Acetabular Dysplasia in the Reduced Or Subluxated Hip

Home , Acetabulum, Dysplasia, Genu varum, Hip dysplasia, Hip dysplasia (canine), Hip pain

1 Acetabular Dysplasia 5 2 in the Reduced or Subluxated Hip

3 Jonathan G. Schoenecker, Ira Zaltz, Justin Roth, 4 and Perry L. Schoenecker

5 Introduction include: dysplasia, impingement and avascular 26 necrosis. The purpose of this chapter is to review 27 6 As first proposed by Dr. William Harris in the the pathologic processes of acetabular and proxi- 28 7 early 1980s, it has become clear that osteoarthri- mal femoral development that lead to acetabular 29 8 tis (OA) of the hip does not exist as a primary dysplasia in a located, or subluxated, hip. 30 9AU2 disease, or if it does, it is extraordinarily rare [1]. Emphasis will be placed upon understanding 31 10 The extensive experience in total hip replacement how the developmental milestones of the acetab- 32 11 surgeries over the last four decades have provided ulum influence the surgeon’s decision to operate, 33 12 extensive insight into the pathological hip joint and if so, whether to perform an acetabuloplasty, 34 13 processes that lead to hip OA [2]. In particular, redirectional, salvage or replacement procedure. 35 14 mechanical pathologies that cause damage to “Mechanical pathologies that cause dam- 36 15 either the labrum or the chondrolabral junction age to either the labrum or the chondro- 37 16 are often the initiating processes which instigate labral junction are often the initiating 38 17 acetabular and femoral head arthritis (Fig. 5.1) processes which instigate acetabular and 39 18 [3]. These key observations have stimulated the femoral head arthritis” 40 19 field of hip preservation, which focuses on deter- 20 mining the mechanisms that cause damage to 21 these structures and the development of surgical Pathophysiology 41 22 approaches that comprehensively correct these 23 pathomorphologies [4–8]. The three pathological Normal anatomical development of the hip 42 24 processes that lead to injury and degeneration of requires coordinated growth of both the acetab- 43 25 the labrum and the chondrolabral junction [1, 2] ulum and proximal femur that provides essential 44 femoral head coverage and clinical stability by 45 J. G. Schoenecker (*) the time the child is skeletally mature [9]. 46 AU1 Department of Orthopaedics, Vanderbilt University Normal acetabular development results in a con- 47 Medical Center, Nashville, TN, USA gruent hip joint with approximately 15° of ace- 48 e-mail: [email protected] tabular anteversion and sufficient coverage of 49 I. Zaltz the femoral head. At skeletal maturity, an intact 50 William Beaumont Hospital, Royal Oak, MI, USA hip joint is stable during weight bearing and 51 J. Roth · P. L. Schoenecker physiologic range of motion, without inappro- 52 Department of Orthopaedics, Washington University priate stresses on the chondrolabral junction. 53 Medical Center, St. Louis, MO, USA e-mail: [email protected]; Normal proximal femoral development results 54 [email protected] in a spherical femoral head with approximately 55

a bc d

Fig. 5.1 Prevailing theory of osteoarthritis of the hip. Years of improper loading of the hip results in tearing of Mechanical pathology leads to labral pathology and hip the labrum or the chondrolabral junction (yellow arrow). osteoarthritis. (a) Radiographs of a mildly dysplastic hip (d) Progression of the tear, or increased pathologic load- in 34-year old female with right hip pain (white arrow rep- ing leads to arthritis of the femoral head or the acetabulum resents position of patient chondrolabral junction). (b, c) (red arrow)

56 15° of femoral version and the tip of the greater motion and pain [10]. During ambulation, hip 87 57 trochanter at the level of the center of the femo- dysplasia may result in excessive stress on the 88 58 ral head. This normal hip development allows labrum and/or chondrolabral junction (Fig. 5.2), 89 59 for joint congruency during physiologic activi- abnormal abductor muscle tension (with gait dis- 90 60 ties, with physiologic motion of 90° of flexion, turbance), and malalignment of the limb leading 91 61 15° of internal rotation at 90° of flexion and a to distal joint pathologies. With these in mind, 92 62 90° arc of rotation with equal internal/external surgical approaches have been designed to pre- 93 63 rotation (45°) in the prone position. Proper fem- serve the hip joint, addressing the pathological 94 64 oral neck offset and alignment of the greater and mechanical problems presented by these pro- 95 65 lesser trochanters assures both normal muscle cesses. The goals of hip joint preservation sur- 96 66 tension and force vectors for hip rotation while gery is to restore stable acetabular coverage of 97 67 avoiding extracapsular impingement on the pel- the femoral head and achieve a near normal range 98 68 vis during physiologic joint motion. Adequate of motion, without femoral acetabular/pelvic 99 69 acetabular coverage, proper acetabular and impingement. Proximal femoral dysplasia may 100 70 proximal femoral version and 15° of external occur from primary developmental pathologies, 101 71 tibial torsion, results in a stable base to support such as proximal femoral focal deficiency, coxa 102 72 the torso over the limb with a foot-forward gait valga/vara or excessive version. It can also 103 73 during single leg stance. develop secondarily, from diseases such as Legg- 104 74 Hip dysplasia with a located, or subluxed, Calve-Perthes disease, slipped capital femoral 105 75 femoroacetabular joint is associated with inap- epiphysis or avascular necrosis. These conditions 106 76 propriate development of either the acetabulum, are presented in detail in other chapters. 107 77 proximal femur or both. Either alone or in combi- Acetabular dysplasia may occur primarily from 108 78 nations, the resulting pathomorphologies cause failure of development or secondarily from 109 79 damage to the labrum/chondrolabral junction and improper loading by the proximal femur. The 110 80 articular cartilage, leading to premature degener- morphologic characteristics are dependent upon 111 81 ation of the hip joint [4–8]. Acetabular under- the stage of acetabular development at the time of 112 82 coverage of the femoral head produces instability insult. 113 83 of the femoroacetabular joint. In addition to dam- Acetabular development (Fig. 5.3) is a 114 84 aging intracapsular structures of the hip, intra- dynamic process of endochondral ossification 115 85 capsular/extracapsular impingement of the femur involving the cartilaginous anlage that includes 116 86 on the acetabulum or pelvis causes restricted two essential growth centers: the triradiate 117 5 Acetabular Dysplasia in the Reduced or Subluxated Hip

ab cd

Fig. 5.2 Micro-instability of the dysplastic hip damages micro-instability of the femoroacetabular joint during the chondrolabral junction. Hip dysplasia with a located, daily activities. (c) This instability ultimately leads to or subluxed, femoroacetabular joint refers to inappropri- damage of the (c) labrum/chondrolabral junction (red ate development of either the acetabulum, proximal femur arrow) or even (d) fracture of the acetabular epiphysis (red and or both. (a) Angle arrows represent insufficient lateral arrow). Ultimately, this damage leads to premature degen- center edge angle (LCEA) of the ossifying acetabular eration of the hip joint epiphysis. (b) The resulting pathomorphologies leads to

118 cartilage and the acetabular epiphysis (os acetab- response to the increased size of the femoral 148 AU3119 uli) [11–13]. During the first 4 years of life the epiphysis [12, 13]. 149 120 majority of acetabular development occurs via Acetabular dysplasia can therefore be broken 150 121 biomechanical molding, with sequential ossifica- down to three categories: (1) improper shape and/ 151 122 tion of the acetabular cartilaginous anlage and or delay in ossification of the cartilaginous anlage, 152 123 radial growth of the acetabulum (by the triradiate (2) damage to the triradiate cartilage, or (3) prob- 153 124 cartilage). The shape of the acetabular cartilagi- lems of shape and/or delayed ossification of the 154 125 nous anlage is primarily influenced through acetabular epiphysis. Problems of shape and/or 155 126 direct contact (articulation) with the femoral delay in ossification of the cartilaginous anlage 156 127 head. The femoral head must be stably reduced in occur early in life. As the cartilaginous anlage is 157 128 the true acetabulum for optimal acetabular growth considerably plastic, malformation most com- 158 129 and development. The cartilaginous anlage is monly occurs as a result of eccentric loading of the 159 130 considerably plastic during the cartilaginous proximal femur. This results in an altered hip cen- 160 131 phase and becomes much less plastic later on, ter which is typically superiorly migrated, 161 132 following vascular invasion and subsequent ossi- observed as a “break in Shelton’s line” on a weight 162 133 fication. The triradiate cartilage is responsible for bearing AP pelvis with femoral version neutral- 163 134 growth of acetabular width, which must match ized (Fig. 5.4). Severe subluxation may cause 164 135 the growth of the femoral epiphysis. In a normal more significant morphologic changes to the carti- 165 136 hip, the majority of the cartilaginous anlage has laginous anlage and resemble a dislocated hip on 166 137 ossified by 4 years of age 12[ , 13]. After 4 years radiographs. Additionally, inappropriate biome- 167 138 of age, triradiate cartilage growth continues to chanical loading may also delay the vascular inva- 168 139 widen the developing acetabulum to accommo- sion and ossification of the cartilaginous anlage 169 140 date a larger proximal femoral epiphysis [12, 13]. which is observed as an abnormal acetabular index 170 141 Triradiate cartilage growth is typically complete (AI) (Fig. 5.5). Although the cartilaginous anlage 171 142 by 12 years of age in girls and 14 years of age in has a significant capacity to remodel, it cannot do 172 143 boys [12, 13]. Starting around age 4 years, and so without restoration of the appropriate hip cen- 173 144 continuing to skeletal maturity, an increase in ter. Additionally, there is no evidence that once an 174 145 acetabular depth occurs secondary to growth of anlage has undergone a morphologic change in the 175 146 the acetabular epiphysis. This growth is essential hip center (broken Shelton’s line) that it is capable 176 147 in providing adequate coverage of a hip in of restoring its normal shape, and hip center, 177 J. G. Schoenecker et al.

c d

Fig. 5.3 The dynamic process of acetabular develop- the growth of the femoral epiphysis. (c) After 4 years of ment. (a) Acetabular development is a dynamic process of age, triradiate cartilage growth continues to widen the endochondral ossification that occurs through the carti- developing acetabulum to accommodate a larger proximal laginous anlage that includes two essential growth cen- femoral epiphysis. Starting around the age of 4 and con- ters: the triradiate cartilage and the acetabular epiphysis tinuing to skeletal maturity, an increase in acetabular (os acetabuli). (b) During the first 4 years of life, the depth occurs secondary to growth of the acetabular epiph- greater majority of acetabular development occurs through ysis. (d) Triradiate cartilage growth is typically complete the biomechanical molding and sequential ossification of by 12 years of age in girls and 14 years of age in boys, the acetabular cartilaginous anlage (big blue arrows) and around which time the acetabular epiphysis initiates its the radial growth of the acetabulum by the triradiate carti- ossification. (e) At skeletal maturity, the acetabular epiph- lage (small blue arrows). The triradiate cartilage is respon- ysis is completely ossified and acetabular development is sible for growth of acetabular width, which must match complete 5 Acetabular Dysplasia in the Reduced or Subluxated Hip a b

c d

e f

Fig. 5.4 Deformation of the cartilaginous anlage. point, although delayed in its ossification, the cartilaginous Problems of shape and/or delay in ossification of the carti- anlage observed in (c) is sufficient to maintain hip congru- laginous anlage occur early in life. As the cartilaginous ity. (e) As the child grows, if the acetabular anlage fails to anlage is considerably plastic, malformation most com- ossify and deform, the hip will migrate superior lateral monly occurs from eccentric loading of the proximal femur. without dislocation. (f) This migration is observed on a In this case an 8-month old female (a) with a dislocated hip standing radiograph with migration of the ossification cen- observed by (b) radiographs with an ossification center in ter back towards the superior lateral quadrant formed by the superior lateral quadrant defined by Hilgenreiner’s line Hilgenreiner and Perkin’s lines, a break in Shenton’s line (white dashed line) and Perkin’s line (yellow dashed line). and increased acetabular index (AI) as compared to the (c) The patient undergoes successful closed reduction with contralateral side. Together, these pathologic changes in the (d) restoration of the ossification center to the inferior anlage results in an altered hip center, which has not been medial quadrant of Hilgenreiner’s and Perkin’s line. At this demonstrated to spontaneously recover J. G. Schoenecker et al.

Fig. 5.5 Acetabular index. The acetabular index (a) mea- maintains the hip center in the appropriate position (yel- sures the ossification of the cartilaginous anlage. The nor- low arrow c). With pathologic development (right hip and mal values per age are presented in Table 5.1. In a b) the anlage may deform leading to a delay in ossification normally forming hip (left hip and c), the ossification of and migration of the hip center laterally (yellow arrow b) the anlage results in an index of 20° by the age of 3. This

ab c

Fig. 5.6 Severe deformation of the cartilaginous anlage ing (c) of a 10-year-old boy demonstrates a subluxed hip in untreated dysplasia. Although the cartilaginous anlage with lateral migration and break in Shenton’s line. This has a significant capacity to remodel, it cannot do so with- migration places the labrum (yellow arrow) cartilaginous out restoration of the appropriate hip center. Severe defor- epiphysis at the junction with the labrum (red arrow) in a mity of an untreated subluxed, but not dislocated, hip biomechanically unfavorable position to function. often leads to permanent deformity of the vital developing Additionally, the pathologic forces deform and delay the structures of the hip. Radiographs (a), MRI (b) and draw- ossification of the cartilaginous anlage (blue arrow)

178 without surgical intervention. Delay in ossification labrum, may result in an intra-articular deformity 185 179 of the acetabular cartilaginous anlage, observed as with dual hip centers that present few reconstruc- 186 180 a delay in acetabular index normalization, may tive possibilities other than salvage procedures 187 181 also occur in idiopathic cases without morpho- (Fig. 5.6). Conditions affecting triradiate cartilage 188 182 logic change in the anlage. Additionally, if left growth are typically caused by trauma, infection, 189 183 uncorrected, the acetabular anlage shape and the cancer or iatrogenic (secondary to surgery) [15]. 190 184 resultant position of the acetabular epiphysis and Abnormal triradiate cartilage growth often results 191 5 Acetabular Dysplasia in the Reduced or Subluxated Hip

abc

Fig. 5.7 Late pathology of the acetabular epiphysis: nous growth (red arrow) and ossification (blue arrow) of Problems of development, shape or delay of ossification the anterior and lateral acetabular epiphysis accounts for of the acetabular epiphysis occur close to skeletal matu- the majority of late-presenting acetabular dysplasia. These rity. They typically present radiographically as an insuffi- developmental conditions lead to improper loading of the cient anterior or lateral center edge angle (a) labrum (yellow arrow) and chondrolabral junction AU4 radiographically or (b) by MRI. Failure of both cartilagi-

