Transient Synovitis of the Hip
Transient synovitis of the hip is a benign, nontraumatic, self-limited disorder that mimics septic hip in clinical presentation. The physician confronting this condition must exclude septic hip, which is a surgical emergency.
Although the cause of transient synovitis is unclear, evidence suggests it is associated with immune responses to viral or bacterial antigens, mediated through the synovial membrane. Aseptic synovial fluid rapidly accumulates under pressure in the hip joint, and there may be severe pain from capsular distension. The fluid is resorbed within 3–7 days, with no long-term sequelae.
As with septic hip, upper respiratory tract infections often precede transient synovitis by a few days to 2 weeks. The hip contains excess synovial fluid and is held in flexion, abduction, and external rotation because this is the joint's position of maximum capacity. The joint may be sore and resistant to movement, but subluxation does not occur. Usually, the patient allows careful passive movement.
Leukocytosis is absent, and ESR and CRP are not elevated. Synovial fluid does not show elevation of the white blood cell count, and bacterial cultures are negative.
Radiographs reveal only capsular swelling, and effusion may be detected on ultrasound. Although experienced physicians frequently suspect transient synovitis based only on clinical examination, aspiration of the hip following confirmation of needle position by radiograph or ultrasound is the safest approach.
The most important differential diagnosis is septic hip, which must be excluded. Also, early stages of Legg-Calvé-Perthes disease (see section on Legg-Calvé-Perthes disease) may include a synovitic stage that, until the development of characteristic radiograph findings, is indistinguishable from transient synovitis. No evidence indicates that transient synovitis leads to Legg-Calvé-Perthes disease itself. Typically, the pain is less severe than in transient synovitis, the children are a bit older (older than 4–5 years), and there is no history of recent illness.
Treatment of transient synovitis includes simple analgesics and splintage, usually by bed rest, until symptoms resolve.
Sultan J, Hughes PJ: Septic arthritis or transient synovitis of the hip in children: the value of clinical prediction algorithms. J Bone Joint Surg Br
Developmental Dysplasia of the Hip
- Certain infants (breech babies, babies with a family history, and females) are at higher risk for developmental dysplasia of the hip.
- Diagnosis is made clinically or by ultrasound.
- Early treatment gives the best results.
Developmental dysplasia of the hip is one of the most serious problems in pediatric orthopedics. The neonatal hip is a relatively unstable joint because the muscle is undeveloped, the soft cartilaginous surfaces are easily deformed, and the ligaments are lax. Exaggerated positioning in acute flexion and adduction in utero may occur, especially in breech presentation. This situation may cause excess stretching of the posterior hip capsule, which renders the joint unstable after delivery. Laxity may reflect family history or the presence of maternal relaxin hormone in the fetal circulatory system.
This relative instability may lead to asymptomatic subluxation (partial displacement) or dislocation (complete displacement) of the hip joint. Displacement of the femoral head in the infant is proximal (posterior and superior) because of the pull of the gluteal and hip flexor muscles. In the subluxated hip, asymmetric pressure causes progressive flattening of the posterior and superior acetabular rim and medial femoral head (dysplasia is the term to describe these structural deviations from normal).
In the completely dislocated hip, dysplasia also occurs because normal joint development requires concentric motion with normally mated joint surfaces. The shallow, deformed dysplastic joint surfaces predispose to further mechanical instability and the inexorable progression of the disorder.
Developmental dysplasia of the hip (DDH) occurs in approximately 1 in 1000 live births in whites, is less common in blacks, and may be more common in certain ethnic groups such as North American Indians. In all groups, this disorder is more likely if certain risk factors are present, such as positive family history, ligamentous laxity, breech presentation (and, by association, cesarean delivery), female gender, large fetal size, and first-born status. Dislocations may be bilateral but are more often unilateral and on the left side.
Reversal of dysplasia and subsequent normal hip development depend on early detection of DDH. Early detection is made more challenging by lack of a definitive test or finding on examination. Moreover, because this disorder is painless, there are no symptoms in the infant. Detection of bilateral dislocations may be particularly difficult.
Radiographs are usually not useful in newborn infants because the femoral head is composed of radiolucent cartilage. Ultrasound examination is helpful, but false-positive results are common before 8–10 weeks of age. The test is expensive, and interpretation requires comprehensive training. Thus, the best test for this disorder is careful physical examination at birth, repeated at each well-infant check until the child is walking normally. A high index of suspicion is mandatory, especially if risk factors are present.
