Treatment modalities for the long-term sequelae of infantile septic arthritis of the hip are outlined in Table 31.1. The recommended primary and secondary treatment methods are as varied as the types of deformities. Unfortunately, no definite primary treatment for a severely damaged hip joint makes the affected joint capable of withstanding the forces imposed on it by otherwise healthy children with their long-term physical demands [1]. Thus, any surgical treatment for severe sequelae must be regarded as a measure that temporarily improves the clinical function and delays the more definitive procedures that are reserved for adult patients [1, 2]. The pearls and pitfalls in the management of late sequelae of infantile septic arthritis of the hip are summarized in Table 31.2.

Type II and III hips are fundamentally the result of an abnormally shaped, sized, or oriented FH and neck, altered head-neck offset, and acetabular dysplasia. A wide variety of residual deformities of the FH have been observed in Type II and III hips, ranging from deformities similar to those in Perthes disease with coxa vara/valga, coxa plana, coxa breva, coxa magna, coxa irregularis, relative greater trochanteric overriding, sagging rope sign [15], and acetabular dysplasia to the more deformed proximal femur visualized as beard, collared, staghorn, or rugby ball-shaped FH [16, 17].

Children with Type II or III deformities may remain asymptomatic in their younger age, but, in (pre)adolescence, these children often present with clinical problems such as pain, limp, joint instability or contracture, restriction of motion, LLD, spinal disorders, and even emotional disturbances. According to the author’s experience, in older children with Type II and III hips, a painful limp is usually associated with femoroacetabular impingement (FAI) with or without damaged acetabular cartilage and/or labrum.

Figure 31.2 depicts a stepwise algorithmic approach to FAI in Perthes-like deformities at the author’s institute. First, the extent of asphericity is assessed; if it is mild and the FH is well contained within the acetabulum, osteochondroplasty of the head and neck junction alone is indicated. Next, the presence or absence of a labral tear is determined. If a labral tear is present, labral debridement or refixation is necessary. Similarly, the presence of coexisting acetabular dysplasia is assessed. If the hip becomes congruent in abduction, relative femoral neck lengthening combined with periacetabular osteotomy (PAO) or triple innominate osteotomy (TIO) is indicated. In the author’s institute, Bernese PAO is preferred for correction of acetabular dysplasia in adolescents and young adults with closed triradiate cartilage (around 12 years in girls and 14 years in boys) [18], whereas a TIO, in (pre)adolescents with open triradiate cartilage [19]. If the hip becomes congruent in adduction, proximal femoral valgus osteotomy and PAO or TIO are indicated. The next step is to check whether coxa breva and coxa vara associated with relatively greater trochanteric overriding are severe enough to cause FAI, and if so, a relative or true femoral neck lengthening combined with distal advancement of the greater trochanter (GT) is indicated [20–23]. When the FH asphericity is too severe and the FH is “irreducible,” the following procedures should be considered. If the hip becomes cong-ruent in extension and adduction, femoral valgus-flexion osteotomy plus/minus PAO or TIO should be considered. If the hip becomes congruent in any rotational position, rotational osteotomy with or without PAO or TIO may be indicated. If the FH with a central depression is too severely deformed such that the FH cannot be contained within the acetabulum in any position, Chiari osteotomy or FH reduction osteotomy [20, 21, 24] plus/minus PAO or TIO can be considered. In addition, combination of osteochondroplasty, labral debridement/refixation, and distal advancement of the greater trochanter should be performed, if necessary.

The available reconstructive procedures for the treatment of Type IV hips are limited, and, in general, have not yielded satisfactory long-term results [1, 2, 7, 11, 25–29]. When only a remnant of the FH and neck is present, it is difficult to maintain a stable reduction; and if instability and dislocation persist, the surgeon can either leave the deformity uncorrected or can attempt reconstruction of femoro-pelvic articulation [25]. In young children in whom the FH and neck have been destroyed, as in Type IVA sequelae, a new femoral neck can be fashioned to articulate with the acetabulum by utilizing the L’Episcopo [30], Harmon [31], or Albee [32] reconstruction methods. When a reasonably sized unossified cartilaginous cap persists as a femoral neck remnant, open reduction can be attempted. The repositioning of the femoral remnant into the acetabular socket can be facilitated using a modification of the Harmon technique [31]. An incomplete, spring osteotomy is made at the base of the femoral remnant adjoining the greater trochanter and the resulting opening wedged gap is filled with a block of cartilage graft taken from the iliac apophysis. This procedure produces a femoral neck-lengthening effect [28]. In older children, gradual lengthening of the remnant femoral neck using the Ilizarov technique may be indicated. Nonetheless, the author believes that open reduction in children more than 6 years of age is not likely to be beneficial because of the high risk of developing stiffness and pain. Therefore, the author recommends that in children older than 6 years of age, Type IVA hips should be treated in the same manner as hips with Type IVB sequelae [2].

Postponing the treatment of Type IVB hips will result in proximal iliac dislocation with a marked abductor lurch, telescoping, limp, and LLD [8, 26]. Although these patients may remain asymptomatic for a number of years [3, 7, 12] they are at a risk of developing degenerative changes in the lumbosacral spine and hips [25]. Therefore, various treatment modalities for reconstructing a femoro-pelvic articulation in Type IVB hips have been reported: hip reconstruction with vascularized iliac crest grafting [33], arthrodesis, greater trochanteric arthroplasty (GTA) [25, 26, 34–39] with adjunctive or secondary procedures, pelvic support osteotomy (PSO) [40–44], and Ilizarov hip reconstruction (IHR) [44–58]. Of these treatment modalities, the two most commonly performed procedures are GTA and IHR.

The rate of overall unsatisfactory results in terms of residual deformities after infantile or childhood septic arthritis of the knee and ankle joints is less as compared to that after septic arthritis of the hip [5, 6], because the infection in these joints can be diagnosed sooner than that in the hip [9]. Long-term assessment is essential because radiographic improvement in the involved epiphyseal region can occur several months to years after the infection. In younger children in whom the secondary ossification center has not yet developed, vascular damage can lead to a marked delay in the formation of the ossific center, but the cartilage model continues to grow. Therefore, even when bone deficiency is seen on plain radiography, it is necessary to perform advanced imaging studies such as ultrasonography, arthrography, or MR imaging [9] in order to better visualize the cartilaginous epiphysis (chondroepiphysis) and assess the potential growth of the adjacent physis. When the appropriate treatment is delayed, growth disturbance with a resultant angular deformity, joint incongruity, impingement, and accompanying ligamentous laxity and joint instability may develop gradually. Postinfectious juxta-articular deformity of the knee usually develops as a result of metaphyseal osteomyelitis or primary septic arthritis of the knee, involving the distal femoral physis or the proximal tibial physis, or both. The distal femur is more prone to growth-related sequelae than the proximal tibia. Angular deformities due to partial distal femoral physeal destruction are far more common than complete symmetric growth cessation [9]. The most serious growth sequelae occur following neonatal sepsis and to a lesser extent within the first 2 years of life [6, 9] (Fig. 31.5). In particular, meningococcemia caused by Neisseria meningitides or meningococcus, which is found only in human respiratory secretions, is a devastating illness that primarily affects young children. The disseminated intravascular coagulation and focal infections of the acute phase are primarily responsible for the vascular injuries to the growing chondro-osseous tissues and contiguous soft tissues. Ischemic changes also selectively involve the physeal circulation, which adversely affect longitudinal and transverse growth of bone. Therefore, children who survive meningococcal septicemia are prone to develop complex deformities of the lower limb due to multiple areas of growth disturbance [59–61].