192 in the development of a severe pincer type acetab- The main principle in the treatment of acetab- 208 193 ulum. Fortunately, likely secondary to the robust ular dysplasia involves maintaining hip joint 209 194 blood supply of the pelvis, premature triradiate reduction to provide an optimum environment for 210 195 cartilage arrest is rare. There are few reports of acetabular and femoral head development. 211 196 successfully restoring the normal development of Intervention should be considered to alter an 212 197 a failed triradiate growth center. Problems of shape adverse natural history of pathologic acetabular 213 198 or delayed ossification of the acetabular epiphysis cartilaginous anlage, triradiate cartilage and ace- 214 199 occur closer to skeletal maturity. They typically tabular epiphysis. 215 200 present radiographically as an insufficient anterior 201 or lateral center edge angle radiographically or by 202 MRI. Failure of both cartilaginous growth and Essential Pathophysiology Leading to Early 203 ossification of the anterior and lateral acetabular Hip Degeneration 204 epiphysis accounts for the majority of late-pre- • Primary Dysplasia (conferred by devel- 205 senting acetabular dysplasia (Fig. 5.7). Primary opmental pathology): 206 acetabular dysplasia occurs typically in females, –– Acetabular dysplasia (e.g. failure of 207 the etiology is unknown. ossification of the acetabular cartilaginous anlage or epiphysis) –– Proximal femoral dysplasia (e.g. congenital femoral deficiency, coxa Acetabular dysplasia can occur from either: vara/valga, excessive femoral ante/ (1) improper shape and/or delay in ossifica- retro-version) tion of the cartilaginous anlage, (2) damage • Secondary Dysplasia (conferred by to the triradiate cartilage, or (3) problems other diseases): of shape and/or delayed ossification of the –– Perthes disease (or other avascular acetabular epiphysis. necrosis) with resulting coxa magna, J. G. Schoenecker et al.

have symptoms. However, there is good evidence 248 with late symptomatic impingement that dysplasia alone, particularly in females, 249 and acetabular dysplasia (variable) leads to degenerative joint disease in adults [1, 250 –– Slipped capital femoral epiphysis 25, 27, 28]. The question of when hip dysplasia 251 (SCFE) associated with metaphyseal patients will become symptomatic in the absence 252 CAM deformity and femoroacetabu- of treatment was evaluated by Hartofilakidis 253 lar impingement et al. In their series of 202 dysplastic hips, the 254 –– Neuromuscular acetabular dysplasia average age for onset of symptoms was 255 and coxa valga occurring secondary 34.5 years. In patients with a low and high 256 to spasticity, muscle imbalance, etc. dislocation, pain from degenerative arthritis asso- 257 (e.g. cerebral palsy; Charcot-Marie ciated with a false acetabulum started at an aver- 258 tooth peripheral neuropathy). age of 32.5 and 31.2 years, respectively. If there 259 was no false acetabulum, pain onset did not occur 260 until 46.4 years, and was mostly secondary to 261 muscle fatigue [30]. 262 216 Natural History The natural history of hip dysplasia and sub- 263 luxation in untreated adults can be extrapolated 264 217 The lack of femoral head coverage exists along a to residual dysplasia and subluxation after treat- 265 218 spectrum; from under-coverage leading to ment in the pediatric patient [1, 27, 28]. In a study 266 219 improper joint loading and subluxation to over- of 152 pediatric hips treated with closed reduc- 267 220 coverage resulting in femoroacetabular impinge- tion and followed for 31 years, the authors 268 221 ment (FAI) [16–18]. Both morphologies reported that dysplastic hips often went on to 269 222 predispose the hip to damage of the labrum/chon- subluxation and the development of degenerative 270 223 drolabral junction and articular cartilage; potenti- joint disease [27]. The cause of degenerative 271 224 ating the premature development of OA [10, 16, changes in dysplastic hips is probably mechani- 272 225 18–22]. Nevertheless, the factors which predis- cal in nature and related to increased contact 273 226 pose certain hips to eventual degenerative change stress, especially to the labrum/chondrolabral 274 227 remain uncertain [23, 24]. Early in life, the fate of junction, leading to damages articular cartilage 275 228 a congenital hip dislocation has been well docu- over time. There is a clear association between 276 229 mented. However, the natural history of acetabu- excessive contact stress and late degenerative 277 230 lar dysplasia in the pediatric and young adult joint diseases for other abnormal anatomical 278 231 patient remains largely undescribed; with the morphologies, such as genu varum and genu val- 279 232 exception of a few studies that have formed the gum. This same association seems to occur in 280 233 basis of surgical indications for hip preservation dysplastic hips with relation to the development 281 234 [18, 24–28]. Understanding how acetabular mor- of degenerative joint disease at long-term follow- 282 235 phological characteristics affect the rate of up [31, 32]. 283 236 degenerative change in the hip has substantial Untreated severe dysplasia of the hip fre- 284 237 implications for prognostic assessment and joint quently leads to osteoarthrosis [14, 25, 31, 33, 285 238 preservation patient selection at all ages [29]. The 34]. While there is no debate that severe dyspla- 286 239 natural history of acetabular dysplasia with sub- sia of the hip should be treated operatively, objec- 287 240 luxation is clear; degenerative joint disease will tive criteria on which to base the treatment of 288 241 develop in all patients, usually in the third to mild and moderate dysplasia was not available 289 242 fourth decade of life [25, 27, 28]. Additionally, as until the mid-1990s and continues to be refined as 290 243 LCEA decreases, subluxation increases [25]. The we learn more about the natural history. 291 244 natural history of untreated adults with dysplasia Therefore, operative treatment for residual dys- 292 245 is more difficult to predict because patients com- plasia of the hip after skeletal maturity assumes 293 246 pensate well and present with dysplasia only as that the dysplasia, if left untreated, will lead to 294 247 an incidental finding on radiographs or if they secondary osteoarthrosis of the hip [14, 16, 295 5 Acetabular Dysplasia in the Reduced or Subluxated Hip

296 35–41]. Without long-term studies with matched >31% or a peak-to-edge distance of 0 mm. While 344 297 pairs and clearly defined parameters of dysplasia, they clearly showed that for patients, whom have 345 298 the natural history of what is now often consid- a hip replacement for dysplasia in one hip, severe 346 299 ered an operative indication may never be real- OA will inevitably develop in the contralateral 347 300 ized. In an attempt to provide objective parameters hip if the aforementioned acetabular criteria are 348 301 to follow the natural history of acetabular dyspla- not met. However, this investigation lacked a true 349 302 sia, Murphy and colleagues first defined the dys- non-operated control group but did have a com- 350 303 plastic acetabulum using CT to assess the parison group (171 pts) without progression of 351 304 morphological differences between two matched OA over the same timeframe. Unfortunately, a 352 305 cohorts of females with mean age 20 years [42]. major limitation to the study was that a substan- 353 306 In their study, the first cohort all went on to pelvic tial portion of the patients that progressed to OA 354 307 osteotomies for symptomatic dysplasia and the had evidence of mild OA at the time of inclusion 355 308 control group was obtained from patients who thus the outcomes are to some degree measure- 356 309 had CT scans obtained for alternate pelvic pathol- ments of secondary OA progression [43]. 357 310 ogies. Comparing the cohorts, acetabular ante- Further confounding our understanding of the 358 311 version was consistent (mean, 20°) and abduction natural history of acetabular dysplasia, patients 359 312 was moderately increased in the dysplastic group often have additional pathologies. For example, 360 313 (mean 62° vs. 53° in controls). The most signifi- many patients have combined acetabular dyspla- 361 314 cant difference was in the mean lateral center sia with FAI. It is not clear to what extent FAI 362 315 edge angle with the normal hips measuring 31° impacts hip dysplasia and the development of 363 316 and the dysplastic hips measuring 6°. This reduc- OA. Bardakos et al. showed that mild to moder- 364 317 tion in femoral head lateral coverage was shown ate OA in hips with a pistol-grip CAM deformity 365 318 to be part of a more global acetabular deficiency does not progress rapidly in all patients, with 366 319 in the dysplastic hip. The normal acetabular vol- one-third of their patients taking at least 10 years 367 320 ume equated to a hemisphere while the dysplastic to manifest signs of OA with some never showing 368 321 only measured one third of a sphere. radiologic signs [24]. Further analysis found two 369 322 Operative treatment for residual dysplasia of important variables associated with those that did 370 323 the hip after skeletal maturity assumes that the progress; the height of the trochanter relative to 371 324 dysplasia, if left untreated, will lead to second- the center of the femoral head and the presence of 372 325 ary osteoarthrosis of the hip. acetabular retroversion. Their conclusion was 373 326 From these objective determinates, Murphy that a hip with cam impingement is not always 374 327 et al. [43] then published the first significant nat- destined for end-stage arthritic degeneration [24]. 375 328 ural history study of the skeletally mature dys- Other studies have found even larger percentages 376 329 plastic hip. This study retrospectively evaluated of asymptomatic patients with cam deformity 377 330 286 young patients with previous unilateral THA that do not progress to OA. In the study by 378 331 for dysplasia and focused on the contralateral Hartofilakidis et al., 82.3% of asymptomatic hips 379 332 non-operated hip. Ultimately, 115 of the patients with a CAM deformity remained free of OA for a 380 333 developed severe OA in the contralateral hip by mean of 18.5 years [26]. Clearly the role of FAI 381 334 65 years of age. These patients also had statisti- in the natural history of hip dysplasia requires 382 335 cally greater derangement of all measured radio- more study to determine which hips are at higher 383 336 graphic features of dysplasia; including lateral risk of progression. 384 337 center edge angle (LCEA), acetabular index of Recently, Wyles et al. published the most 385 338 depth to width (D/W), vertical distance, lateral comprehensive study of the natural history of 386 339 distance, peak-to-edge distance, femoral extru- OA in patients with hip dysplasia [18]. Similar to 387 340 sion distance and acetabular index (AI). Key Murphy et al., they retrospectively studied 172 388 341 findings were that no patient in whom the hip young patients (mean, 47 years-old) that had 389 342 functioned well until age 65 had a LCEA <16°, undergone unilateral total hip arthroplasty 390 343 D/W <38%, AI >15°, femoral head uncovering (THA). While the Murphy et al. study contained 391 J. G. Schoenecker et al.

392 patients with advanced Tönnis grades, all Epidemiology 426 393 patients in the Wyles et al. study had a Tönnis 394 grade 0 grade for the contralateral hip. These Acetabular dysplasia is one of the most common 427 395 hips were given a structural diagnosis of acetab- causes of pre-arthritic hip pain, hip dysfunction, 428 396 ular dysplasia (48 patients), FAI (74 patients) and secondary OA [1, 2, 4, 44]. The infantile form 429 397 and normal (40 patients) and were evaluated for of acetabular dysplasia is considered a multifacto- 430 398 OA progression. At a mean follow-up of rial disease with genetic, ethnic and environmen- 431 399 20 years, 35 patients underwent contralateral tal risk factors [45, 46]. The intrauterine 432 400 THA; 16 (33%) with acetabular dysplasia, 13 environmental associations include decreased 433 401 (18%) with FAI and 6 (15%) patients with nor- uterine size with first-born children and breech 434 402 mal morphology. They showed degenerative presentation, both of which restrict fetal leg 435 403 changes progressed more rapidly in the acetabu- mobility. The incidence of breech birth is 2–4% in 436 404 lar dysplasia group with an increased probability the general population but 17–23% among 437 405 of undergoing a THA at 10- and 20-year follow- patients with infantile hip dysplasia [45, 47]. The 438 406 up compared to the FAI and normal morphology left hip is more commonly affected because of its 439 407 cohorts. FAI was similar to structurally normal fetal position adducted against the sacrum [48]. 440 408 hips in terms of progression to THA but patient Although no genetic locus has been identified, a 441 409 with a CAM deformity and concomitant acetab- hereditary component of developmental dysplasia 442 410 ular dysplasia developed OA more rapidly. From of the hip (DDH) is strongly supported on the 443 411 their data they created 10- and 20-year prognos- basis of increased risk in patients with a positive 444 412 tic tables predictive of osteoarthritic progression family history and varying rates by ethnicity. 445 413 (by Tönnis grade) based on the structural diag- Extremely low rates of DDH are seen in the 446 414 nosis and initial Tönnis grade. Furthermore, African populations [49, 50] with the African 447 415 based on their continuous multistate Markov Bantu having an incidence of essentially zero 448 416 models, they proposed the following new thresh- [51]. Much higher rates have been reported in 449 417 olds for an increased risk for OA progression Native Americans [52] and the Sami in Norway 450 418 and thus an indication for hip preservation sur- [53]. DDH is much more common in females but 451 419 gery: femoral head lateralization >8 mm, femo- the exact cause is uncertain; one theory being 452 420 ral head extrusion index >0.20, acetabular depth increased joint laxity during the neonatal period 453 421 to width index <0.30, LCEA <25° and Tönnis secondary to increased female sensitivity to the 454 422 angle >8°. A major limitation of this study is that maternal hormone relaxin [11, 54]. Another is that 455 423 all patients underwent an index THA and thus females are twice as likely as males to be born 456 424 the findings cannot be directly correlated to breech [9, 54]. 457 425 highly active patients. The prevalence of asymptomatic dysplasia in 458 the general population varies with ethnicity. 459 Caucasians have a 3–4% prevalence of hip dys- 460 Acetabular dysplasia can be classified plasia, with females having a higher prevalence 461 into mild, moderate and severe forms than males [55–60]. Inoue et al. showed the prev- 462 using several well-established measure- alence in men and women respectively to be 463 ments. However, its diagnosis and natu- 5.1% and 11.6% for the Japanese and 1.7% and 464 ral history are complicated by the effects 5.6% for the French [56]. Another study by Lau 465 of acetabular and proximal femoral ver- et al. found the prevalence of dysplasia 466 sion as well as FAI. While the progres- (CEA < 25°) to be similar between Chinese and 467 sion to OA in severe dysplasia is clear, British men at 4.5% and 3.6% respectively, how- 468 surgical indications in mild and moder- ever the same cohort showed a 50% reduction in 469 ate forms continue to be refined. OA prevalence in the Chinese group (5.4% vs. 470 11.0%) [58]. It was not clear why the Chinese 471 5 Acetabular Dysplasia in the Reduced or Subluxated Hip