Several examination maneuvers require a quiet, relaxed infant and commonly produce false-negative findings. Although it is imperative to detect subluxated or dislocated hips, it is also helpful to identify the very lax (unstable) but still located hip. This type of joint may either dislocate later or exhibit subtle dysplasia during growth that can cause premature osteoarthritis.
A dislocated hip displaces proximally, causing the leg to be marginally shorter. This occasionally leads to the accordion phenomenon, with wrinkling of thigh skin folds. The most significant fold is between the genitals and gluteus maximus region. This test is not very reliable, frequently producing false-positive and false-negative results (Figure 10–4A).
Clinical examination of developmental dislocation of the hip. In all pictures, the child's left hip is the abnormal side. A: Asymmetric skin folds. B: Galeazzi test. C: Limitation of abduction. D, E, F: Ortolani and Barlow tests (see text).
With the child lying on a flat surface, flex the hips and knees so the heels rest flat on the table, just distal to the buttock (Figure 10–4B). A dislocated hip is signaled by relative shortening of the thigh compared with the normal leg, as shown by the difference in knee height level. This test is almost always useless in children younger than 1 year and is negative if dislocation is bilateral.
The flexed hips are gently abducted as far as possible (Figure 10–4C). If one or both hips are dislocated, the femoral head (the pivot point during abduction) is posterior, causing relative tightness of the adductor muscles. Asymmetric abduction or limited abduction (usually <70 degrees from the midline) is a positive finding. When the hip is lax (dislocatable but not dislocated), the abduction test is normal despite the presence of subluxation or dislocation.
A provocative test that picks up an unstable but located hip, the Barlow test is unsuitable for a dislocated hip. The flexed calf and knee are gently grasped in the hand, with the thumb at the lesser trochanter and fingers at the greater trochanter (knee flexion relaxes the hamstrings). The hip is adducted slightly and gently pushed posteriorly and laterally with the palm (Figure 10–4D, F). Detection of so-called pistoning, or the sensation of the femoral head subluxating over the posterior rim of the acetabulum, is a positive finding.
This test detects hips that are already dislocated. The flexed limb is grasped as in the Barlow test. The hip is abducted while the femur is gently lifted with the fingers at the greater trochanter (Figure 10–4D, E). In a positive test, there is a sensation of the hip reducing back into the acetabulum. Reduction is felt but not heard: The old concept of a so-called hip click is incorrect. The Ortolani test may be negative at 2–3 months of age, even when the hip is dislocated, because of the development of soft-tissue contracture.
In the infant, diagnosis is made by physical examination alone, and radiographs are generally unnecessary. Dysplasia, instability, and dislocation may appear on ultrasound studies, which can allow visualization of hip contour and stability before ossification is present. Sonography is a dynamic examination that requires an experienced interpreter, and there can be false positives prior to 6–10 weeks of age. Radiographs may be used at any age, but the absence of ossified structures renders them inaccurate in the newborn. After 4–6 months, when the ossific nucleus appears in the femoral head, radiographs are more helpful. Because much of the skeleton is cartilaginous at this age, certain lines and angles may be drawn on radiographs to allow estimates of geometric parameters (Figure 10–5). These may suggest evidence of acetabular dysplasia (a more vertical slope of the acetabular roof, measured as the acetabular index), femoral dysplasia (small or absent ossification center in the femoral head), or lateral superior displacement of the femoral head.
Lines drawn for measurement in developmental dysplasia of the hip. In the figure, the patient's left hip (on the right of the figure) is the subluxated one. A: Hilgenreiner line is a horizontal line of the pelvis, drawn between the triradiate cartilages. The proximal femoral ossification center should be below this line. B: Perkins line is a vertical line (perpendicular to Hilgenreiner line) drawn down from the lateral edge of the acetabulum. The femoral head ossification center, as well as the medial beak of the proximal metaphysis, should fall medial to this line. C: The acetabular index is the angle between Hilgenreiner line and a line joining the acetabular center (triradiate) with the acetabular edge as it intersects Perkins line. It measures acetabular depth and should be below 30 degrees by 1 year of age and below 25 degrees by 2 years of age. D: The center-edge angle is the angle between Perkins line and a line joining the lateral edge of the acetabulum with the center of the femoral head. It is a measure of lateral subluxation that becomes smaller as the hip subluxates laterally. Normal is 20 degrees or greater.
Increased femoral anteversion (external rotation of the femoral head and neck) is often present in DDH but not visible. Increased anteversion may be seen as an increase in relative femoral neck valgus in the older child.
