography, the reported average pain from the arthrogram was low. Despite its invasiveness, clinicians should not hesitate to order MR arthrography when clinically indicated.
The joint puncture procedure is identical to MR arthrography and is usually performed in the fluoroscopy unit. However, in several institutions, the procedure is done directly under CT guidance. Although it differs slightly between institutions performing CT arthrography, a good option for preparation of the mixture is 10 mL normal saline solution and 10 mL iodinated contrast material (370 mg/cc). Normally, a volume of about 12 to 17 mL is needed for a reasonable injection and joint distention. In some institutions, 1 mL of lidocaine is added to this solution to reduce eventual complaints. In case MR arthrography and CT arthrography are considered to be performed in the same patient, the following mixture can be used: First, 2 mL of gadolinium (Gd-DTPA) is added in 250 mL of normal saline solution. Then, 10 mL of that solution is mixed with either (a) 10 mL of iodinated contrast material (370 mg/cc) or (b) 9 mL of iodinated contrast material (370 mm/cc) and 1 mL of lidocaine. CT arthrography with its superior spatial resolution offers several advantages over plain MRI for the evaluation of intraarticular structures. In particular, image acquisition at a submillimeter scale together with the availability of multiplanar reformations can help evaluate intraarticular pathology. Therefore, CT arthrography might serve as an excellent alternative in cases where MR is contraindicated.
Osteonecrosis of the adult represents a well-defined circulatory osteopathy that progresses in different stages. The early (preradiographic) stages with nonspecific imaging findings are potentially reversible. Manifest osteonecrosis, defined by a subchondral defect in the weight-bearing zone of the femoral head surrounded by a reactive interface that separates the necrotic area from living bone, is irreversible in almost all cases. Osteonecrosis is also known as avascular necrosis (AVN) and ischemic or aseptic femoral head necrosis . Osteonecrosis after a fracture of the femoral neck (posttraumatic) or hip dislocation is caused by an acute ischemia due to damage of the vascular supply of the femoral head. In nontraumatic osteonecrosis, 80% of patients show several risk factors, which are associated with a heterogeneous group of disorders such as caisson disease, sickle cell anemia, Gaucher disease, systemic lupus erythematosus, hyperuricemia, pancreatitis, alcoholism, and cortisone therapy. Therefore, multiple theories about the pathogenesis of developing osteonecrosis exist. However, all finally lead to a common pathway of interruption of the local subchondral circulation of the affected bone.
In nontraumatic osteonecrosis, the incidence has been estimated to be approximately 0.01% of the population, and about 10% of all total hip replacements are performed because of osteonecrosis. Bilateral involvement of the femoral head is frequent. The consensus is that most cases of osteonecrosis have no clinical symptoms at the early beginning of the disease (“silent hip”). In this early phase, the patients usually are not seeing a physician, and therefore silent hips were diagnosed incidentally, in most of the cases by MRI due to a painful contralateral hip or by serial MR examinations in high-risk patients.
Histologically in the subchondral zone, necrotic bone trabeculae are embedded in necrotic marrow without any signs of remodeling or an insufficient repair only. The necrotic tissue is separated by a reactive interface from adjacent bony structures and marrow. The reactive interface consists of well-vascularized granulation tissue and thickened bone trabeculae covered with new bone formation representing an active repair process. Edematous bone marrow changes can sometimes be observed peripherally to the reactive interface. These latter morphologic changes beyond the necrotic lesion might represent the morphologic link between the focal changes of classic osteonecrosis and the diffuse changes in bone marrow edema syndrome (BMES).
Imaging findings of osteonecrosis of the hip should be reported according to the international classification system of the Association Research Circulation Osseous (ARCO), which should replace the several different staging systems used so far.
MR imaging is highly sensitive in depicting early AVN and is considered to be the method of choice for accurate diagnosis and staging of the disease.
In ARCO stage 0, all imaging findings are normal or nondiagnostic, and, because this initial stage without repair lasts for a few days only, it normally will not be observed in clinical practice. There are only subtle histologic findings indicating the existence of this very early phase.
In ARCO stage I, only reversible bone marrow changes had occurred, and therefore radiographs and CT still remain normal.
Scintiscans can show a nonspecific “hot spot” with increased radionuclide uptake, indicating enhanced vascularity caused by the repair process.