472 group did not progress to radiographic OA at the based on when the diagnosis was first obtained: 519 473 same rate. A recent study by Engesaeter et al. infancy, adolescence or adulthood [54]. They 520 474 looked at 2081 Norwegians (mean age, 19 years) found demographic differences between patients 521 475 and found the prevalence of a Wiberg center- diagnosed with hip dysplasia in infancy versus 522 476 edge-angle (CEA) less than 20° to be 3.3% (4.3% adolescence/adulthood. There were more females 523 477 in women and 2.4% in men) [61]. If the Wiberg with left hip involvement and breech presentation 524 478 CEA threshold was increased to less than 25°, in the infant/DDH population while bilateral dis- 525 479 20% (23% in women and 16% in men) of the ease (61% vs. 45%) was more common in the 526 480 cohort had hip dysplasia [61]. This further con- adolescent population. The same study also 527 481 firmed the higher prevalence of hip dysplasia in looked and family history and found that >50% 528 482 Norway and agreed with previous Nordic of all respondents had a family history of hip dis- 529 483 Arthroplasty Registry findings [62, 63]. Although ease with >40% being first order relatives. first 530 484 the percentage of patients with dysplasia who order relatives of adolescent/adult diagnosed 531 485 will ultimately progress to end-stage OA is patients had a twofold increase in incidence of 532 486 unknown, it has been documented that 25–50% hip replacement by age 65 compared to infant/ 533 487 of primary hip OA is due to acetabular dysplasia DDH first order relatives (50% vs. 22%). 534 488 [30, 34, 64]. However, first order family members of infant/ 535 489 Despite the plethora of studies investigating DDH patients were four times more likely to 536 490 risk factors for infantile hip dysplasia, there is a have DDH themselves (59% vs. 16%). 537 491 scarcity of literature describing patient demo- “Rates of acetabular dysplasia vary widely 538 492 graphics and disease epidemiology for adoles- by gender and cultural origin with several 539 493 cent and adult patients, with most data coming well accepted patient characteristics being 540 494 from single surgeon series reporting on symp- predictive of increased risk during 541 495 tomatic acetabular dysplasia [16, 65–68]. In a infancy. Once a dysplastic hip is present, 542 496 series of 337 patients undergoing total hip arthro- whether that hip will become symptomatic 543 497 plasty, Clohisy et al. found that 48% less than age is directly related to the necessity of treat- 544 498 50 had acetabular dysplasia as the predisposing ment. Severity of dislocation and family 545 499 factor for their OA [69]. A recent large multi- history along with cultural origin again 546 500 center study by Sankar et al. looked at disease influence that symptomatology. The peri- 547 501 epidemiology and patient demographics in dys- acetabular osteotomy is commonly 548 502 plastic patients treated with a periacetabular oste- employed for younger (<40yo) symptom- 549 503 otomy (PAO) in 950 consecutive patients [44]. atic patients while a total hip replacement 550 504 They demonstrated that symptomatic acetabular is indicated for older patients (>40yo) with 551 505 dysplasia starts 1–3 years before surgical inter- Tönnis 2 changes or greater”. 552 506 vention and occurs predominantly in young 507 (average 25.3 years), female, Caucasian patients 508 with a normal BMI (average 24.6). These find- Clinical Presentation 553 509 ings are consistent with other reports in the litera-

510 ture [70–73]. The same study found baseline Young children with hip dysplasia with or with- 554 511 functional scores to be mean modified Harris Hip out subluxation typically do not present with any 555 512 Score (mHHS) of 61.8 and a mean UCLA activ- complaints of hip pain or any apparent functional 556 513 ity score of 6.6. The mean mHHS is slightly limitations. More likely, children in the first 557 514 lower than published elsewhere (61.8 vs. 66–70) 6–8 years of life will have relatively normal hip 558 515 [71, 74] but the mean UCLA activity score is function despite radiographic evidence of notable 559 516 comparable with other authors [75]. hip dysplasia. However, with growth and 560 517 Lee et al. further evaluated the differences in increased body mass during and post puberty, 561 518 symptomatic hip dysplasia treated with PAO older children and adolescents with acetabular 562 J. G. Schoenecker et al.

563 deficiency will variably become symptomatic, adolescents, further visualization of the anterior 608 564 particularly in the presence of hip joint sublux- acetabulum can be seen with the standing false 609 565 ation. Signs include functional hip joint associ- profile lateral radiograph 4[ ]. Persistent hip sub- 610 566 ated fatigue and often a subtle, though progressive, luxation after the age of 6 years portends a 611 567 gluteus medius weakness limp (Trendelenburg). guarded prognosis for maximal acetabular devel- 612 568 This early onset weight bearing pain typically is opment for any given hip dysplasia [9]. If sublux- 613 569 located laterally (trochanteric) and occurs sec- ation is noted on the standing AP pelvic 614 570 ondary to chronic gluteus medius fatigue. Later, radiograph, a functional view (AP with hip 615 571 anterolateral groin pain secondary to chondro- abducted and internally rotated) is obtained to 616 572 labral strain and or injury variably develops. In assess if the femoral head positionally reduces 617 573 these relatively older patients, groin pain is back into the true acetabulum. Knowing that 618 574 characteristically described as an anterior hip positional reduction of femoral head subluxation 619 575 centered discomfort often with catching or snap- is possible, is very helpful in the preoperative 620 576 ping. Groin pain typically occurs with hip motion planning of joint reconstruction surgery. 621 577 such as in pivoting, twisting, running, when aris- 578 ing from a sitting position, and on initiating 579 walking. Essential Imaging 580 On physical examination, the gait of most of • Plain radiographs: For measurement of 581 the younger children will appear to be normal. AI, LCEA, Tonnis sourcil angle, tear- 582 On careful observation of older children and or drop morphology, and femoral 583 adolescents, there may be an abductor limp and/ deformity 584 or a positive Trendelenburg sign on single leg • MRI: Used on occasion to assess devel- 585 stance examination. The hip abductors may be opment of the cartilaginous acetabulum 586 weak on resistance testing. Passive hip range of and/or version 587 motion is initially normal and often increased in • MRI arthrogram (MRA): For assess- 588 all planes, secondary to both relative joint laxity ment of chondrolabral integrity in 589 and a variably deficient anterolateral acetabulum. adolescents 590 Later as the hip disease progresses, range of • CT: For either assessment of version 591 motion can become restricted, associated with (femoral and acetabular) or for concom- 592 the onset of painful impingement at the acetabu- itant FAI 593 lar chondrolabral junction.

Normative values for acetabular index (AI) 622 594 Imaging (Coleman 1968; Tönnis 1976), lateral center angle 623AU5 (LCEA) [4, 34], Tonnis sourcil angle [4, 14] are 624 595 Hip joint dysplasia in the child occurs secondary helpful in decision-making and are summarized 625 596 to abnormal growth of either the acetabulum, in Tables 5.1 and 5.2. We also assess the anterior 626 597 femoral head, or both, in a non-dislocated hip CEA [4, 14] in our older patients. The acetabular 627 598 joint. The shape of the acetabular anlage and its tear drop morphology can be useful in assessing 628 599 functional capacity to support weight bearing is acetabular development in late infancy/early 629 600 evaluated with a standing anterior posterior (AP) 601 radiograph. Typically the acetabular development

602 will be deficient anterolaterally. In addition, the Table 5.1 Suggested acetabular index (AI) guideline t1.1 603 absence (or presence) of hip joint subluxation values [14] t1.2

604 (i.e. Shenton’s line intact or not) is assessed. The Age Acetabular index t1.3 605 contour of the anterior and posterior edges of the 1 <25 t1.4 606 proximal femurs are visualized on the supine 3 <20 t1.5 607 frog lateral radiographs. In older children and 6 <18 t1.6 5 Acetabular Dysplasia in the Reduced or Subluxated Hip

Table 5.2 Lateral center-edge angle (LCEA) guideline t2.1 values at skeletal maturity dysplasia with simpler procedures t2.2 LCEA (acetabuloplasty and/or Salter innomi- t2.3 Normal ≥30 nate osteotomy) t2.4 Minimum ≥25 • Failure to continue essential radio- t2.5 Poor prognosis <20 t2.6 graphic and clinical monitoring for min- imally or asymptomatic adolescents/ 630 childhood (Albinana et al. 1996; Smith et al. young adults with hips at risk (acetabu- 631 1997). Similarly, Shenton’s line, intact or not, is lar dysplasia and subluxation) 632 very important in decision making, with chronic 633 subluxation always being a concern for a guarded 634 prognosis [9]. Operative Management 652

Essential Surgical Techniques 653 635 Non-operative Management in Childhood (4–10 Years Old) 654

636 Childhood (4–10 Years Old) Direct surgical correction of acetabular dysplasia 655 can be broken into three different types: (1) ace- 656 637 If sufficient femoral head coverage is present and tabuloplasty, (2) redirectional osteotomies, and 657 638 the child is asymptomatic, one may observe until (3) salvage procedures (Fig. 5.8). The decision as 658 639 there is evidence of failure to improve radio- to which procedure is most appropriate in 659 640 graphically or until pain develops (Chap. 4, attempting to achieve correction of a specific 660 641 Developmental Dysplasia of the Hip in Young acetabular dysplasia is dictated by the principal 661 642 Children). Deferring operative treatment after deficiency of development (acetabular anlage, tri- 662 643 age 6 years (with or without symptoms) is not radiate cartilage or acetabular epiphysis), the age 663 644 indicated if hip is subluxated and/or there is per- of the patient, and whether the hip is completely 664 645 sistent acetabular dysplasia in girls ≥8 years or reduced. Currently, the incomplete acetabulo- 665 646 boys ≥9 years. plasties [76–80] have become the most popular 666AU6 surgical approach in the correction of residual 667 dysplasia in the skeletal immature pelvis 668 647 Older Child (≥11 Years/Adolescent) (<11 years). 669

648 Observe if asymptomatic, but it is essential to fol- 649 low at least annually. Prognosis relatively guarded Acetabuloplasty 670AU8 650 in proportion to degree of subluxation and/or 651 acetabular dysplasia. Pathologic shape or delay of the acetabular car- 671 tilaginous anlage is often characterized by an 672 acetabulum with a relatively larger arc of curva- 673 Non-operative Pitfalls ture then of the femoral epiphysis (Fig. 5.4). 674 • Inappropriate continued observation in The intent of the acetabuloplasty is to correct 675 childhood despite subluxation and or the pathological increased slope of the superior 676 lack of progressive improvement in ace- anterolateral acetabulum (Fig. 5.9). Correcting 677 tabular development (AI) and femoral the acetabular insufficiency (abnormal shape) 678 head coverage (LCEA) without damaging the triradiate cartilage redi- 679 • Loss of opportunity in younger patients rects the hip center to its natural location, reduc- 680 (<10 years of age) of correcting ing femoral head subluxation. These acetabular 681 osteotomies compress the cartilaginous anlage 682 J. G. Schoenecker et al.

ab c

Acetabuloplasty Redirectional Salvage

AU7 Fig. 5.8 Types of acetabular corrective surgeries: Direct otomies, such as the periacetabular osteotomy (PAO) surgical correction of acetabular dysplasia can be broken shown here and (c) salvage procedures, such as the ace- into three different types: (a) acetabuloplasty, such as the tabular shelf procedure shown here Pemberton osteotomy shown here (b) redirectional oste-

683 which restores endochondral ossification pro- acetabuloplasty in the correction of ace- 707 684 viding needed support for functional loading tabular dysplasia. Over correction is very 708 685 (Fig. 5.10). Acetabuloplasty is best indicated in possible which can potentiate late occur- 709 686 conditions with remaining acetabular cartilagi- ring femoral acetabular impingement”. 710 687 nous anlage, a relatively capacious acetabulum 688 and or subluxation. Alternatively, satisfactory Surgical Technique: Pemberton 711 689 correction can be achieved with a single innomi- Acetabuloplasty (Figs. 5.9–5.11) 712 690 nate (Salter) osteotomy. If the femoral head is With the patient positioned supine on the operat- 713 691 relatively large, the Salter redirectional osteot- ing room table, a small circular roll is placed 714 692 omy can be the preferred technique in attempt- behind the buttock in back of the affected extrem- 715 693 ing to correct acetabular dysplasia in a younger ity. The approach to the hip and pelvis is made 716 694 child. Following surgical correction of acetabu- through a skin excision located lateral to and par- 717 695 lar dysplasia, an intraoperative arthrogram can alleling the iliac crest extending a couple of cen- 718 696 be very helpful in assessing femoral head cover- timeters distal to the anterior superior iliac spine. 719 697 age achieved, both laterally and anteriorly Using the electrocautery, subcutaneous flaps are 720 698 (Fig. 5.11). raised both medially and laterally to the superfi- 721 699 “Success is often judged by a radio- cial fascia. The fascia overlying the tensor fascia 722 700 graphically noting a reduction of the lata muscle is incised longitudinally and dissec- 723 701 acetabular index, a medialized hip cen- tion directed medially over the tensor and under 724 702 ter, (from abnormally lateral to more the sartorius, which protects the lateral femoral 725 703 normally medial), and a restored cutaneous nerve lying just under the sartorius fas- 726 704 Shenton’s line. It is important to be cia. Dissection is continued bluntly until the lat- 727 705 aware of the extent of the acetabular car- eral aspect of the rectus femoris tendon and 728 706 tilaginous anlage when performing an muscle are identified. The external oblique mus- 729 5 Acetabular Dysplasia in the Reduced or Subluxated Hip

Fig. 5.9 Acetabuloplasty: (a) Pathologic shape or ab delay of the acetabular cartilaginous anlage is often characterized by an acetabulum with a relatively larger arc of curvature then of the femoral epiphysis and a break in Shenton’s Line (black arrow). (b) The intent of the acetabuloplasty is to correct the pathological increased slope of the superior anterolateral acetabulum anlage (also see Fig. 5.11 arthrogram). (c) Correcting the acetabular insufficiency cd redirects the hip center to its natural location, here shown with an ‘Inge’ retractor. The intent is to restore Shenton’s line, and the proper position of the chondrolabral junction (red arrow). (d) Bone graft (green arrow) is then placed to hold this new position. Healing of the bone graft ensues, often restoring normal hip development (see Fig. 5.10)

730 cle is reflected of the iliac apophysis from lateral anterior and lateral line of the cut should be made 743 731 to medial, exposing the apophyseal cartilage at least 1½ cm proximal to the edge of the acetab- 744 732 which is sharply divided in half from anterior to ulum. The cut is initiated with a straight narrow 745 733 posterior so as to achieve exposure of the ilium. osteotome extending in a posterior direction then 746 734 The lateral ilium is subperiosteally exposed to with a narrow curved osteotome around the ace- 747 735 the palpable edge of the acetabulum then posteri- tabulum toward the triradiate cartilage. The 748 736 orly down to the lateral entrance of the sciatic C-arm is brought in across from the surgeon and 749 737 notch (which can be probed with blunt dissecting the hip joint and posterior column are visualized 750 738 instrument). The lateral iliac cut is made first. with 45° iliac oblique view. As monitored with 751 739 The course of the osteotomy begins anteriorly, the C-arm, the course and extent of the curved 752 740 mid distance between the anterior superior iliac osteotomy can be precisely located one half way 753 741 spine (ASIS) and the anterior inferior iliac spine between the acetabulum and the medial edge of 754 742 (AIIS), and extends in a posterior direction. The the posterior column. 755 J. G. Schoenecker et al.

a b

c d

e f

Fig. 5.10 Restoration of hip development after an acetabu- junction, however, note that initially the cartilaginous anlage loplasty: (a, b) Patient from Fig. 5.4 with pathologic carti- still appears under-ossified (yellow arrow) as indicated by an laginous anlage (black arrow on drawing and yellow arrow increased acetabular anlage at age 2. (e, f) Four years later, at on radiographs). (c, d) A Pemberton type osteotomy restores age 6, the anlage has ossified and the hip position has been Shenton’s line and the proper position of the chondrolabral maintained without iatrogenic over-coverage of the hip 5 Acetabular Dysplasia in the Reduced or Subluxated Hip

a b

c d

e f

Fig. 5.11 Measuring correction during an acetabulo- tion (black arrow and “thorn”). (b) The gap between the plasty: (a) Correction of acetabular anlage under-coverage iliac fragments is filled with an allograft (white arrow) and AU9 is often monitored by an arthrogram in order to visualize typically inherently stable after graft insertion restoration of proper position of the chondrolabral junc- J. G. Schoenecker et al.