Detection of Dysplasia in the Older Child
As the infant grows older, many diagnostic maneuvers that are positive in a young infant become negative because soft-tissue changes accommodate the displaced structures. Thus, the Ortolani and Barlow signs can be negative, even in the face of grossly abnormal hip development, making detection particularly difficult (especially between 4 and 15 months of age). The first signs of developmental dysplasia may then not be recognized until the child begins to walk and demonstrates a waddling gait with excessive lumbar lordosis. Radiographs at this age are diagnostic.
Treatment of DDH should be initiated as soon as the diagnosis is suspected. Early treatment is generally successful, whereas a delay in treatment may result in permanent dysplastic changes. Exact treatment depends on patient age at presentation and degree of involvement. Regardless of age, treatment may fail, and the physician may need to institute a more complex treatment plan. The current recommendations described next.
A dislocated hip at this age may spontaneously reduce over 2–3 weeks if the hip is held in a position of flexion. This is best accomplished with the Pavlik harness (Figure 10–6), a canvas device that holds the hips flexed at 100 degrees and prevents adduction but does not limit further flexion. Movement in the harness is beneficial for the joint and helps achieve gradual spontaneous reduction and stabilization of the hip. Treatment with a Pavlik harness has a low risk of avascular necrosis (see section on avascular necrosis of the hip). This treatment should not be continued beyond 3–4 weeks if there is no improvement. The failure rate of the Pavlik harness is approximately 10%, necessitating more invasive treatment, such as closed or open reduction.
The Pavlik harness, a device used for treatment of hip dislocation, subluxation, and dysplasia.
Age 6–12 Months (before Walking)
Gentle manipulative reduction of the dislocation under a general anesthetic and maintenance of a located position for 2–3 months in a spica cast usually stabilizes the joint. Even after the hip is stable, any residual dysplasia must be treated by bracing or surgery. In the past, prereduction skin traction was thought to reduce the risk of avascular necrosis. It is now believed that adequate hip flexion and limited abduction in the spica cast are the most important safety factors, and most surgeons no longer use traction.
In toddlers or young children in whom closed reduction failed, open reduction of the hip is required. Severe flattening of the acetabulum with distortion of the normal spherical femoral head shape is found on opening the hip. The limbus (acetabular rim) may be flattened and inverted, and the ligamentum teres is always hypertrophic. Fibrofatty tissue occupying the center of the acetabulum must be removed. Femoral shortening osteotomy may be required at the time of open reduction to reduce soft-tissue tension and minimize the risk of avascular necrosis. After reduction, the position is maintained by capsular repair (capsulorrhaphy) and a cast, until stability is achieved. Prolonged bracing or surgery is often required to resolve the residual dysplasia that accompanies untreated dysplasia in this group of children.
Significant residual dysplasia is present in children with DDH who are untreated at this age. Dysplasia may also persist despite successful reduction performed by any method at an earlier age. The dysplasia may be accompanied by a limp, and radiographs show a high acetabular index (more vertical acetabular roof), increased valgus of the femoral neck, and subluxation of the femoral head.
Surgical correction of dysplasia creates a stable mechanical environment that permits remodeling to a more normal joint during growth. Treatment requires bony procedures, either on the acetabular or femoral sides of the joint, or on both sides. Acetabular procedures, such as the Salter or Pemberton osteotomies, improve the acetabular index and increase the mechanical stability of the joint.
Femoral osteotomy corrects the anteversion and femoral neck valgus that characterize femoral dysplasia. The exact selection of osteotomy site may be based on maximum radiographic dysplasia or on the individual surgeon's preference. All of the osteotomies require that the femoral head be spherical and the hip joint concentrically reduced before an attempt can be made to correct the dysplasia. In general, the osteotomy should address the site of dysplasia, that is, acetabular dysplasia is not ideally treated with femoral osteotomy. Nevertheless, femoral osteotomy, if performed before 4 years of age, stimulates a dysplastic shallow acetabulum to remodel into a more normal shape. This occurs because the femoral osteotomy renders the hip joint more stable, thus allowing the normal mechanisms of growth to take over. Similarly, patients exhibit a progressive decrease in femoral dysplasia following successful acetabular osteotomy.
Salter osteotomy is a surgical procedure to redirect the acetabulum in DDH (Figure 10–7). Animal models demonstrate that residual hip dysplasia is accompanied by acetabular malrotation and deficiency in the anterolateral acetabular rim. Salter osteotomy corrects this deficiency by rotating the acetabular region anteriorly and laterally.
