Click here to view next page of this article
LCPD is idiopathic osteonecrosis or avascular necrosis of the CFE, and the associated complications thereof, occurring in an immature, growing child. This osteochondrosis is caused by an interruption of the CFE blood supply. It is primarily a disorder affecting males (4-5:1) and is bilateral in approximately 20% of children. Children with LCPD also often have delayed bone ages, disproportionate growth, and mild short stature.
The clinical onset of LCPD typically is between the ages of 2 and 12 yr (mean, 7 yr). Most children present with mild or intermittent pain in the anterior thigh and a limp. The classic presentation has been described as a "painless limp." The pertinent early physical findings include antalgic gait; muscle spasm with mild restriction of motion, especially abduction and internal rotation; proximal thigh atrophy.
Anteroposterior and Lauenstein (frog) lateral radiographs of the pelvis should be obtained to establish the diagnosis. The radiographic characteristics can be divided into five distinct stages representing a continuum of the disease process: (1) cessation of CFE growth, (2) subchondral fracture.
There are three radiographic classification systems of the extent of CFE involvement. Catterall developed a four-group classification on the basis of the appearance of the CFE at maximum resorption. Although this classification has been helpful in retrospective analysis of results, it has limited prognostic value because it is difficult to apply in the earliest phases of the disease process. Salter-Thompson used two groups and Herring and colleagues, three groups, depending on involvement or extent.
LCPD is a local, self-healing disorder. Prevention of femoral head deformity and secondary osteoarthritis are the only justifications for treatment. The treatment goals are (1) elimination of hip irritability, (2) restoration and maintenance of a good range of hip motion, (3) prevention of CFE collapse, extrusion, or subluxation, and (4) attainment of a spherical femoral head.
Temporary or periodic treatment with bed rest or abduction stretching exercises to maintain mobility can be used in conjunction with observation. Recurrent episodes of hip irritability with a temporary decrease in motion commonly occur during the phases of subchondral fracture and fragmentation, and the child may benefit.
Nonsurgical or surgical containment of the femoral head in the course of the disease is indicated when (1) the age at clinical onset is 6 yr or older (possibly 5 yr in girls), (2) the lateral column or pillar of the CFE is involved, or (3) there is a loss of containment, as manifested by extrusion of the femoral head.
Abduction casts (Petrie) or orthoses are commonly used to contain the femoral head within the acetabulum. Containment is continued only until there is early radiographic subchondral reossification. Because this usually occurs 12-17 mo after clinical onset, nonsurgical containment methods can be limited to 18 mo or less with no adverse effect on the outcome. Currently, the Atlanta Scottish Rite Hospital orthosis is the most widely used because it allows reciprocal motion and ambulation without crutches or external support. The success of nonsurgical containment has recently been challenged on the grounds that it does not alter the natural history of untreated LCPD.
The selection of pelvic or femoral osteotomy for surgical containment is based on the philosophy and technical expertise of the surgeon. The results of surgical containment appear to be better than those of nonsurgical containment.
If significant femoral head deformity prevents reduction of the femoral head into the acetabulum, an alternative method must be considered. Several surgical procedures at least partially correct the various existing deformities.