756 The medial ilium is subperiosteally exposed to The anteriorly prominent spike of bone on the 803 757 and beyond the brim of the pelvis; incising the acetabulum fragment is subperiosteally exposed 804 758 periosteum facilitates this exposure. A small and resected. The apophyseal cartilage is securely 805 759 straight osteotome is then directed through the repaired with interrupted #1 absorbable sutures, 806 760 lateral cut in a medial direction and is visualized the tensor-sartorius facia reapproximated and the 807 761 cutting through the most anterior 2–3 cm of the external oblique muscle reattached just lateral to 808 762 medial wall of the ilium. A transverse cut potenti- the apophyseal cartilage with running #1 absorb- 809 763 ates anterior coverage and a more oblique cut able sutures. The subcutaneous and skin tissues 810 764 (medial cut made more distal than lateral) greater are closed with absorbable sutures. To protect the 811 765 lateral coverage. The medial cut is continued osteotomy in children less than 4 years of age, a 812 766 with a curved osteotome, extending over the pel- one and half spica cast is placed. In older patients, 813 767 vic brim, towards but not through the triradiate an abduction pillow is used for 6 weeks. Typically, 814 768 cartilage, monitored with the C-arm [15]. At this healing of the osteotomy is sufficient to allow 815 769 point the osteotomy will be near complete. weight bearing as tolerated at 6–8 weeks post 816 operatively. 817 770 “As the two fragments are separated with 771 a laminar spreader, displacement of the 772 typical oblique cut (from proximal lateral Pelvic Redirectional Osteotomies 818 773 to distal medial) of the acetabular frag- 774 ment allows for marked improvement in A pelvic redirectional osteotomy can be single 819 775 lateral and anterior femoral head innominate (childhood) or triple pelvic (adoles- 820 776 coverage”. cents/young adults) both being effective in cor- 821 777 Improved femoral head coverage is moni- recting pathological acetabular insufficiency. 822 778 tored by the C-arm using both an AP and false Salter [39] pioneered operative pelvic redirec- 823 779 profile lateral views. In the younger child, femo- tional osteotomy correction of congenital acetab- 824 780 ral head coverage is provided by both the bony ular deficiency [39, 81]. The single horizontal 825 781 acetabulum and by the cartilage anlage. An osteotomy through the ilium allows for a consid- 826 782 arthrogram can be very helpful showing the true erable anterolateral acetabular redirection around 827 783 extent of combined bone and cartilage head cov- the relatively flexible pubic symphysis. 828 784 erage (Fig. 5.11). Correction achieved should be “In years past, the Salter osteotomy was 829 785 correlated with range of motion and adjusted to the procedure of choice in younger chil- 830 786 assure there is 90–95° of passive hip flexion fol- dren. It is now used less frequently given 831 787 lowing turning down the acetabular fragment. the current popularity of acetabuloplas- 832 788 The gap between the fragments is filled with a ties. However, the Salter osteotomy is still 833 789 structural allograft which is typically inherently the preferred surgical approach in the 834 790 stable after graft impaction. Optionally, if needed correction of residual acetabular dyspla- 835 791 to assure graft stability, a small K-wire may be sia in the very young child (<5 yrs of age) 836 792 used in smaller children and/or a 3.5 mm cortical in which there is relatively little sublux- 837 793 screw in older children, inserted in an antegrade ation and an arc of curvature of the ace- 838 794 direction starting in the proximal iliac crest and tabulum that is quite similar to the 839 795 directed across the osteotomy (through the bone corresponding arc of curvature of the 840 796 graft) and into the ilium medially, just short of femoral head”. 841 797 the roof of the acetabulum. Bilateral Pemberton 798 osteotomies can be performed if needed. In Surgical Technique: Single Innominate 842 799 patients with either excessive femoral antever- (Salter) Pelvic Osteotomy 843 800 sion and or coxa valga deformity, a proximal The patient positioning and initial exposure to the 844 801 redirectional femoral osteotomy can be concom- ilium is as described above for performing the 845 802 itantly performed. Pemberton acetabuloplasty. Following division 846 5 Acetabular Dysplasia in the Reduced or Subluxated Hip

847 of the iliac apophysis, both tables of the ilium are approximately 2 weeks for clinical and radio- 895 848 dissected subperiosteally until the sciatic notch is graphic assessment. The cast is removed at 6 896 849 encountered, both medially and laterally. Care is weeks post-operatively and ambulation initiated 897 850 taken to avoid penetrating the periosteum as the with a walker until healing is confirmed 898 851 sciatic notch is dissected subperiosteally. A small radiographically. 899 852 curved clamp, such as a Satinsky, is used to pass 853 a # 1 Vicryl suture through the sciatic notch 854 which is then tied to a Gigli saw, so that the saw Essential Surgical Techniques 900 855 then carefully passed through the sciatic notch. in Childhood (>11 Years Old to Young 901 856 Crego or similar retractors are inserted into the Adults) 902 857 sciatic notch medially and laterally in order to 858 protect the adjacent soft tissues. An oscillating Addressing Pathology Subsequent 903 859 saw is used to cut the ilium beginning just distal to Ossification of the Acetabular 904 860 to the ASIS and directed towards the sciatic Anlage 905 861 notch, terminating about 1 cm anterior to it. The Once the acetabular cartilaginous anlage has 906 862 Gigli saw is then used to complete the iliac oste- completely ossified and if the triradiate cartilage 907 863 otomy so that an angle is created between the is still biologically active, a triple innominate 908 864 posteriorly directed saw cut and the anteriorly osteotomy should be considered when attempting 909 865 directed Gigli cut. Creating such an angle will to achieve satisfactory mobility of the acetabular 910 866 assist in stabilizing the rotated acetabular frag- fragment and, in turn, adequate redirection and 911 867 ment against the ilium. The ischiopubic fragment correction of acetabular dysplasia (Fig. 5.12). For 912 868 is grasped with a pointed bone forceps just ante- older children and young adolescents, especially 913 869 rior to the sciatic notch osteotomy which effec- those with significant remaining triradiate 914 870 tively helps rotate the acetabulum anteriorly in growth, greater acetabular mobility is desirable/ 915 871 order to improve anterior and lateral coverage of necessary so as to achieve optimal hip joint sta- 916 872 the femoral epiphysis. The prominent anterior bility not only laterally but also anteriorly and 917 873 extension of the acetabular fragment is osteoto- posteriorly as needed [14, 76, 77, 82, 83]. With 918 874 mized (which will be a tricortical bone graft the triple innominate redirectional osteotomy, the 919 875 wedge) to be impacted into the gap between the surgeon can satisfactorily mobilize the acetabular 920 876 ilium and the acetabular fragment. The osteot- fragment in attempting to achieve redirection of 921 877 omy is transfixed with two threaded Kirschner the acetabulum and optimal hip joint stability. 922 878 wires inserted antegrade under AP fluoroscopy, In the younger child, the surgical exposure 923 879 just proximal to the triradiate cartilage. The sta- during triple innominate osteotomy is extra- 924 880 bility of the osteotomy is assessed manually. The periosteal, an essential modification so as to not 925 881 C-arm, with or without a concomitant arthro- injure the triradiate cartilage and to facilitate 926 882 gram, is used to assure that satisfactory femoral greater mobility with less stress on fixation 927 883 head coverage has been achieved. devices. This technique allows for optimal ace- 928 884 Repair of the split apophyseal cartilage is tabular redirection (achieving desirable acetabu- 929 885 achieved securely with interrupted absorbable lar version) in restoring hip stability; particularly 930 886 sutures. The threaded Kirschner wires are then for the younger child with global deficiency (e.g. 931 887 cut about 1 cm proud from the iliac repaired Down syndrome, Spina Bifida). 932 888 apophysis in order to facilitate easier removal. 889 Closure of the tensor—Sartorius fascia, reattach- Surgical Technique: Triple Innominate 933 890 ment of the external oblique muscle and subcuta- Osteotomy (Fig. 5.12) 934 891 neous and skin tissues is as previously described The patient is positioned supine on a flat radiolu- 935 892 for the Pemberton acetabuloplasty. Following cent table. A roll is placed behind the contralat- 936 893 wound dressing application, a single-leg hip eral knee in order to maintain hip flexion, which 937 894 spica is applied. The patient is followed up in helps both to flex the pelvis and to flatten the 938 J. G. Schoenecker et al.

ab c

Fig. 5.12 Triple innominate osteotomy. A 9-year-old pain with insufficient lateral and superior coverage of the male (bone age, 7 years) with a history of viral transverse left hip (a). The patient underwent a triple innominate myelitis secondary to chemotherapy who is functionally a osteotomy (b, 3 months post-operatively). (c) Two-years mild diplegic. He is a community ambulator (GMFCS II) later, after hardware removal, the patient had restoration with AFO braces and presented with gait deterioration and of coverage, increased function and resolution of pain

939 lumbar lordosis. The initial approach for the tri- released from the iliopectineal line. The golden 972 940 ple innominate is as previously described for the coloured retroperitoneal fat is exposed, and the 973 941 Pemberton Acetabuloplasty. Following exposure obturator vein and nerve are carefully identified 974 942 of the ilium, the interval between the tensor and and protected by packing a Ray-Tec sponge 975 943 sartorius is identified. Dissection then proceeds extraperiosteally along the quadrilateral surface 976 944 within this interval proximal to the brim of the of the acetabulum. The pubic periosteum can be 977 945 pelvis. The lateral iliac apophysis is then reflected incised and the remaining iliopectineal fascia 978 946 and the lateral ilium dissected subperiosteally released from the iliopectineal line. The true pel- 979 947 until the sciatic notch is identified. The sciatic vis is then exposed extraperiosteally from the 980 948 notch is also identified medially. The subsequent ischial tuberosity to the iliopectineal line. 981 949 dissection involves an extraperiosteal exposure of The pubic osteotomy is performed medial to 982 950 the ischium and pubis while visualizing and pro- the pubic limb of the triradiate cartilage using a 983 951 tecting the obturator nerve within the retroperito- Gigli saw. In older children the pubis can be dis- 984 952 neum. In order to accomplish this exposure, the sected subperiosteally; however, in younger chil- 985 953 fascia of the iliacus is released from the rectus dren the periosteum is cut with the osteotomy. The 986 954 tendon and the hip is flexed in order to relax the anterior pubic periosteum is incised and the root of 987 955 iliacus and psoas muscles. This relaxation allows the pubis carefully dissected subperiosteally using 988 956 identification of the iliopectineal bursa just a right-angled clamp. The obturator nerve is pro- 989 957 medial to the AIIS with blunt dissection medially tected during this part of the procedure. 990 958 to expose the pubis. A double-pronged Hohmann Alternatively, the entire pubic root can be exposed 991 959 retractor is then inserted into the superior pubic extraperiosteally. A #1 Vicryl suture is passed 992 960 ramus medially to retract the iliopsoas while through the obturator foramen and used to pass a 993 961 maintaining the hip in flexion to protect the fem- Gigli saw. The root of the pubis is protected either 994 962 oral nerve. The interval between the psoas tendon in an extra- or sub-periosteal fashion and a trans- 995 963 sheath and the hip capsule is developed by open- verse pubic osteotomy performed using the Gigli 996 964 ing the iliopectineal bursa medial to the hip cap- saw. Care is taken to orient the osteotomy as per- 997 965 sule in order to access the ischium. Next, with the pendicular as possible to the long axis of the pubis. 998 966 hip still held in flexion, the iliacus muscle is gen- “To achieve maximal mobility of the ace- 999 967 tly separated from the periosteum of the ilium so tabular fragment in children and adoles- 1000 968 that the iliopectineal fascia can be exposed at the cents, it is very helpful to cut the 1001 969 attachment to the iliopectineal line. In order to surrounding periosteum to effectively 1002 970 access the retroperitoneum and to protect the mobilize the superior pubic ramus frag- 1003 971 obturator nerve, the fascia is then incised and ments after the osteotomy”. 1004 5 Acetabular Dysplasia in the Reduced or Subluxated Hip