Salter innominate osteotomy, used for managing acetabular dysplasia. After a transverse cut is made above the acetabulum (A), the acetabular fragment is rotated forward and outward (B) to improve acetabular coverage.
The procedure is indicated in children 18 months to 10 years of age in whom concentric reduction of the hip was achieved. It is used to correct moderate acetabular dysplasia and can improve the acetabular index by 15 degrees. It may also be used to stabilize the hip at the time of open reduction. The pelvis above the hip joint is exposed subperiosteally. A transverse cut is made, using a wire saw, from the sciatic notch to the anteroinferior iliac spine, and the entire distal fragment (including the acetabulum) is spun on the pivot points of the notch and the pubic symphysis. This redirects the entire dysplastic acetabulum to a more horizontal stable position. A bone graft and pins hold the osteotomy open until it heals. A spica cast is used for 6 weeks to protect the graft during healing.
Salter osteotomy requires a second operation to remove the fixation pins. Because the geometric reorientation afforded is limited, there may be residual dysplasia. In addition, failure to achieve a concentric reduction before pelvic osteotomy usually renders the procedure ineffective.
Indications for the Pemberton osteotomy (Figure 10–8) are similar to those of the Salter osteotomy, and frequently one or the other is selected according to the surgeon's experience or preference. The Pemberton procedure is particularly suited for correction of the long stretched-out dysplastic acetabulum because it reduces the capacity of an overly spacious acetabulum. This is done by cutting above the acetabular roof, down to the flexible triradiate cartilage (the growth plate of the center of the acetabulum). The roof fragment is then pried down to a more horizontal position and held in place by wedging a bone graft into the resulting defect. The fold thus produced in the center of the acetabulum may cause temporary stiffness. In younger children, this quickly remodels, but it is the major reason many surgeons do not perform this procedure on children older than 7–8 years.
Pemberton pericapsular iliac osteotomy. An osteotomy cut is made above the acetabulum down to the flexible triradiate cartilage (A). The fragment is pried down to improve acetabular coverage and held with a bone graft (B).
Like the Salter procedure, Pemberton osteotomy requires concentric reduction before it is performed. For the Pemberton osteotomy, the pelvis is exposed above the joint. Under radiographic guidance, a curved osteotome is used to cut the pelvic bone from the acetabular roof down to the triradiate cartilage (the central growth plate of the acetabulum). The flexible cartilage allows the fragment to be hinged down over the femoral head, producing a more horizontal acetabular roof. A bone graft from the upper ilium wedges into the osteotomy site to maintain correction, and a spica cast is used until healing, which takes approximately 6 weeks.
Rarely, early extrusion or graft collapse occurs, and transient stiffness may be seen in older children. Because there is no internal fixation, a second procedure is unnecessary.
Femoral osteotomy (Figure 10–9) may be used to correct severe increased femoral anteversion or coxa valga (a high neck-shaft angle), conditions that are sometimes seen in residual DDH.
Femoral osteotomy is performed at the intertrochanteric level and fixed with a plate and screws.
The procedure is particularly indicated when radiographs taken with the hip in abduction and internal rotation show improvement in the overall congruency of the hip. Redirection of an anteverted, valgus hip stimulates spontaneous improvement in dysplastic acetabula in children younger than 4 years.
Femoral osteotomy is performed using a lateral approach, with the cut made across the intertrochanteric region of the femur. This site is chosen both because it is distal to the blood supply of the femoral head and because the cancellous bone heals easily. A metal blade-plate is placed in the proximal (femoral neck) fragment, usually after positioning with a provisional guidewire. The femoral neck fragment is rotated into a more horizontal position (varus) and is then internally rotated to correct excessive anteversion. The exact degree of correction is determined by preoperative radiograph positioning to achieve maximum congruence and correction of radiographic dysplasia. The plate portion is then clamped to the shaft of the bone and fixed with screws. A spica cast is usually used to supplement fixation.
After healing (6 weeks), the patient may resume walking. A Trendelenburg limp is common for 1–2 years after femoral osteotomy because of the geometric distortion of the relationship between the joint and insertion of the abductor muscles. This resolves as the femur remodels with growth and does not present a long-term problem.
After age 6–10 years, reduction and reconstruction of severely dysplastic or dislocated hips may be impossible. If acetabular coverage is poor but the joint is concentric, major reorientation of the acetabulum may be indicated. Salter osteotomy (see above) may be inadequate for this degree of reorientation, necessitating the addition of osteotomy cuts in the pubis and ischium to allow more aggressive repositioning of the joint surface (triple innominate osteotomy).
