Legg-Calve-Perthes disease (LCPD) is a pediatric disorder characterized by osteonecrosis of the capital femoral epiphysis. The osteonecrosis progresses to fragmentation of the femoral head and eventual revascularization and reossification. Ultimately, LCPD leaves a residual deformity of the proximal femur and acetabulum that can be a cause of progressive hip pain and dysfunction later in life. Previous reports have noted that anywhere between 30% and 50% of individuals affected by LCPD have residual hip symptoms that persist into adulthood.¹,²,³ The resultant deformities of the hip can lead to pathologic mechanics of femoroacetabular impingement (FAI), hip instability, or a combination of both pathologies.⁴ The long-term prognosis of the hip is associated with femoral head sphericity and joint congruence.⁵,⁶,⁷ Femoral deformity includes loss of epiphyseal sphericity, coxa magna or breva, a high-riding greater trochanter, and relative retroversion of the femoral head. On the acetabular side, retroversion is commonly encountered, but the acetabular remodeling in response to significant proximal femoral deformity may lead to an adaptive form of acetabular dysplasia.⁸ Successful treatment of deformity following LCPD requires an ability to accurately identify and subsequently correct the varied pathomorphology encountered. The goal of treatment is a stable, concentrically reduced joint with an optimized range of motion.

Symptoms caused by the morphologic abnormalities encountered in healed LCPD deformities reflect those encountered in the idiopathic cases of FAI and dysplasia. Classically, FAI is characterized by the abnormal, repetitive contact of the anterior femoral head and neck with the anterior acetabulum. In the healed LCPD hip, this impingement can result from morphologic changes on either the proximal femur or the acetabulum. This abnormal contact leads to progressive damage to the acetabular cartilage, acetabular labrum, or both.⁹ Patients with FAI tend to have anterior groin pain and pain in the “c-sign” region of the hip, which is aggravated by physical activity, prolonged sitting, and positions of flexion and internal rotation. Stiffness or loss of motion is also quite common and can at times become symptomatic prior to the onset of pain. Extra-articular FAI, involving contact between the trochanters and the pelvis, can also be seen in the healed LCPD hip. It presents as posterolateral hip pain with extension activities when localized to the greater trochanter and posterior groin pain with extension activities when localized to the lesser trochanter.

Instability symptoms typically manifest during upright activities such as walking or running. Pain may be localized to the anterolateral aspect of the hip and can be associated with pain along the psoas muscle and abductor musculature. Abductor fatigue and a perceived limp can be related to instability but may also be a product of the high-riding greater trochanter and associated inefficiency of the abductor musculature. Symptoms of locking or “catching” of the hip joint with activity may be indicative of articular pathology such as labral tears, cartilage flaps, or loose bodies (Figure 9.1).

Initial imaging of patients with healed LCPD deformity should provide a thorough analysis of both proximal femoral and acetabular morphology. Routine radiographs should include a standing anteroposterior (AP) view of the pelvis, lateral view of the proximal femur (45° Dunn or frog-leg lateral), and a false profile view of the acetabulum. Measurements of proximal femoral deformity include assessment of the femoral head-neck sphericity (alpha angle, head-neck offset ratio), the position of the greater trochanter with respect to the femoral head (articulotrochanteric distance), and femoral neck-shaft axis. On the acetabular side, measurements of acetabular coverage (lateral center edge angle, Tönnis roof angle, anterior center edge angle, anterior/posterior wall indices) should be performed. Markers of acetabular retroversion include
assessment of the crossover sign, posterior wall sign, and prominent ischial spine sign. Owing to the often significant deformity associated with LCPD, we recommend routine cross-sectional imaging. Computed tomography of the pelvis, including the distal femur, should be obtained for assessment of the bony morphology, including three-dimensional reconstruction and femoral version. Magnetic resonance imaging is important to determine the extent of articular cartilage and acetabular labral damage.

Management of patients with symptomatic healed LCPD requires identification of individual pathomorphologies and associated soft-tissue abnormalities that contribute to the patient’s symptoms. It is crucial to distinguish hips with isolated FAI from hips with secondary acetabular dysplasia and instability and from hips with both. Moreover, it is essential to understand the source of the conflict between the proximal femur and the acetabulum rim (femoral vs. acetabular or combined; intra-articular vs. extra-articular) to design the surgical strategy. The most common treatment options on the femoral side of the hip joint include intertrochanteric osteotomy, relative neck lengthening, true femoral neck lengthening, trochanteric advancement, and osteochondroplasty of the head and neck junction. In very severe dysmorphic hips with an incongruent joint, the femoral head reduction osteotomy has recently been described as an option. On the acetabular side, extra-articular procedures include acetabular shelf osteotomy and redirectional osteotomies. In the healed LCPD hip, complex deformities of both femur and acetabulum leading to instability and FAI usually require a combined approach. A comprehensive assessment of the femoral and pelvic pathomorphology
allows for identification of different subtypes and planned treatment according to the altered anatomy. Our strategy for the treatment of symptomatic hip deformity secondary to healed LCPD involves the surgical hip dislocation approach¹⁰ to assess and treat the femoral deformity and intra-articular pathology and the Bernese Periacetabular Osteotomy (PAO)¹¹ for the treatment of the acetabular deformity (Figure 9.2).

A detailed description of the surgical hip dislocation is provided in Chapter 12 and a description of the dissection of the retinacular flap in Chapter 7. Briefly, the surgery is performed with the patient in the lateral decubitus position using a straight lateral incision.¹² The fascia lata is split in line with the femoral shaft, and the interval between the gluteus maximus and medius is dissected. The gluteus medius is retracted, allowing for exposure of the gluteus minimus and the piriformis tendon. The interval between the piriformis tendon and the gluteus minimus is opened by sharp dissection, and the inferior border of the gluteus minimus is dissected from underlying capsule (Figure 9.3). Next, a 1 to 1.5-cm thick trochanteric osteotomy is performed with an oscillating saw, leaving the piriformis tendon and short external rotators intact on the base of the stable trochanter (Figure 9.4). The trochanteric piece is reflected and flipped anteriorly with the attached vastus lateralis and gluteus medius. The previously exposed capsular
minimus is further elevated anteriorly off the hip capsule. The anterolateral portion of the vastus lateralis is released from the femur, with the hip in external rotation, until the level of the gluteus maximus insertion. A capsulotomy is performed in a Z-shape fashion (right hip) or reverse Z-shape (left hip), with the longitudinal arm of the Z in line with the anterior femoral neck. With the capsule opened, intra-articular and extra-articular causes of FAI can be dynamically determined. Flexion, adduction, and external rotation allow for the hip to partially dislocate, and the ligamentum teres is divided to allow complete dislocation of the femoral head. The femoral and the acetabular articular cartilage and the labrum are inspected for the presence of labral and chondral lesions.