On MRI, a focal subchondral marrow defect shows the nonspecific pattern of bone marrow edema but no reactive interface. At this early stage, MRI is not able to differentiate this nonspecific pattern from other subchondral entities with similar bone edema.
In ARCO stage II, radiographs and CT images are still equivocal, showing only a more or less mottled radiolucent area with osteosclerotic or cystic lesions due to the bony repair activity. Later, a sclerotic rim surrounds this subchondral lesion, indicating the new bone formation at the reactive interface ( Figs. 23-1 and 23-2 ).
On scintiscans, an area of decreased tracer accumulation of the central necrotic lesion can be surrounded by increased tracer uptake at the reactive interface and residual femoral head. This “cold in hot” spot is pathognomonic of osteonecrosis.
On MRI, the subchondral necrotic defect now shows different signal alterations that are surrounded by a band of low signal intensity on T1-weighted images, representing new bone formation at the reactive interface. In most of the cases, on T2-weighted and contrast-enhanced images, a high signal intensity line central to the low signal line (double-line sign) is characteristic for the well-vascularized granulation tissue of the focal lesion, but insufficient repair can be seen. These MRI patterns are pathognomonic. Beginning with stage II, osteonecrosis can be sufficiently diagnosed by MRI and differentiated from pathologic alterations such as fissure, fracture, or contusion. At this point, osteonecrosis has become irreversible, and the necrotic area has been walled off from the living bone. This “point of no return” occurs much earlier than was presumed in the pre-MRI era, when the collapse of the femoral head was regarded as the point of no return. Some investigators have reported follow-up MR studies showing apparent healing of osteonecrotic lesions in high-risk patients. At least some of these cases included focal bone marrow edema lesions without a reactive interface, thereby representing ARCO stage I lesions, which are reversible.
In ARCO stages III and IV, the femoral head becomes mechanically unstable, and a subchondral fracture, collapse of the femoral head, and, subsequently, secondary arthritic changes occur and can be identified on radiographs and CT images ( Fig. 23-3 ). Although focal osteonecrotic lesions of all stages are significantly different from the diffuse bone marrow edema pattern, combinations of both imaging patterns can be observed.
Characteristic MR findings for osteonecrosis in one hip joint and a typical edema pattern on the contralateral side are reported ( Figs. 23-4 and 23-5 ). Osteonecrosis is generally accepted to be a progressive disease with a rate of collapse higher than 80% after 2 to 4 years, if it is symptomatic and left untreated. In the past few years, MRI could clearly demonstrate that the stage, the extension, and the location of the defect are the most important prognostic factors.
Conservative management alone with partial weight bearing or medication is generally regarded to produce unacceptable results. The clinical outcomes of electrical stimulation, magnetic fields, hyperbaric oxygenation, and extracorporeal shock wave therapy have not been successful in controlled studies, so far.
If left untreated, the disease progresses in about 80% of cases, and, sooner or later, an operative intervention (total hip arthroplasty) is generally recommended and cannot be avoided. Because treatment at an early stage is directly associated with a better prognosis and may prevent or delay at least total hip arthroplasty, early diagnosis and accurate staging of AVN are crucial.
Legg-Calvé-Perthes disease is a juvenile aseptic osteonecrosis of the femoral head that is not an uncommon disease of childhood. The incidence varies widely between 5.5 and 15.6 per 100,000 children younger than 15 years of age. Legg-Calvé-Perthes disease often leads to distortion of the size and shape of the proximal femur and results in disability. Prognosis in this disease is worsened by a deformity of the femoral head and abnormal growth of the proximal femur, which may be observed as a consequence of severe epiphyseal or physeal involvement. Children suffering from Legg-Calvé-Perthes disease may even have growth disturbances caused by premature physeal closure.
The radiographically unremarkable initial phase of the disease is followed by advancing sclerosis and a fragmentation as well as a reparation phase. Imaging includes plain film radiography, scintigraphy, and MRI.
More than 20 years ago, Catterall and colleagues characterized the different histologic phases of Legg-Calvé-Perthes disease. The extent of necrosis using the Catterall classification provides valuable radiologic information for prognostic significance.
In grade I, only the anterior part of the epiphysis is affected. There is no collapse or sequestration. In the early stage of the disease, metaphyseal changes are unusual.
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