For children older than 10 years with hip pain and nonreconstructable joints, Chiari osteotomy reliably improves pain. After a slightly upwardly angled cut is made through the ilium just at the proximal edge of the hip capsule, the hip joint is medially displaced half the width of the iliac cut. After healing, the lateral protruding shelf of the ilium blends with the hip capsule to create a functional equivalent of an augmented hip socket, lined with the smooth capsule, which serves as part of the joint surface.
Complications of Surgery for DDH
Avascular Necrosis of the Hip
If a reduction maneuver for DDH was forceful or if there is tension in the soft tissues around the hip, the resulting compression of the joint may cause transient blockage of the blood supply to the femoral head. The subsequent death of the ossific nucleus and proximal growth plate of the femur (avascular necrosis) is a complication of treatment rather than of the disorder itself. A well-recognized cause of avascular necrosis is exaggerated forced abduction in the spica cast used after closed or open reduction. Avascular necrosis may be mild (involving a small fraction of the ossific nucleus), in which case it may go undetected and be of little significance. At the other extreme, avascular necrosis may lead to complete femoral head death and loss of future growth at the proximal physis. As it revascularizes, a dead femoral head may deform significantly, subluxate further, and require abduction bracing or osteotomy. Thus, it can cause leg-length inequality or early osteoarthritis of the hip. The best treatment for avascular necrosis is prevention.
Residual Dysplasia and Degenerative Arthritis
No form of treatment uniformly resolves hip dysplasia, and residual dysplasia is common. It may lead to resubluxation or cause failure of remodeling. Older children are more prone to residual problems and may require repeat surgery to help resolve them. Dysplasia is a major cause of premature osteoarthritis of the hip.
Lehmann HP, Hinton R, Morello P, et al: Developmental dysplasia of the hip practice guideline: technical report. Committee on Quality Improvement, and Subcommittee on Developmental Dysplasia of the Hip. Pediatrics
Rejholec M: Combined pelvic osteotomy for the bipartite acetabulum in late developmental dysplasia of the hip: a ten-year prospective study. J Bone Joint Surg Br
Walton MJ, Isaacson Z, McMillan D, Hawkes R, Atherton WG: The success of management with the Pavlik harness for developmental dysplasia of the hip using a United Kingdom screening programme and ultrasound-guided supervision. J Bone Joint Surg Br
Weinstein SL, Mubarak SJ, Wenger DR: Developmental hip dysplasia and dislocation: part II. Instr Course Lect
- Legg-Calvé-Perthes disease is most common in children age 4–8 years and is largely self-healing.
- Flexion contracture and loss of abduction are uniform and characteristic.
- There may be a small subgroup of patients with Legg-Calvé-Perthes disease who benefit from surgical treatment.
Legg-Calvé-Perthes disease (LCP, Perthes disease) is a serious but mostly self-limited pediatric hip disorder. Although its cause is unknown, the disease is thought to be related to avascular necrosis of the hip. It affects children between 4 and 10 years of age and is somewhat more common in boys. Children with the disease are often small for their age and have retarded bone age. The disease is generally unilateral. Although bilateral LCP of the hips occurs in about 10% of cases, in patients with symmetric changes/stages, other conditions such as Gaucher disease or multiple epiphyseal dysplasia must be considered. Multiple epiphyseal dysplasia is most readily diagnosed by evaluation of other radiographs, in particular of the knee and, if confirmatory, of the spine to assess for spondyloepiphyseal dysplasia. Patients with multiple epiphyseal dysplasia generally have heights in the fifth percentile or below. Newer investigations suggesting that some cases of LCP might be related to a variety of transient or permanent hypercoagulation states are intriguing but not confirmed in multiple centers. Surprisingly, trauma is not considered a causative factor in LCP.
