1 Introduction

Posttraumatic dysplasia of the acetabulum is a rare, yet distinct, deformity usually caused by traumatically induced closure of the triradiate cartilage of the acetabulum. It differs substantially from the pattern of developmental acetabular dysplasia. All observed cases show a rather uniform pathomorphology that toward the end of growth results in a deformity of the entire hemipelvis. In one reported case of bilateral involvement [1], the deformity led to a symmetrical transverse elongation of the pelvis. Traumatic involvement of the acetabulum is rather uncommon in children but becomes more frequent in adolescents. Incidences reported in the literature vary from 0.8−15.2% [2–4]; however, later growth disturbances develop in only a selected few of these injured hips [2–5]. Experimental fusion of the triradiate cartilage in a rabbit model resulted in acetabular deformity and dislocation of the femoral head [6]. Marked thickening of the medial acetabular wall also is not an uncommon observation after pediatric pelvic surgery, and similar deformities have been observed after septic arthritis causing destruction of the triradiate cartilage [7, 8].

2 Pathophysiology

The acetabulum is formed from the iliac, ischial, and pubic bones. Growth of the acetabulum occurs via an interposed and confluent physis—the triradiate cartilage. The triradiate cartilage has a bipolar growth potential; constant pressure of the femoral head provides the appropriate molding stimulus, whereas peripheral growth centers are responsible for the final depth of the acetabulum, which is an ongoing process until age 16−18 years [9]. Fusion of the triradiate cartilage in animal models revealed that isolated fusion of the ilioischial limb of the triradiate cartilage caused the same deformity as fusion of all three limbs, whereas isolated iliopubic fusion did not substantially influence acetabular growth [6, 10]. In patients, however, it is difficult to determine the mechanism and amount of injury to the acetabular physis. Fusion could occur via formation of a bony bridge over the inner border of the physis, as observed by Rodriguez [11]. Ponseti [9] focused on the perichondrium of the inner physeal border, which may rupture and be repaired by callus formation; while Buchholz et al [3] proposed that destructive injury to the stratum germinativum of the physis is necessary to produce such a deformity. Another influential factor is the patient’s age at the time of injury, when 5 years seems to be the threshold. In a study [3] of nine patients, the five with evidence of premature partial closure of the growth plate who did not subsequently develop dysplasia had an average age of 13 years at time of injury. Dora et al [12] compiled eight posttraumatic dysplasia cases from the literature; the average age at injury was 5 years and the late deformity was identical. In their series of ten hips with post-traumatic acetabular dysplasia, the average age at the initial trauma was 3 years (range, 2–5 years).

3 Pathomorphology

Dora et al [12] aimed to analyze and quantify the complex deformity by measuring standard AP pelvic x-rays from these patients. Computed tomography was available for five hips, which confirmed some measurements; five hips also had a false profile view available for further evaluation. In four cases, injury radiographs and follow-up x-rays were available. Three were Salter-Harris type II injuries, and one was a Salter-Harris type I or V injury [13]. For all cases, premature closure of the triradiate cartilage was evident within the first year after the injury. Evaluation of the ten AP x-rays revealed a uniform distortion of the true pelvis with an angular deformity in the region of the acetabular fossa. This deformation created a lateral, caudal, and posterior shift of the acetabulum and femoral head.

Although the ilioischial line and the center of the femoral head were both relatively lateralized, the center of the femoral head was disproportionally further lateral. This was due in part because the width of the acetabular teardrop and inner wall increased, and also because the femoral head subluxated laterally with an increased distance between the acetabular fossa and the center of the head. The inner symmetry of the anterior part of the pelvis was preserved. In all cases, the acetabular deformity consisted of a marked deficit of lateral coverage. Considerable retroversion, as acquired using Hefti’s semiquantitative method [14], was also a constant finding that is consistent with only moderate deficiency anteriorly. This was confirmed with computed tomography in five cases. On the involved side, the femoral head tended to be slightly smaller, which may have been caused by the x-ray projection as the pelvic rotation deformity causes the involved head to be closer to the x-ray plate ( Fig 2.17-1 ).

In classic developmental dysplasia, the outer surface of the pelvic ring may be deformed by surgery but the true pelvis remains symmetrical. Thickening of the medial wall can be observed, although this occurs mainly after acetabular surgery to a lesser degree. In developmental dysplasia, the femoral head may migrate cranially and the femoral neck is often anteverted. In contrast, the acetabulum in post-traumatic dysplasia displaces caudally, resulting in a leg-length discrepancy with the leg on the involved side longer, even though femoral growth is not affected by the deformity ( Fig 2.17-2 ).