1005 Next the ischial osteotomy is performed using acetabular fragment is osteotomized and used as 1053 1006 a Ganz osteotome that is passed between the ilio- a tricortical graft within the supra-acetabular 1054 1007 pectineal bursa and the hip capsule and posi- ilium. The graft is transfixed with one anterior 1055 1008 tioned at the level of the infracotyloid groove. cortical iliac screw. The hip range of motion is 1056 1009 Using both a 50° cephalad and oblique radio- assessed for impingement. 1057 1010 graphic (C-arm) guidance, the medial and lateral Closure is performed in a layered fashion. If 1058 1011 cortices of the ischium are osteotomized com- the anterior superior iliac spine has been osteoto- 1059 1012 pletely, terminating just distal to the ischial mized, it is reattached with intraosseous O-Vicryl. 1060 1013 spine. The osteotome as visualized on the 50° Repair of the iliac apophysis, closure of the 1061 1014 cephalad view is rotated back and forth in the tensor-sartorius interval, reattachment of the 1062 1015 transverse anatomic plane in order to confirm external oblique, subcutaneous and skin closure 1063 1016 that the ischium is completely cut. Similar to the are as previously described. Typically, fixation is 1064 1017 pubic cut, the ischial periosteum is cut simulta- sufficient to obviate the need for spica casting, 1065 1018 neously while performing the osteotomy. AP patients are mobilized as appropriate on post- 1066 1019 fluoroscopy is used to select the line of the operative day #1. Neurologically disabled chil- 1067 1020 intended iliac osteotomy sufficiently proximal to dren are, as necessary, immobilized in an 1068 1021 the acetabulum to allow for later stabilization abduction pillow. 1069 1022 with screws and/or threaded guide wires. A #1 1023 Vicryl suture is passed through the sciatic notch Surgical Technique: Ganz 1070 1024 and used to pass a Gigli saw. The adjacent soft Periacetabular Osteotomy (PAO) 1071 1025 tissue are protected with Hohmann retractors. (Figs. 5.13, 5.14, 5.15, and 5.16) 1072 1026 An oscillating saw is used to divide the ilium If the triradiate cartilage appears to be closing or 1073 1027 from anterior to posterior aiming slightly in a is closed, performing a periacetabular osteotomy 1074 1028 caudal direction and terminating approximately (Ganz) achieves both maximal mobility and the 1075 1029 1 cm anterior to the iliopectineal line. The Gigli potential to redirect the acetabulum into the 1076 1030 saw that has been passed through the sciatic desired location (Fig. 5.12) [5, 8, 16, 84]. The 1077 1031 notch is used to complete the iliac osteotomy in patient is positioned supine on a radiolucent 1078 1032 order to create a small cephalad directed angle table. The skin excision again parallels the iliac 1079 1033 into which the rotated acetabulum can be stabi- crest laterally and extends more distally down 1080 1034 lized. To redirect and control the position of the onto the thigh. Exposure is as described for the 1081 1035 acetabulum, a 4 mm Schanz screw is inserted Pemberton acetabuloplasty, as is the initial ilio- 1082 1036 into the supra-acetabular ilium and a pointed femoral dissection. When reflecting the external 1083 1037 bone clamp applied to the root of the pubis. The oblique muscle from lateral to medial in a skele- 1084 1038 acetabulum is redirected such that the sourcil is tally mature patient, the apophysis will be ossi- 1085 1039 oriented horizontally and the anterior-posterior fied, so the tissue plane is between the external 1086 1040 acetabular walls are balanced appropriately oblique and the periosteum of the iliac crest. 1087 1041 across the femoral head (i.e. no “crossover” Next, the medial ilium is subperiosteally 1088 1042 sign). Provisional fixation is obtained using exposed and an interval is developed between 1089 1043 2 mm Kirschner wires and an intraoperative the sartorius and rectus tendon. The ASIS (with 1090 1044 radiographs obtained to confirm appropriate the attached sartorius muscle) is osteotomized 1091 1045 reorientation of the acetabulum. On occasion, an through an approximately 3 cm oblique cut in a 1092 1046 intraoperative arthrogram is performed to con- lateral to medial, proximal to distal direction. 1093 1047 firm that the hip is well reduced. The “thorn The interval between the sartorius and the 1094 1048 sign” is used to identify lateral coverage of the attached ASIS medially and the rectus muscle/ 1095 1049 head of the femur and overall rotation of the ace- tendon complex laterally is developed. Deeper 1096 1050 tabulum. The provisional fixation is then to this, the same interval is further developed 1097 1051 removed and replaced with cortical screws or between the rectus laterally and the iliacus, ilio- 1098 1052 Steinmann pins. The anterior extension of the capsularis, and iliopsoas muscles medially. With 1099 J. G. Schoenecker et al.

Fig. 5.13 Periacetabular osteotomy (PAO) Ischial Cuts: teriorly to allow the final posterior column cut (Fig. 5.14) The ischium is partially cut (a) medially (b) centrally and to connect (c) laterally in sequence. (d) The cuts should extend pos-

1100 the hip slightly flexed, the dissection extends in ischium with the hip skid protecting the sur- 1111 1101 a posterior direction medial to the hip capsule rounding soft tissues. The ischial cut starts in 1112 1102 and lateral to the psoas tendon. A long large the infracotyloid groove just inferior to the ace- 1113 1103 Mayo type sutures is essential in expanding this tabulum, extending the cut posteriorly around 1114 1104 interval around the hip capsule posteriorly down the acetabulum and then proximally, ending 1115 1105 to the ischium inferior to the acetabulum. The near the level of the base of the ischial spine. AP 1116 1106 anterior, medial and lateral cortical surface of and 45° iliac oblique C-arm views are essential 1117 1107 the ischium is palpated with the scissors tip. in assuring the correct placement of the osteo- 1118 1108 This interval is developed so as to allow for pas- tome. The medial ischial cortex is cut first, in 1119 1109 sage of first a hip skid (if possible), then the turn, the middle and lateral cuts are completed. 1120 1110 Ganz angled osteotome inserted down to the The lateral cut will be shorter (<1½ cm), the 1121 5 Acetabular Dysplasia in the Reduced or Subluxated Hip

Fig. 5.14 Periacetabular osteotomy (PAO) Posterior rior column on the lateral view. (b) It should connect with Column Cuts: The final cut of the PAO is to split the pos- the medial cut of the ischium (see Fig. 5.13a). (c) A terior column. It is important to complete this cut both straight osteotome is used complete the cut—aligning the medially (a, b) and laterally (c, d). (a) A “flag” osteotome lateral edge with the lateral edge of the ischium (see can be used to follow the false and true pelvis for the Fig. 5.13c) medial cut while monitoring the position within the poste-

1122 osteotome directed posteriorly and medially exposure is extended to and beyond the iliopec- 1131 1123 away from the adjacent sciatic nerve. The leg is tineal eminence onto the superior pelvic ramus. A 1132 1124 externally rotated and a foot hand-held to detect pointed Homan type is driven into the most 1133 1125 any muscle contraction which might suggest medial anterior ramus as a retractor for the ilio- 1134 1126 sciatic nerve irritation. psoas muscle and neurovascular bundle. 1135 1127 The second cut is an osteotomy of the superior Subperiosteal (Crego) type retractors are inserted 1136 1128 pubic ramus. The medial ilium is subperiosteally around the ramus through the obturator foramen 1137 1129 exposed down to the pelvic brim medially then proximally (first) and then distally, protecting the 1138 1130 distally to the obturator foramen. Anteriorly, obturator nerve. The distal retractor should be 1139 J. G. Schoenecker et al.

Fig. 5.15 Periacetabular osteotomy (PAO) Correction: to provide significant lateral coverage as judged by an AP Once free, the acetabular fragment is repositioned to pro- radiograph. (d) An arthrogram can help judge the position vide anterior coverage (a) that permits 90° of hip flexion of the un-ossified cartilaginous epiphysis and position of (b). Additionally, (c) the fragment should be repositioned the labrum

1140 slightly medial to the proximal retractor. The To perform the iliac osteotomy followed by 1151 1141 superior ramus osteotomy should slope from lat- the posterior column osteotomy, further expo- 1152 1142 eral to medial beginning at a point at least 1 cm sure is necessary. The quadrilateral plate is sub- 1153 1143 medial to the iliopectineal eminence to assure the periosteally exposed down to the sciatic notch 1154 1144 hip joint is not entered during the completion of and base of the ischial spine. A point is marked 1155 1145 the osteotomy. on the false pelvis just lateral to the brim of the 1156 pelvis which corresponds with the proximal 1157 1146 “Palpating the adductor muscle for con- extent of the sciatic notch. To further protect soft 1158 1147 tracture when placing the Crego retrac- tissues, a sub-periosteal retractor is placed along 1159 1148 tors and/or cutting the superior pubic the lateral wall of the ilium in line with the 1160 1149 ramus helps to further protect the obtura- intended course of the iliac osteotomy. The ilium 1161 1150 tor nerve”. 5 Acetabular Dysplasia in the Reduced or Subluxated Hip

Fig. 5.16 Periacetabular osteotomy (PAO): (a) A the osteotomy is well healed, note the restoration of 16-year-old female with significant lateral and anterior Shenton’s line and hip center. The patient is now pain free under-coverage, pain but no labral tear or signs of arthritis returned to sport underwent a PAO (Figs. 5.13–5.16). (b) Two years later

1162 is cut with a power saw to point marked (see attached. The fragment is carefully mobilized 1181 1163 above) on false pelvis. which effectively completes the osteotomies, 1182 freeing the fragment from the surrounding intact 1183 1164 “The posterior column cut begins at the periosteum. The T-handle is further secured to the 1184 1165 end of the iliac cut and extends distally to acetabular fragment with a curved (lobster claw) 1185 1166 a point near or at the most proximal extent bone fragment. Correction desired is typically 1186 1167 of the initial ischial cut (first cut). The cut achieved by adducting, medializing and anterior 1187 1168 should be centered equal distance from tilting (extending) of the acetabular fragment. 1188 1169 the posterior edge of the acetabulum and Provisional fixation is achieved with 3/32 K-wires. 1189 1170 the edge of the posterior column. The 1171 C-arm (45° iliac oblique view) is critical in “Correction achieved is assessed with the 1190 1172 monitoring the direction of the osteotomy. C-arm. Adjustments are made so as to 1191 1173 As the distal portions of the lateral cortex optimize coverage, medialization and ace- 1192 1174 is osteotomized, care must be taken to min- tabular version. The range of motion is 1193 1175 imize injury to the sciatic nerve. The hip is assessed, flexion to 90° and abduction to 1194 1176 extended, abducted and externally rotated 30° should be present. If not, the correc- 1195 1177 and a hand is placed on the foot”. tion obtained should be decreased”. 1196

1178 Having completed all osteotomies, a Shantz The acetabular fragment is secured with corti- 1197 1179 screw is inserted into the acetabular fragment just cal screws, inserted in the same direction as the 1198 1180 superior to the acetabulum and a T-handle chuck previously placed K-wires. Final correction is 1199 J. G. Schoenecker et al.

abc

AU10 Fig. 5.17 Salvage procedure: Shelf Arthroplasty. (a) A patient has healed the shelf and the extracapsular arthro- patient with in incongruent femoral head and acetabulum plasty has influenced restoration of the hip shape (white underwent a shelf osteotomy (b). Two years later, the arrow)

1200 again assessed by C-arm and hip motion again type procedure should be considered so as 1232 1201 assessed. If internal rotation in 90° of flexion is to provide extracapsular stability of the 1233 1202 limited (<15–20°) and a head-neck offset defi- hip joint Fig. 5.17)”. 1234 1203 ciency is noted on pre-operative radiographs, an 1204 anterior arthrotomy is performed and an antero- Surgical Technique: Chiari Osteotomy 1235 1205 lateral head-neck osteochondroplasty performed The approach for the Chiari osteotomy is quite 1236 1206 which typically allows for improved internal rota- similar as to the approach for Bernese PAO and or 1237 1207 tion in flexion [85]. If opened, the capsule is triple innominate osteotomy. Subperiosteal expo- 1238 1208 closed. The ASIS and attached sartorius muscle sure of both the lateral and medial walls of the 1239 1209 are reattached with #5 permanent suture, placed ilium is obtained. Medially, the subperiosteal dis- 1240 1210 through the drill holes in the ilium and around the section extends to and beyond the brim of the pel- 1241 1211 base of the ASIS. The tensor/sartorius fascia is vis down to and into the sciatic notch, and distally 1242 1212 reapproximated and the external oblique muscle to the base of the ischial spine. Laterally, the 1243 1213 sutured to the soft tissue on the anterolateral edge abductor muscle is detached from the iliac crest 1244 1214 of the ilium. The subcutaneous and skin tissues and subperiosteal dissection extended down to 1245 1215 are closed in layers. Patients are mobilized on and into the sciatic notch. When exposing later- 1246 1216 post-operative day #1, and early weight bearing is ally, subperiosteal exposure is carried as far dis- 1247 1217 encouraged for patients with good bone quality. tally as possible. In some instances, this may 1248 include distally elevating proximally displaced 1249 lateral labral chondral tissues (distally, without 1250 1218 Irreducible Hip Joint violating the lateral capsule). Dissecting in the 1251 notch with a sponge facilitates exposure. The 1252 1219 For those hips unable to achieve a concentric osteotomy begins anteriorly at a point half way 1253 1220 reduction, salvage procedures, rather than redi- between the ASIS and AIIS and extends posteri- 1254 1221 rectional, are indicated. These involve either orly (similar to the iliac cut of the previously 1255 1222 moving the ilium itself laterally (i.e. Chiari-type) described Ganz PAO) but extends across and 1256 1223 [86–89] or augmenting extracapsular bone with a through the posterior column, exiting at the sciatic 1257 1224 bone graft (i.e. shelf arthroplasty) to provide fem- notch. To both optimize the eventual displace- 1258 1225 oral head coverage [90, 91]. ment of the fragments and provide enhanced oste- 1259

1226 “Importantly, for satisfactory outcome of otomy stabilization, the osteotomy should be 1260 1227 either a pelvic redirectional osteotomy or angulated approximately 15° cephalad in the 1261 1228 an acetabuloplasty, it is essential that ana- frontal plane. Completion of the osteotomy is per- 1262 1229 tomical reduction of the femoral head into formed with a power saw beginning anteriorly 1263 1230 the true acetabulum is possible. In cases and extending towards the sciatic notch. 1264 1231 in which this is not possible, a salvage Completion of osteotomy within the notch can be 1265 5 Acetabular Dysplasia in the Reduced or Subluxated Hip