Although early radiographs may be negative, they eventually show fragmentation, irregularity, and collapse of part or the entire femoral head ossification center (Figure 10–10). The few pathologic specimens that were examined suggest that multiple rather than single episodes of avascular necrosis occur over a period of months. Early bone scans may show a filling defect corresponding to areas of necrosis, and MRI is typical of avascular necrosis. The disease has a characteristic course (see Figure 10–10). Initially, the avascular episodes are silent and the child is asymptomatic. As the disease progresses, the necrotic femoral epiphysis is revascularized. Osteoclasts remove dead bone while osteoblasts simultaneously lay down new bone on the dead trabeculae (a process known as creeping substitution). During this phase, the femoral head is mechanically weak. Fragmentation and collapse of the bony structure may then occur, causing geometric flattening and deformity of the ossific nucleus and femoral head. The newly replaced bone takes the shape of the collapsed head. At this point, continued growth may allow gradual remodeling and improvement of the femoral head shape until maturity. The symptomatic collapse phase rarely exceeds 1–1.5 years, but full revascularization and remodeling may continue silently for several years thereafter. Although cartilage is not specifically injured by the avascular events, hyperemia can cause articular cartilage thickening, ectopic ossification, and physeal damage that affects femoral neck growth.
Legg-Calvé-Perthes disease. A: Central necrotic fragment with collapse. B: Same patient after healing and partial remodeling.
Clinical Findings and Classification
The initial presentation of LCP is usually a painless limp, with aching pain in older children. If pain is present, it may be mild and referred to the thigh or knee. Physical examination discloses atrophy of the thigh on the affected side and, usually, limited hip motion. The typical patient has a flexion contracture of 0–30 degrees, loss of abduction compared with the opposite side (in severe cases, no abduction beyond 0 degrees), and loss of internal rotation of the hip.
Radiographs may be negative at first, probably because the initial softening of the femoral head is sufficient to cause symptoms but insufficient to change the radiographic appearance of the femoral head. The eventual characteristic collapse of portions of the femoral head is diagnostic of the disease, however.
The exact extent of necrosis, which is estimated in fourths of the head using the Catterall classification (Figure 10–11), is helpful in determining whom to treat. This may require additional radiographs.
The Catterall classification is used to determine probable course and prognosis of Legg-Calvé-Perthes disease. It is based on progressive involvement of approximate fourths of the femoral head. AP, anteroposterior.
An alternative radiograph classification uses the lateral third of the femoral epiphysis (the so-called lateral pillar). Collapse of this structure suggests a poor prognosis for late deformity (class C), whereas maintenance of pillar height correlates with good long-term results (class A). Partial collapse suggests an intermediate prognosis (class B). The difficulty with all classification systems is their reproducibility and the need to delay until the collapse phase before the exact extent of involvement is clear.
There is little value in bone scans or MRI in the clinical management of LCP.
Age at presentation and range of motion (ROM) of the hip are the two most significant predictors of long-term outcome. Children with bone age less than 5 years and children who exhibit relatively minor involvement (less than half of the femoral head) rarely need treatment. In these children, so much of the femoral head is cartilage, and therefore unaffected by necrosis, that mechanical collapse does not markedly decrease sphericity. Also, younger children have tremendous remodeling potential, and minor collapse can be outgrown before maturity. Limited hip ROM may be due to muscle spasm early on, or synovitis; but in late disease, it may reflect incongruity of the joint. Older children who exhibit some radiographic changes but have excellent ROM may require only observation and serial reexamination.
Nonoperative and Operative Treatment
The issues surrounding selection of patients with LCP who need treatment are as highly controversial as the treatment itself. Most experts agree that children who maintain excellent motion (particularly abduction greater than 30 degrees in the absence of flexion contracture) may not require intervention. In children older than 4–5 years with significant collapse or progressive loss of abduction, treatment is frequently recommended.
No evidence indicates that use of crutches or relief of weight bearing has any effect on femoral head collapse in this disease. For those children requiring it, however, treatment should minimize the effects of collapse and subluxation that often occur when the femoral head deforms. This is best achieved by abduction of the hip until subluxation resolves. The molding action of the acetabular shape is thought to help improve the contour of the collapsing femoral head. Abduction can be accomplished nonoperatively by holding the legs in abduction (Petrie) casts or using an ambulatory brace (Figure 10–12).
Abduction bracing is one method used for ambulatory treatment of Legg-Calvé-Perthes disease.
Operative procedures are advocated by some and include varus femoral osteotomy and Salter osteotomy, which were adapted from hip dysplasia treatment to control the subluxation seen in some cases of LCP. Healing usually occurs within 18 months. The best current investigations suggest that children over 8 years who have partial head collapse (lateral pillar B-C or Catterall III) may ultimately have better radiographic outcome if treated by surgery.
Despite many studies, there is still no consensus for the best method of treatment; some patients do well without treatment, whereas others have a poor result after aggressive treatment. Prognosis can often be predicted from the knowledge of certain factors (Table 10–5), with age being the most important.