1266 achieved with a Gigli saw, cutting anteriorly and In younger patients, hips are protected with an 1313 1267 laterally out of the notch, or with an osteotome abduction pillow, and kept non-weightbearing for 1314 1268 cutting into the notch. In doing so, medial and lat- 5–6 weeks. Younger patients are then mobilized 1315 1269 eral large Hohmann retractors are subperiosteally as possible with protected weight bearing using a 1316 1270 placed in the notch, serving to protect the gluteal walker and/or crutches. Older patients whose 1317 1271 vessels and sciatic nerve. osteotomies have been fixed with cortical screws 1318 are mobilized as possible post operatively. Weight 1319 1272 “Once completed, the distal fragment is bearing is limited until early bone healing is pres- 1320 1273 displaced medially, which variably effects ent (6–8 weeks) and then weight bearing is grad- 1321 1274 improved superior capsular coverage by ually increased. 1322 1275 the osteotomy surface of the proximal 1276 fragment. Effort must be made to assure Surgical Technique: Shelf Arthroplasty 1323 1277 that sufficient displacement occurs but (Figs. 5.8 and 5.17) 1324 1278 also that the distal fragment does not dis- Shelf arthroplasty can at times be very effective 1325 1279 place too posteriorly”. in the treatment of problematic hip joint sublux- 1326 1280 Improved lateral coverage can be augmented ation secondary to various developmental hip 1327 1281 with insertion of a shelf augmentation, which joint pathologies, in older children and adoles- 1328 1282 also helps to minimize the variably occurring cents. The surgical approach in all cases includes 1329 1283 osseous offset between the two pelvic fragments. first achieving femoral head reduction and then 1330 1284 The osteotomy is transfixed with K-wires providing stabilization of what often is a complex 1331 1285 (inserted proximal-distal/lateral-medial) in hip joint subluxation. For the shelf arthroplasty, it 1332 1286 younger patients (<10 years). For older patients, is desirable to use either a screw-plate or screw- 1333 1287 and/or when no cast immobilization is planned, washer stabilization of the shelf to optimize 1334 1288 the osteotomy is fixated with large fragment immediate post-operative early hip joint stabili- 1335 1289 (4.5 mm) cortical screws and cast immobilization zation. The combination of surgical reduction as 1336 1290 is not required. necessary and secured shelf arthroplasty has 1337 1291 Typically, a capsulotomy is not performed. proven to be very effective for the patient with 1338 1292 However, if there is considerable subluxation, severe hip subluxation and deformity. 1339 1293 performing an anterior capsulotomy can help “A relatively “fixed” shelf provides imme- 1340 1294 minimize the extent of subsequent hip joint insta- diate/early important stabilization follow- 1341 1295 bility. The capsulotomy is performed anteriorly, ing surgical reduction of the previously 1342 1296 does not extend superolaterally, but correctly subluxated hip in patients with severe 1343 1297 extends through the most medial capsule to the acetabular insufficiency secondary to 1344 1298 medial edge of the true acetabulum. This potenti- neuromuscular disorders such as cerebral 1345 1299 ates femoral head medialization which in turn palsy and Charcot-Marie-Tooth Disease. 1346 1300 makes it possible to perform a more distal Chiari A surgically secured shelf also provides 1347 1301 osteotomy cut (which is desired). When repairing early stability in the containment treat- 1348 1302 the capsulotomy, it is critical to achieve a very ment of Perthes disease”. 1349 1303 competent capsulorrhaphy as the capsule later 1304 serves as an interpositional arthroplasty, essential The procedure is performed with the patient 1350 1305 in performing a Chiari displacement osteotomy. positioned supine on a flat radiolucent table with 1351 1306 The medial and lateral ilial soft tissues are a small bump under the buttock and lower back. 1352 1307 securely repaired both to each other and to the The hip and pelvis are exposed anteriorly through 1353 1308 iliac crest with #1 Vicryl suture. The tensor sarto- an iliofemoral approach identical to that described 1354 1309 rius interval is closed and the external oblique is for the Pemberton Acetabuloplasty. If the femoral 1355 1310 also reattached to the soft tissues just lateral to head is notably subluxated and a capsulotomy 1356 1311 the iliac crest. The subcutaneous and skin tissues and capsulorrhaphy are to be performed, the rec- 1357 1312 are closed in layers. tus tendon is transected 1 cm distal to insertion 1358 J. G. Schoenecker et al.

1359 and the muscle complex reflected distally to graft. An oscillating saw is used to cut off the top 1406 1360 achieve complete capsular exposure. A near hori- of the iliac crest (saved as a source of bone graft) 1407 1361 zontal capsulotomy is performed, starting 1 cm and then a curved osteotome is used to cut three 1408 1362 lateral to the acetabular rim sloping slightly from adjacent longitudinal Cortico-Cancellous strips 1409 1363 proximal lateral to distal medial. To facilitate from the outer (or inner table). The strips should 1410 1364 essential medialization of the head into the true be made as long as possible, but be sure to leave 1411 1365 acetabulum, the capsulotomy must be extended enough intact. One should leave room in the dis- 1412 1366 to the medial rim of the acetabulum. Problematic tal outer table to accommodate subsequent plate 1413 1367 musculotendinous and ligamentous contractures fixation of the shelf. The total width of the com- 1414 1368 may preclude obtaining a satisfactory reduction bined strips should be roughly the length of the 1415 1369 of the femoral head into the true acetabulum and/ previously constructed trough. Depending on the 1416 1370 or achieving satisfactory hip motion after reduc- volume of graft harvested, you may have to fash- 1417 1371 tion. To deal with this, a proximal femoral oste- ion additional corticocancellous strips from a tri- 1418 1372 otomy (PFO) is designed as dictated by the cortical allograft to augment both the thickness 1419 1373 patient pathology. Components of the PFO and width of the bony shelf. 1420 1374 include shortening of the femur by ~1.5 cm, rota- The shelf is constructed by laying the graft 1421 1375 tion as indicated to correct excessive anteversion strips in the trough side-by-side starting posterior 1422 1376 and increasing varus of neck shaft angle to better and moving anterior. Tamp each individual strip 1423 1377 seat the femoral head into the acetabulum. The deep into the trough abutting immediately on the 1424 1378 PFO is completed through a second incision capsule. Use the initially obtained osteotomized 1425 1379 using a standard lateral approach to the proximal top of the ilium (a tricortical autograft) to press fit 1426 1380 femur. The timing of the PFO during the proce- and backfill the superior aspect of the trough and 1427 1381 dure is based on need. If femoral shortening is reinforce the shelf. The shelf will become more 1428 1382 required then the PFO should be done prior to stable as the trough is tightly filled with graft 1429 1383 attempting open reduction. reinforcing its superior surface. A Freer elevator 1430 1384 Once the head is reduced into the acetabulum is inserted between the shelf and the capsule and 1431 1385 and the capsulorrhaphy complete (if necessary), the C-arm is used to assess there is a tight fit 1432 1386 the shelf acetabuloplasty is performed. The anter- between shelf and capsule. 1433 1387 osuperior aspect of the acetabulum is located uti- To assure the shelf remains impacted against 1434 1388 lizing an AP fluoroscopic image. A series of the capsule, the shelf is secured in place with 1435 1389 unicortical holes are made just above the acetab- either a plate and/or abutting screws. A small 1436 1390 ulum, using a 3.2 mm drill through the outer table fragment (distal radius type) T-plate is appro- 1437 1391 (2 cm deep, directed 20° cephalad) priately bent and secured with 2–3 bicortical 1438 screws through the ilium and 2 locking screws 1439 1392 “Starting anterior and moving posterior – through the shelf. The plate is contoured and 1440 1393 just above and as close as possible to the fixated between the pelvis and graft so as to 1441 1394 superior acetabular – the shelf must ana- both hold the composite graft in-place and 1442 1395 tomically about the hip capsule without compress the shelf against the capsule. 1443 1396 penetrating into acetabular articular Alternatively stabilize the shelf by inserting 1444 1397 surface”. two cortical screws abutting firmly against the 1445 1398 Once the line of drill holes is complete, they proximal surface of the bony shelf in a blocking 1446 1399 are connected from anterior to posterior using strategy (washers with points are essential in 1447 1400 small curettes and dental burrs, directing the dis- achieving secure screw head purchase on the 1448 1401 section so the slot being created is immediately lateral edges of the shelf). 1449 1402 adjacent to the capsule and directed proximally. “Once the shelf arthroplasty has been 1450 1403 The trough should be deep enough to abut but not secured. Final C-arm views include an AP 1451 1404 penetrate the inner table. After the trough is cre- (in abduction and adduction) and false 1452 1405 ated, proceed in harvesting the outer table bone profile lateral (in neutral extension and 1453 5 Acetabular Dysplasia in the Reduced or Subluxated Hip

1454 flexion). Assess femoral head coverage 1455 and the desired immediate adjacent con- innominate osteotomy) and an overzeal- 1456 tact, with the capsule interposed between ous proximal femoral derotational oste- 1457 the head and the shelf. Also, hip motion otomy that corrects for anteversion. 1458 should be confirmed, with flexion to 90° • Attempting to correct global deficiency 1459 and abduction to 25–30° mandatory so as associated with myelodysplasia or 1460 to avoid impingement”. Down syndrome, with either an acetabuloplasty or single innominate, may fail 1461 In closing the conjoined rectus tendon (if tran- because of posterior acetabular defi- 1462 sected in the approach) repaired with #1 Ethibond. ciency. In these cases, a triple innomi- 1463 Repair of the apophyseal cartilage, closure of the nate osteotomy is typically necessary. 1464 tensor-sartorius interval, and reattachment of the • Lack of familiarity of the modification 1465 external oblique and subcutaneous and cutaneous of the Smith Peterson approach neces- 1466 is performed, as previously described. The patient sary to achieve access to anterior ischial 1467 is placed into an A-frame long leg cast bilaterally and superior pubic ramus will make it 1468 with the knees slightly flexed. After 5–6 weeks in technically near impossible to safely 1469 the A-frame cast the patient is converted to an complete either a triple innominate or 1470 A-frame brace and three times daily range of PAO osteotomy. 1471 motion exercises initiated. At 3 months, the • Failure to complete the posterior col- 1472 patients can begin weightbearing based on X-ray umn osteotomy of an attempted Ganz 1473 evidence of graft incorporation, continuing with PAO and mobilize the acetabulum frag- 1474 the A-frame brace at night. ment will limit achieving both satisfactory redirection and medialization of the Operative Pitfalls acetabulum. • Failure to use C-arm monitoring while • Failure to stabilize a triple innominate performing an acetabuloplasty risks or Ganz PAO risks early post-operative inadvertently extending the osteotome loss of acetabular reorientation. into the acetabulum and/or the bone graft • If a Chiari osteotomy is too proximal, into and through the tri-radiate cartilage. relative to the joint capsule, the potential • Overcorrective anterolateral coverage, for improved stability provided to the particularly when performing an acetab- femoral head is notably compromised. uloplasty, risks later development of • Allowing excessive posterior displace- symptomatic FAI. ment of the distal Chiari fragment risks • Inadequate fixation risks a post- injury to the sciatic nerve. operative loss of reduction following • Failing to obtain intimate contact of the Salter osteotomy; especially in a small capsule and femoral head when per- pelvis. forming a shelf arthroplasty minimizes • Attempting to achieve improved cover- any subsequent beneficial supportive age with a pelvic procedure without function of the shelf. first obtaining satisfactory reduction of the femoral head into the true acetabulum risks persistent postoperative subluxation. Classic Papers 1475 • Exacerbating posterior deficiency and the potential for early redislocation by Harris WH. Etiology of OA of the hip. Instr 1476 overcorrection can occur with a combi- Coume Lect 1986. Proposed that OA of the hip 1477 nation of acetabuloplasty (or single typically does not exist as a primary disease, a 1478 change in our thinking. 1479 J. G. Schoenecker et al.

1480 Klaue K. The acetabular rim syndrome. A complete cut through the entire ilium, i.e. 1527 1481 clinical presentation of dysplasia of the hip J “acetabuloplasty”. 1528 1482 Bone Joint Surg Br 1991. Hip pathology that Wyles EC. The John Charnley Award: 1529 1483 leads to damage to the labrum and/or chondrolat- Redefining the natural history of osteoarthri- 1530 1484 eral junction is what typically leads to acetabular tis in patients with hip dysplasia and impinge- 1531 1485 and femoral head arthritis. ment. Clin Orthop Relat Res 2017. 1532 1486 Ponsetti IV. Morphology of the acetabulum Comprehensive comparison in longitudinal study 1533 1487 in congenital dislocation of the hip, gross, his- of frequency of total hip replacement necessary 1534 1488 tological and roentgenographic studies. J in patients with either FAI, dysplasia or normal 1535 1489 Bone and Joint Am 1976. Detailed description morphology. 1536 1490 of the cartilaginous anatomy of the acetabulum Smith-Petersen MN. The Classic: 1537 1491 and its growth and development. Treatment of malum coxae senilis, old slipped 1538 1492 Weinstein SL. Natural history of congenital upper femoral epiphysis, intra pelvic protru- 1539 1493 hip dislocation (CDH) and hip dysplasia. Clin sion of the acetabulum, and coxa plana by 1540 1494 Orthop Relat Res 1987. Extensive description means of acetabuloplasty in 1936 (reprinted in 1541 1495 of the normal and abnormal radiological features Clin Orthop Relat Res 2009). Original descrip- 1542 1496 of hip development and factors, most important tion on the technique of what is now the standard 1543 1497 in clinical outcome. anterior approach to the pelvis and hip joint. 1544 1498 Tonnis D. Congenital dysplasia and dislo- Betz RR. Chiari pelvic osteotomy in chil- 1545 1499 cation of the Hip in children and Adults. dren and young adults. J Bone Joint Surg Am 1546 1500 Springer 1987. The most informative/authorita- 1988. Indications for and technique of perform- 1547 1501 tive text on hip dysplasia (a “must” for hip ing a Chiari osteotomy. 1548 1502 aficionados). Kuwajima SS. Comparison between 1549 1503 Cooperman DR. Acetabulum dysplasia in Salter’s innominate osteotomy and augmented 1550 1504 the adult. Clin Orthop Relat Res. 1983. acetabuloplasty in the treatment of patients 1551 1505 Documented that degenerative hip joint disease with severe Legg Calve-Perthes disease. J 1552 1506 will eventually develop in all patients with hip Pediatr Orthop B 2002. The author demon- 1553 1507 subluxation. strated the slot-secured shelf arthroplasty in the 1554 1508 Wiberg G. Studies on dysplastic acetabular treatment of problematic Coxa Plana. 1555 1509 and congenital subluxation of the hip joint with Faciszewski T. Triple innominate osteotomy 1556 1510 special reference to the complication of for acetabular dysplasia. J Pediatr Orthop 1557 1511 OA. ACTA Chine Scandinavia 1939. Very early 1993. Publication with a substantial number of 1558 1512 definitive description of radiographic acetabular patients (other than Steel’s original article) of 1559 1513 deficiency, what was felt to be normal and abnormal successful treatment of residual dysplasia utiliz- 1560 1514 and its association with the development of OA. ing the Steel triple innominate osteotomies. 1561 1515 Salter RB. Innominate osteotomy in the Ganz R. A new periacetabular osteotomy 1562 1516 treatment of congenital dislocation and sub- for the treatment of hip dysplasia. Technique 1563 1517 luxation of the hip. J Bone Joint Surg Br 1961. and preliminary results. Clin Orthop Relat 1564 1518 First publication of its kind describing a com- Res 1988. “The” article that introduced the 1565 1519 plete iliac pelvic osteotomy allowing for antero- Bernese PAO as an alternate to a triple innomi- 1566 1520 lateral redirection of the congenitally deficient nate or dial osteotomy in correcting acetabular 1567 1521 acetabulum. dysplasia. 1568 1522 Pemberton PA. Pericapsular osteotomy of Wells J. Intermediate-term hip survivor- 1569 1523 the ilium for treatment of congenital sublux- ship and patient-reported outcomes of peri- 1570 1524 ation and dislocation of the hip. J Bone Joint acetabular osteotomy: The Washington 1571 1525 Am. 1965. Also a first in the description of University experience. J Bone Joint Surg Am 1572 1526 redirecting the acetabulum without making a 2018. Comprehensive review of both local, 1573 5 Acetabular Dysplasia in the Reduced or Subluxated Hip