Table 10–5. Factors in Long-Term Prognosis for Patients with Legg-Calvé-Perthes Disease. ||Download (.pdf)
Table 10–5. Factors in Long-Term Prognosis for Patients with Legg-Calvé-Perthes Disease.
Age at diagnosis
Maintained (abduction >30 degrees)
Stiff (abduction <15 degrees)
Extent of involvement
<50% of femoral head
>50% or total femoral head
Little or no subluxation
Subluxation, lateral calcification
Herring JA, Kim HT, Browne R: Legg-Calvé-Perthes disease. Part II: prospective multicenter study of the effect of treatment on outcome. J Bone Joint Surg Am
Karol LA: Legg-Calvé-Perthes disease 100 years on: what have we learned? J Am Acad Orthop Surg
Kim HK: Legg-Calvé-Perthes disease. J Am Acad Orthop Surg
Terjesen T, Wiig O, Svenningsen S: The natural history of Perthes' disease. Acta Orthop
Slipped Capital Femoral Epiphysis
- Slipped capital femoral epiphysis is most common in overweight children entering puberty.
- Early diagnosis and surgical management give the best results.
Slipped capital femoral epiphysis is an adolescent hip disorder characterized by displacement of the femoral head on the femoral neck through failure of the proximal femoral physis (growth plate). Displacement changes the geometry of the upper end of the femur and hinders hip function (Figure 10–13). This disorder is one of the main causes of premature osteoarthritis in young adults.
Anteroposterior (AP) and frog-leg views of a slipped epiphysis. The dotted lines show the normal position of the femoral head.
Slipped capital femoral epiphysis affects both male and female adolescents 11–13 years of age. In 30–40% of patients, the condition is bilateral, although both legs are not always affected simultaneously. The typical patient is overweight—often markedly so—and is in either late prepuberty or early puberty. Rarely, the patient is tall, asthenic, and rapidly growing.
This disorder occurs at a time when the cartilage physis of the proximal femur is thickening rapidly under the influence of growth hormone. The vigorous secretion of sex hormone has not yet begun, however, so the biological effect of sex hormones on closure and stabilization of the growth plate is absent. This combination of thick growth plate cartilage (weaker than bone and subject to shear), lack of sexual maturity (which would stabilize the physis), mechanical stress (caused by obesity), and the peculiar anatomic mechanics of the hip joint renders the growth plate susceptible to slippage.
The direction of the slip is always posterior and often medial, and the mechanical bases of chronic and acute disorders are the same. In chronic slipped capital femoral epiphysis, the most common form (90% of patients), the femoral head slips insidiously at the growth plate over the course of several months. In the acute form, the femoral head is suddenly displaced, a condition that can be superimposed on chronic changes. Displacement may occur during normal activity or following minor trauma.
Because slipped capital femoral epiphysis is a progressive disorder and the prognosis depends on the severity of the slippage, early detection and prompt treatment are imperative.
There are two forms of the disorder: chronic and acute. The onset of chronic slipped capital femoral epiphysis is usually insidious, with a history of a painful limp for 1 to several months prior. The pain is characteristically aching and located in the thigh or knee rather than the hip. This referred pain to the knee is responsible for many misdiagnoses. Patients may be seen for knee pain and dismissed as normal after a negative knee examination and radiographs. A high index of suspicion is required to detect slipped capital femoral epiphysis in the obese limping adolescent complaining of knee pain. The change in hip ROM is usually diagnostic: loss of abduction and internal rotation of the hip are evident, although these may be difficult to identify in the grossly overweight child. There is almost always a characteristic obligatory external rotation of the hip when it is flexed because of the distorted hip anatomy caused by the disorder. The femoral head is posterior to its normal position, so the flexed hip must externally rotate to keep the head within the acetabulum.
Acute slipped capital femoral epiphysis is accompanied by severe pain and limping, which may render the patient immobile. The onset is sudden, following little or no trauma, and examination discloses a painful, guarded, restricted range of hip motion. An acute slip is analogous to an epiphyseal fracture. In its unstable form, the patient is unable to bear weight, and there is a high rate of avascular necrosis. In its stable form, the sudden increase in displacement is painful, but limited weight bearing is possible and the risk of avascular necrosis appears to be lower.
Slipped capital femoral epiphysis can be difficult to detect on standard AP radiographs (Figure 10–14). A frog-leg lateral view is the best for detecting mild forms because slippage is always posterior. A radiograph also shows changes suggesting acute or chronic forms, information that may be critical to management of the disorder.