1574 national and international outcomes to date of cartilaginous anlage), the indications are some- 1597 1575 treatment of acetabular dysplasia with the what less clear for the surgical correction of 1598 1576 Bernese (Ganz) PAO. residual acetabular dysplasia (Fig. 5.18). There 1599 is a paucity of both natural history and properly 1600 controlled interventional studies of hip dysplasia 1601 1577 Key Evidence in this age group. In these more mature hips, 1602 there will be less potential remodeling following 1603 1578 The indications for performing either a pelvic joint preserving surgery. Precise repositioning of 1604 1579 redirectional osteotomy or an acetabuloplasty in the acetabulum is more critical in assuring satis- 1605 1580 attempting to correct acetabular dysplasia are factory long-term outcome [8, 76, 77]. Most sur- 1606 1581 dependent upon age and cause of the dysplasia. geons consider symptoms of dysplasia (pain, 1607 1582 In the young child (during development of the feeling of instability, and limping), a positive 1608 1583 cartilaginous anlage), indications for surgical Trendelenburg sign on exam and radiographic 1609 1584 correction are dependent on the functional evidence of subluxation as indications for cor- 1610 1585 capacity of the acetabulum to support weight rective surgery in these more skeletally mature 1611 1586 bearing and hip range of motion. For these patients. Outcomes of surgical connection of 1612 1587 patients, radiographic evidence of acetabular acetabular dysplasia have been very favorable, 1613 1588 underdevelopment and subluxation/instability with a reported 95% 15 year survival rate [92– 1614 1589 (i.e. break in Shenton’s line) or symptomatic 95]. Younger patients and the preoperative 1615 1590 dysplasia (pain or feeling of instability) is a absence of arthritis were predictors of poten- 1616 1591 clear indication for surgical intervention [9]. tially better outcomes. The status of the labral 1617 1592 Given the predictable remodeling potential of chondral complex and/or head-neck prominence 1618 1593 the cartilaginous anlage, patients do very well as predictors of outcome is less clear. While 1619 1594 following properly performed interventions [39, techniques have been developed that make it 1620 1595 76, 77]. In relatively older patients (following possible to correct both labral chondral pathol- 1621 1596 near complete development/ossification of the ogy and head-neck junction abnormalities 1622

abc

Fig. 5.18 Current indications of the PAO: Indications for (green arrow). However, evidence is less clear as to the correction of insufficient lateral (black arrow) or anterior outcome of correcting incidentally discovered, asymp- coverage (a) are continually evolving. Current evidence tomatic dysplasia (a). Additionally, with the advent of supports correction of a symptomatic under-covered (see combined arthroscopy, it is unknown if labral repair is AU11 Table 5.1 for values) hip. Current evidence also supports required when addressing dysplasia, or, how much a tear replacement, not preservation, of a (c) symptomatic dys- is too significant to warrant surgical correction of both the plasia with a labral tear (red arrow) and osteoarthritis labrum and dysplasia in favor of replacement J. G. Schoenecker et al.

1623 concomitant with acetabular reorientation, clini- References 1628AU12 1624 cal studies are still ongoing in attempting to show 1625 how effective these adjacent procedures are (or 1. Harris WH. Etiology of osteoarthritis of the hip. Clin 1629 1626 are not) in further improving the outcome of ace- Orthop Relat Res. 1986;(213):20–33. 1630 2. Aronson J. Osteoarthritis of the young adult hip: etiol- 1631 1627 tabular reorientation joint preserving surgery. ogy and treatment. Instr Course Lect. 1986;35:119–28. 1632 3. Klaue K, Durnin CW, Ganz R. The acetabular rim 1633 syndrome. A clinical presentation of dysplasia of the 1634 hip. J Bone Joint Surg Br. 1991;73(3):423–9. 1635 Take Home Message 4. Clohisy JC, Beaule PE, O’Malley A, Safran MR, 1636 • In the last few decades, both our under- Schoenecker P. AOA symposium. Hip disease 1637 standing of what leads to hip joint arthri- in the young adult: current concepts of etiology 1638 tis secondary to acetabular dysplasia and and surgical treatment. J Bone Joint Surg Am. 1639 2008;90(10):2267–81. 1640 the ability to surgically correct it has 5. Leunig M, Siebenrock KA, Ganz R. Rationale of 1641 changed the practice of our hip surgery. periacetabular osteotomy and background work. Instr 1642 • It is essential to be knowledgeable of the Course Lect. 2001;50:229–38. 1643 development of the hip and the pro- 6. Nepple JJ, Byrd JW, Siebenrock KA, Prather H, 1644 Clohisy JC. Overview of treatment options, clinical 1645 cesses by which it can fail when select- results, and controversies in the management of femo- 1646 ing a surgical approach in the correction roacetabular impingement. J Am Acad Orthop Surg. 1647 of residual acetabular dysplasia. 2013;21(Suppl 1):S53–8. 1648 • Having an understanding of both the 7. Schoenecker PL, Clohisy JC, Millis MB, Wenger 1649 DR. Surgical management of the problematic hip 1650 normal and abnormal growth of the ace- in adolescent and young adult patients. J Am Acad 1651 tabulum helps in both the need for tim- Orthop Surg. 2011;19(5):275–86. 1652 ing of and choosing the optimal surgical 8. Siebenrock KA, Leunig M, Ganz R. Periacetabular 1653 technique in correcting acetabular osteotomy: the Bernese experience. Instr Course Lect. 1654 2001;50:239–45. deficiency. 1655 9. Weinstein SL. Natural history of congenital hip dis- 1656 • Further observation is indicated for location (CDH) and hip dysplasia. Clin Orthop Relat 1657 younger children (less than 7 years old) Res. 1987;(225):62–76. 1658 with a progressive decrease of the ace- 10. Beck M, Kalhor M, Leunig M, Ganz R. Hip morphol- 1659 ogy influences the pattern of damage to the acetabular tabular index, an intact Shelton’s line, 1660 cartilage: femoroacetabular impingement as a cause 1661 normal hip motion and no limp. of early osteoarthritis of the hip. J Bone Joint Surg Br. 1662 • Further observation is not indicated for 2005;87(7):1012–8. 1663 older children (7 years and older) with an 11. Aronsson DD, Goldberg MJ, Kling TF Jr, Roy 1664 DR. Developmental dysplasia of the hip. Pediatrics. unchanging acetabular index, break in 1665 1994;94(2 Pt 1):201–8. 1666 Shelton’s line, and a positive 12. Ponseti IV. Growth and development of the acetabu- 1667 Trendelenburg sign. Rather, appropriate lum in the normal child. Anatomical, histological, 1668 surgical correction should be considered. and roentgenographic studies. J Bone Joint Surg Am. 1669 1978a;60(5):575–85. • For skeletally mature patients, surgical 1670 13. Ponseti IV. Morphology of the acetabulum in con- 1671 correction of residual acetabular dyspla- genital dislocation of the hip. Gross, histological and 1672 sia is selectively performed typically roentgenographic studies. J Bone Joint Surg Am. 1673 only for symptomatic patients. 1978b;60(5):586–99. 1674 14. Tonnis D. Congenital dysplasia and dislocation of the • The clinical and radiographic goals at 1675 hip in children and adults. New York: Springer; 1987. 1676 skeletal maturity, whether by natural his- 15. Leet AI, Mackenzie WG, Szoke G, Harcke HT. Injury 1677 tory or following surgical intervention, to the growth plate after Pemberton osteotomy. J Bone 1678 include: lateral and anterior CEA of 25°, Joint Surg Am. 1999;81(2):169–76. 1679 16. Ganz R, Klaue K, Vinh TS, Mast JW. A new periace- less than 20% of the femoral head later- 1680 tabular osteotomy for the treatment of hip dysplasias. 1681 ally uncovered, a “stable” hip (i.e. Tonnis Technique and preliminary results. Clin Orthop Relat 1682 angle <10° and Shelton’s line intact) and, Res. 1988;(232):26–36. 1683 most importantly, a congruent hip with 17. Parvizi J, Leunig M, Ganz R. Femoroacetabular 1684 impingement. J Am Acad Orthop Surg. 2007; satisfactory range of motion. 1685 15(9):561–70. 1686 5 Acetabular Dysplasia in the Reduced or Subluxated Hip

1687 18. Wyles CC, Heidenreich MJ, Jeng J, Larson DR, nonuniform contact models applied to long-term fol- 1748 1688 Trousdale RT, Sierra RJ. The John Charnley Award: low-up of CDH. J Biomech. 1995;28(2):159–66. 1749 1689 redefining the natural history of OA in patients with 33. Wedge JH, Wasylenko MJ. The natural history of con- 1750 1690 hip dysplasia and impingement. Clin Orthop Relat genital dislocation of the hip: a critical review. Clin 1751 1691 Res. 2017;475(2):336–50. Orthop Relat Res. 1978;(137):154–62. 1752 1692 19. Chegini S, Beck M, Ferguson SJ. The effects of 34. Wiberg G. Studies on dysplastic acetabula and congen- 1753 1693 impingement and dysplasia on stress distribu- ital subluxation of the hip joint with special reference to 1754 1694 tions in the hip joint during sitting and walk- the complication of OA. Acta Chir Scand. 1939;83:58. 1755 1695 ing: a finite element analysis. J Orthop Res. 35. Eppright R. Dial osteotomy of the acetabulum in the 1756 1696 2009;27(2):195–201. treatment of dysplasia of the hip. J Bone Joint Surg 1757 1697 20. Ecker TM, Tannast M, Puls M, Siebenrock KA, Am. 1975;57:212–5. 1758 1698 Murphy SB. Pathomorphologic alterations predict 36. Millis MB, Murphy SB. Use of computed tomo- 1759 1699 presence or absence of hip osteoarthrosis. Clin Orthop graphic reconstruction in planning osteotomies of the 1760 1700 Relat Res. 2007;465:46–52. hip. Clin Orthop Relat Res. 1992;(274):154–9. 1761 1701 21. Ganz R, Parvizi J, Beck M, Leunig M, Notzli H, 37. Muller ME. Intertrochanteric osteotomy: indication, 1762 1702 Siebenrock KA. Femoroacetabular impingement: a preoperative planning, technique. In: Schatzker J, 1763 1703 cause for osteoarthritis of the hip. Clin Orthop Relat editor. The intertrochanteric osteotomy. New York: 1764 1704 Res. 2003;(417):112–20. Springer; 1984. p. 25–66. 1765 1705 22. Smith-Petersen MN. The classic: Treatment of malum 38. Pauwels F. Biomechanics of the normal and diseased 1766 1706 coxae senilis, old slipped upper femoral epiphysis, hip. In: Furlong R, Maquet P, editors. Theoretical 1767 1707 intrapelvic protrusion of the acetabulum, and coxa foundation, technique and results of treatment an 1768 1708 plana by means of acetabuloplasty. 1936. Clin Orthop atlas. New York: Springer; 1976. p. 136–43. 1769 1709 Relat Res. 2009;467(3):608–15. 39. Salter RB. The classic. Innominate osteotomy in 1770 1710 23. Allen D, Beaule PE, Ramadan O, Doucette the treatment of congenital dislocation and sublux- 1771 1711 S. Prevalence of associated deformities and hip pain ation of the hip by Robert B. Salter, J Bone Joint 1772 1712 in patients with cam-type femoroacetabular impinge- Surg (Brit) 43B:3:518, 1961. Clin Orthop Relat Res. 1773 1713 ment. J Bone Joint Surg Br. 2009;91(5):589–94. 1978;(137):2–14. 1774 1714 24. Bardakos NV, Villar RN. Predictors of progression 40. Wagner H. Experiences with spherical acetabular 1775 1715 of osteoarthritis in femoroacetabular impingement: osteotomy for the correction of the dysplastic acetab- 1776 1716 a radiological study with a minimum of ten years ulum. In: Weil U, editor. Acetabular dysplasia prog- 1777 1717 follow-up. J Bone Joint Surg Br. 2009;91(2):162–9. ress in orthopaedic surgery, vol. 2. Berlin, Heidelberg: 1778 1718 25. Cooperman DR, Wallensten R, Stulberg Springer; 1978. p. 131–45. 1779 1719 SD. Acetabular dysplasia in the adult. Clin Orthop 41. Wagner H. Osteotomies for congenital hip dislocation. 1780 1720 Relat Res. 1983;(175):79–85. In: The hip proceedings of the fourth open scientific 1781 1721 26. Hartofilakidis G, Bardakos NV, Babis GC, Georgiades meeting of the Hip Society. St Louis: Mosby; 1976. 1782 1722 G. An examination of the association between dif- p. 45–66. 1783 1723 ferent morphotypes of femoroacetabular impinge- 42. Murphy SB, Kijewski PK, Millis MB, Harless 1784 1724 ment in asymptomatic subjects and the development A. Acetabular dysplasia in the adolescent and young 1785 1725 of osteoarthritis of the hip. J Bone Joint Surg Br. adult. Clin Orthop Relat Res. 1990;(261):214–23. 1786 1726 2011;93(5):580–6. 43. Murphy SB, Ganz R, Muller ME. The prognosis in 1787 1727 27. Malvitz TA, Weinstein SL. Closed reduction for con- untreated dysplasia of the hip. A study of radiographic 1788 1728 genital dysplasia of the hip. Functional and radio- factors that predict the outcome. J Bone Joint Surg 1789 1729 graphic results after an average of thirty years. J Bone Am. 1995;77(7):985–9. 1790 1730 Joint Surg Am. 1994;76(12):1777–92. 44. Sankar WN, Duncan ST, Baca GR, Beaule PE, 1791 1731 28. Schwend RM, Pratt WB, Fultz J. Untreated acetabular Millis MB, Kim YJ, et al. Descriptive epidemiology 1792 1732 dysplasia of the hip in the Navajo. A 34 year case series of acetabular dysplasia: The Academic Network of 1793 1733 followup. Clin Orthop Relat Res. 1999;(364):108–16. Conservational Hip Outcomes Research (ANCHOR) 1794 1734 29. Sierra RJ, Trousdale RT, Ganz R, Leunig M. Hip dis- periacetabular osteotomy. J Am Acad Orthop Surg. 1795 1735 ease in the young, active patient: evaluation and non- 2017;25(2):150–9. 1796 1736 arthroplasty surgical options. J Am Acad Orthop Surg. 45. Carter CO, Wilkinson JA. Genetic and environmental 1797 1737 2008;16(12):689–703. factors in the etiology of congenital dislocation of the 1798 1738 30. Hartofilakidis G, Karachalios T, Stamos hip. Clin Orthop Relat Res. 1964;33:119–28. 1799 1739 KG. Epidemiology, demographics, and natural his- 46. Weinstein SL, Mubarak SJ, Wenger 1800 1740 tory of congenital hip disease in adults. Orthopedics. DR. Developmental hip dysplasia and dislocation: 1801 1741 2000;23(8):823–7. Part I. Instr Course Lect. 2004;53:523–30. 1802 1742 31. Hadley NA, Brown TD, Weinstein SL. The effects of 47. Salter RB. Etiology, pathogenesis and possible pre- 1803 1743 contact pressure elevations and aseptic necrosis on vention of congenital dislocation of the hip. Can Med 1804 1744 the long-term outcome of congenital hip dislocation. J Assoc J. 1968;98(20):933–45. 1805 1745 Orthop Res. 1990;8(4):504–13. 48. Dunn PM. Perinatal observations on the etiology of 1806 1746 32. Maxian TA, Brown TD, Weinstein SL. Chronic stress congenital dislocation of the hip. Clin Orthop Relat 1807 1747 tolerance levels for human articular cartilage: two Res. 1976;(119):11–22. 1808 J. G. Schoenecker et al.