Radiograph diagnosis of left slipped capital femoral epiphysis. A: Anteroposterior film shows subtle medial displacement of left epiphysis, best appreciated by drawing a line (Klein line) along the lateral side of the normal and abnormal femoral neck. The slipped epiphysis does not protrude lateral to this line. B: Frog-leg lateral radiograph clearly demonstrates posterior displacement.
Establishing the severity of slippage is important in determining treatment and prognosis. Severity is estimated by the percentage of femoral neck left exposed. Slippage of less than 25% of neck width is mild; 25–50% is moderate; and more than 50% is severe.
Slipped capital femoral epiphysis is usually a progressive disease that requires prompt surgical treatment. Because the changes in the chronic form occur so slowly, it is impossible to manipulate the femoral head into a better position. Treatment consists of fixing the slip in its current position and preventing progression. This is done by inserting one or more screws or pins across the growth plate, regardless of the severity of the slip (pinning in situ).
Following surgery, aching rapidly resolves, and during the remaining 2–3 years of skeletal growth, the extent of remodeling of the distorted proximal femur may be considerable, leading to an improved ROM.
Because of bilateral involvement, some surgeons recommend prophylactic screw fixation of the normal side at the time of initial treatment. This is particularly indicated in children ages 10 years and under.
Acute slips, if unstable, may be gently reduced before fixation, but the risk of further damage to the tenuous blood supply of the proximal femur and subsequent avascular necrosis is always significant. For this reason, many surgeons accept the position of an acute slip and pin it in situ.
In some cases, high-grade slipped capital femoral epiphysis does not remodel sufficiently with growth, despite treatment. In these cases, a residual, chronically painful limp is present, requiring correction by proximal femoral osteotomy. The osteotomy site may be at the level of the slip, which is mechanically effective but relatively risky for the blood supply. Alternatively, osteotomy can be performed at the trochanteric level; this is a safer procedure for correction of the functional deformity but does not resolve the exact anatomic deformity.
In addition to the problems of impingement of the anterior metaphyseal prominence, which can impede motion, patients with slipped capital femoral epiphysis may rarely develop chondrolysis, a poorly understood degeneration of the hip articular cartilage. It may be painful and may progress to severe joint narrowing and degenerative changes within 6 months.
During chondrolysis, cartilage is replaced by fibrous tissue, the joint capsule thickens and contracts, and joint motion is lost. Typically, the joint stiffens in flexion, abduction, and external rotation. Radiographs reveal joint narrowing, irregularity, and subchondral sclerosis, as well as regional osteoporosis from disuse.
Chondrolysis can result from iatrogenic malposition (permanent penetration) of pins or screws used for fixation of slipped capital femoral epiphysis. Although brief penetrations during surgery are probably common and cause no complications, unrecognized permanent pin penetration is disastrous. Chondrolysis also appears without obvious penetration and occasionally is detected in patients before treatment begins.
Chondrolysis is treated by nonsteroidal anti-inflammatory drugs (NSAIDs), aggressive physical therapy and ROM exercises, and observation. Capsular release is sometimes useful in resistant cases. Approximately half of patients eventually recover satisfactory painless motion. The other half may require hip fusion for symptomatic relief.
Patients with an acutely slipped capital femoral epiphysis can develop avascular necrosis of the femoral head (see section on developmental dysplasia of the hip). These patients are usually teenagers so their hips lack potential for remodeling, and the prognosis is therefore poor. Yet, some patients with partial head involvement regain a painless hip after 1–2 years of symptoms. Some patients with painless but abnormal ROM may be treatable by intertrochanteric osteotomy to reorient the arc of motion. Long-term pain following avascular necrosis is treated by hip fusion.
Slipped epiphysis is a major cause of early osteoarthritis. In general, the higher the degree of slip, the earlier the degenerative changes begin. In fact, a statistical increase in degenerative arthritis is evident even in the radiographically normal hip of patients with a contralateral slipped epiphysis. This suggests that subclinical bilateral involvement is more common than recognized.
Loder RT, Greenfield ML: Clinical characteristics of children with atypical and idiopathic slipped capital femoral epiphysis: description of the age-weight test and implications for further diagnostic investigation. J Pediatr Orthop
Peck D: Slipped capital femoral epiphysis: diagnosis and management. Am Fam Physician
Sankar WN, McPartland TG, Millis MB, Kim YJ: The unstable slipped capital femoral epiphysis: risk factors for osteonecrosis. J Pediatr Orthop