1809 49. Bialik V, Berant M. “Immunity” of Ethiopian 64. Murray RO. The etiology of primary osteoarthritis of 1869 1810 Jews to developmental dysplasia of the hip: a pre- the hip. Br J Radiol. 1965;38(455):810–24. 1870 1811 liminary sonographic study. J Pediatr Orthop B. 65. Crockarell J Jr, Trousdale RT, Cabanela ME, Berry 1871 1812 1997;6(4):253–4. DJ. Early experience and results with the periace- 1872 1813 50. Roper A. Hip dysplasia in the African Bantu. J Bone tabular osteotomy. The Mayo Clinic experience. Clin 1873 1814 Joint Surg Br. 1976;58(2):155–8. Orthop Relat Res. 1999;(363):45–53. 1874 1815 51. Skirving AP, Scadden WJ. The African neonatal hip 66. Peters CL, Erickson JA, Hines JL. Early results of the 1875 1816 and its immunity from congenital dislocation. J Bone Bernese periacetabular osteotomy: the learning curve 1876 1817 Joint Surg Br. 1979;61-B(3):339–41. at an academic medical center. J Bone Joint Surg Am. 1877 1818 52. Rabin DL, Barnett CR, Arnold WD, Freiberger 2006;88(9):1920–6. 1878 1819 RH, Brooks G. Untreated congenital hip disease. A 67. Trousdale RT, Ekkernkamp A, Ganz R, Wallrichs 1879 1820 study of the epidemiology, natural history, and social SL. Periacetabular and intertrochanteric osteotomy 1880 1821 aspects of the disease in a Navajo population. Am J for the treatment of osteoarthrosis in dysplastic hips. J 1881 1822 Public Health Nations Health. 1965;55(Suppl):1–44. Bone Joint Surg Am. 1995;77(1):73–85. 1882 1823 53. Johnsen K, Goll R, Reikeras O. Acetabular dyspla- 68. Trumble SJ, Mayo KA, Mast JW. The periacetabular 1883 1824 sia in the Sami population: a population study among osteotomy. Minimum 2 year followup in more than 1884 1825 Sami in north Norway. Int J Circumpolar Health. 100 hips. Clin Orthop Relat Res. 1999;(363):54–63. 1885 1826 2008;67(1):147–53. 69. Clohisy JC, Dobson MA, Robison JF, Warth LC, 1886 1827 54. Lee CB, Mata-Fink A, Millis MB, Kim Zheng J, Liu SS, et al. Radiographic structural abnor- 1887 1828 YJ. Demographic differences in adolescent-diagnosed malities associated with premature, natural hip- 1888 1829 and adult-diagnosed acetabular dysplasia compared joint failure. J Bone Joint Surg Am. 2011;93(Suppl 1889 1830 with infantile developmental dysplasia of the hip. J 2):3–9. 1890 1831 Pediatr Orthop. 2013;33(2):107–11. 70. Clohisy JC, Barrett SE, Gordon JE, Delgado ED, 1891 1832 55. Croft P, Cooper C, Wickham C, Coggon Schoenecker PL. Medial translation of the hip joint 1892 1833 D. Osteoarthritis of the hip and acetabular dysplasia. center associated with the Bernese periacetabular 1893 1834 Ann Rheum Dis. 1991;50(5):308–10. osteotomy. Iowa Orthop J. 2004;24:43–8. 1894 1835 56. Inoue K, Wicart P, Kawasaki T, Huang J, Ushiyama T, 71. Nunley RM, Prather H, Hunt D, Schoenecker PL, 1895 1836 Hukuda S, et al. Prevalence of hip osteoarthritis and Clohisy JC. Clinical presentation of symptomatic 1896 1837 acetabular dysplasia in French and Japanese adults. acetabular dysplasia in skeletally mature patients. J 1897 1838 Rheumatology (Oxford). 2000;39(7):745–8. Bone Joint Surg Am. 2011;93(Suppl 2):17–21. 1898 1839 57. Jacobsen S, Sonne-Holm S, Soballe K, Gebuhr P, 72. Steppacher SD, Tannast M, Ganz R, Siebenrock 1899 1840 Lund B. Hip dysplasia and osteoarthrosis: a survey KA. Mean 20-year followup of Bernese peri- 1900 1841 of 4151 subjects from the Osteoarthrosis Substudy acetabular osteotomy. Clin Orthop Relat Res. 1901 1842 of the Copenhagen City Heart Study. Acta Orthop. 2008;466(7):1633–44. 1902 1843 2005;76(2):149–58. 73. Troelsen A, Elmengaard B, Soballe K. Medium-term 1903 1844 58. Lau EM, Lin F, Lam D, Silman A, Croft P. Hip osteo- outcome of periacetabular osteotomy and predictors 1904 1845 arthritis and dysplasia in Chinese men. Ann Rheum of conversion to total hip replacement. J Bone Joint 1905 1846 Dis. 1995;54(12):965–9. Surg Am. 2009;91(9):2169–79. 1906 1847 59. Lehmann HP, Hinton R, Morello P, Santoli 74. Ito H, Tanino H, Yamanaka Y, Minami A, Matsuno 1907 1848 J. Developmental dysplasia of the hip practice T. Intermediate to long-term results of periace- 1908 1849 guideline: technical report. Committee on Quality tabular osteotomy in patients younger and older 1909 1850 Improvement, and Subcommittee on Developmental than forty years of age. J Bone Joint Surg Am. 1910 1851 Dysplasia of the Hip. Pediatrics. 2000;105(4):E57. 2011;93(14):1347–54. 1911 1852 60. Smith RW, Egger P, Coggon D, Cawley MI, Cooper 75. Novais EN, Heyworth B, Murray K, Johnson VM, 1912 1853 C. Osteoarthritis of the hip joint and acetabular dyspla- Kim YJ, Millis MB. Physical activity level improves 1913 1854 sia in women. Ann Rheum Dis. 1995;54(3):179–81. after periacetabular osteotomy for the treatment of 1914 1855 61. Engesaeter IO, Laborie LB, Lehmann TG, Fevang symptomatic hip dysplasia. Clin Orthop Relat Res. 1915 1856 JM, Lie SA, Engesaeter LB, et al. Prevalence of 2013;471(3):981–8. 1916 1857 radiographic findings associated with hip dysplasia 76. Faciszewski T, Coleman SS, Biddulph G. Triple 1917 1858 in a population-based cohort of 2081 19-year-old innominate osteotomy for acetabular dysplasia. J 1918 1859 Norwegians. Bone Joint J. 2013;95-B(2):279–85. Pediatr Orthop. 1993a;13(4):426–30. 1919 1860 62. Engesaeter LB, Engesaeter IO, Fenstad AM, Havelin 77. Faciszewski T, Kiefer GN, Coleman SS. Pemberton 1920 1861 LI, Karrholm J, Garellick G, et al. Low revision rate osteotomy for residual acetabular dysplasia in chil- 1921 1862 after total hip arthroplasty in patients with pediatric dren who have congenital dislocation of the hip. J 1922 1863 hip diseases. Acta Orthop. 2012;83(5):436–41. Bone Joint Surg Am. 1993b;75(5):643–9. 1923 1864 63. Lohmander LS, Engesaeter LB, Herberts P, Ingvarsson 78. Gordon JE, Capelli AM, Strecker WB, Delgado ED, 1924 1865 T, Lucht U, Puolakka TJ. Standardized incidence rates Schoenecker PL. Pemberton pelvic osteotomy and 1925 1866 of total hip replacement for primary hip osteoarthritis varus rotational osteotomy in the treatment of ace- 1926 1867 in the 5 Nordic countries: similarities and differences. tabular dysplasia in patients who have static encepha- 1927 1868 Acta Orthop. 2006;77(5):733–40. lopathy. J Bone Joint Surg Am. 1996;78(12):1863–71. 1928 5 Acetabular Dysplasia in the Reduced or Subluxated Hip

1929 79. Pemberton PA. Pericapsular osteotomy of the tion of the hip in cerebral palsy. A long-term outcome 1965 1930 ilium for treatment of congenital subluxation study. J Bone Joint Surg Br. 2006;88(10):1373–8. 1966 1931 and dislocation of the hip. J Bone Joint Surg Am. 89. Dietz FR, Knutson LM. Chiari pelvic osteotomy in 1967 1932 1965;47:65–86. cerebral palsy. J Pediatr Orthop. 1995;15(3):372–80. 1968 1933 80. Vedantam R, Capelli AM, Schoenecker PL. Pemberton 90. Kuwajima SS, Crawford AH, Ishida A, Roy DR, Filho 1969 1934 osteotomy for the treatment of developmental dys- JL, Milani C. Comparison between Salter’s innomi- 1970 1935 plasia of the hip in older children. J Pediatr Orthop. nate osteotomy and augmented acetabuloplasty in the 1971 1936 1998;18(2):254–8. treatment of patients with severe Legg-Calve-Perthes 1972 1937 81. Salter RB. Role of innominate osteotomy in the disease. Analysis of 90 hips with special reference to 1973 1938 treatment of congenital dislocation and subluxation roentgenographic sphericity and coverage of the fem- 1974 1939 of the hip in the older child. J Bone Joint Surg Am. oral head. J Pediatr Orthop B. 2002;11(1):15–28. 1975 1940 1966;48(7):1413–39. 91. Staheli LT, Chew DE. Slotted acetabular augmenta- 1976 1941 82. Rebello G, Zilkens C, Dudda M, Matheney T, Kim tion in childhood and adolescence. J Pediatr Orthop. 1977 1942 YJ. Triple pelvic osteotomy in complex hip dysplasia 1992;12(5):569–80. 1978 1943 seen in neuromuscular and teratologic conditions. J 92. Clohisy JC, Ackerman J, Baca G, Baty J, Beaule 1979 1944 Pediatr Orthop. 2009;29(6):527–34. PE, Kim YJ, et al. Patient-reported outcomes of 1980 1945 83. Steel HH. Triple osteotomy of the innominate bone. J periacetabular osteotomy from the prospective 1981 1946 Bone Joint Surg Am. 1973;55(2):343–50. ANCHOR cohort study. J Bone Joint Surg Am. 1982 1947 84. Clohisy JC, Barrett SE, Gordon JE, Delgado ED, 2017;99(1):33–41. 1983 1948 Schoenecker PL. Periacetabular osteotomy in the 93. Lerch TD, Steppacher SD, Liechti EF, Tannast M, 1984 1949 treatment of severe acetabular dysplasia. Surgical Siebenrock KA. One-third of hips after periacetabu- 1985 1950 technique. J Bone Joint Surg Am. 2006;88(Suppl 1 Pt lar osteotomy survive 30 years with good clinical 1986 1951 1):65–83. results, no progression of arthritis, or conversion to 1987 1952 85. Nassif NA, Schoenecker PL, Thorsness R, Clohisy THA. Clin Orthop Relat Res. 2017;475(4):1154–68. 1988 1953 JC. Periacetabular osteotomy and combined femoral 94. Wells J, Millis M, Kim YJ, Bulat E, Miller P, Matheney 1989 1954 head-neck junction osteochondroplasty: a minimum T. Survivorship of the Bernese periacetabular osteot- 1990 1955 two-year follow-up cohort study. J Bone Joint Surg omy: what factors are associated with long-term fail- 1991 1956 Am. 2012;94(21):1959–66. ure? Clin Orthop Relat Res. 2017;475(2):396–405. 1992 1957 86. Bailey TE Jr, Hall JE. Chiari medial displacement 95. Wells J, Schoenecker P, Duncan S, Goss CW, 1993 1958 osteotomy. J Pediatr Orthop. 1985;5(6):635–41. Thomason K, Clohisy JC. Intermediate-term hip survi- 1994 1959 87. Betz RR, Kumar SJ, Palmer CT, MacEwen GD. Chiari vorship and patient-reported outcomes of periacetabu- 1995 1960 pelvic osteotomy in children and young adults. J Bone lar osteotomy: the Washington University experience. 1996 1961 Joint Surg Am. 1988;70(2):182–91. J Bone Joint Surg Am. 2018;100(3):218–25. 1997 1962 88. Debnath UK, Guha AR, Karlakki S, Varghese J, Evans 96. Weinstein SL, Mubarak SJ, Wenger DR. Fundamental 1998 1963 GA. Combined femoral and Chiari osteotomies for concepts of developmental dysplasia of the hip. Instr 1999 1964 reconstruction of the painful subluxation or disloca- Course Lect. 2014;63:299–305. 2000 Author Queries Chapter No.: 5 0004302441

Queries Details Required Author’s Response AU1 Please check and confirm if the affiliations are presented correctly. AU2 As per reference style, name-date references have been changed to numbered references. Please check. AU3 Ref. “Ponseti 1978” has been changed to “Ponseti 1978a, b” to match with the reference list. Please check here and in subsequent occurrences. AU4 Part label (c) is present in the artwork but not mentioned in the caption of Fig. 5.7. Please check. AU5 Refs. “Coleman 1968; Tönnis 1976; Albinana et al. 1996; Smith et al. 1997” are cited in the text but not provided in the reference list. Please check and provide the bibliographic details in the list or delete the citations from the text. AU6 Ref. “Faciszewski et al. (1993)” has been changed to “Faciszewski et al. (1993a, b)” to match with the reference list. Please check here and in subsequent occurrences. AU7 We have relabeled Fig. 5.8. Kindly check and provide better quality figures if any. AU8 Please check the hierarchy of the section headings and confirm if correct. AU9 Part labels (c–f) are present in the artwork but not mentioned in the caption of Fig. 5.11. Please check. AU10 Part label (c) is present in the artwork but not mentioned in the caption of Fig. 5.17. Please check. AU11 Part label (b) is present in the artwork but not mentioned in the caption of Fig. 5.18. Please check. AU12 Reference “96” was not cited anywhere in the text. Please provide in text citation or delete the reference from the reference list.