Springer Nature Switzerland AG 2019 S Alshryda et al eds The P - PDF document

© Springer Nature Switzerland AG 2019 S. Alshryda et al. (eds.), The Pediatric and Adolescent Hip, https://doi.org/10.1007/978-3-030-12003-0_5 IntroductionAs rst proposed by Dr. William Harris in the early 1980s, it has become clear that osteoarthri-tis (OA) of the hip does not exist as a primary disease, or if it does, it is extraordinarily rare [1]. The extensive experience in total hip replacement surgeries over the last four decades have provided extensive insight into the pathological hip joint processes that lead to hip OA [2]. In particular, mechanical pathologies that cause damage to either the labrum or the chondrolabral junction are often the initiating processes which instigate acetabular and femoral head arthritis (Fig.5.1) include: dysplasia, impingement and avascular necrosis. The purpose of this chapter is to review the pathologic processes of acetabular and proxi-mal femoral development that lead to acetabular dysplasia in a located, or subluxated, hip. Emphasis will be placed upon understanding how the developmental milestones of the acetab J. G. Schoenecker (� ) Department of Orthopaedics, Vanderbilt University Medical Center, Nashville, TN, USAe-mail: jon.schoenecker@vumc.org I. Zaltz William Beaumont Hospital, Royal Oak, MI, USA J. Roth · P. L. Schoenecker Department of Orthopaedics, Washington University Medical Center, St. Louis, MO, USAe-mail: justin.s.roth@wustl.edu; pschoenecker@shrinenet.orgAU1 5 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 15° of femoral version and the tip of the greater trochanter at the level of the center of the femo-ral head. This normal hip development allows for joint congruency during physiologic activi-ties, with physiologic motion of 90° of exion, 15° of internal rotation at 90° of exion and a 90° arc of rotation with equal internal/external rotation (45°) in the prone position. Proper fem-oral neck offset and alignment of the greater and lesser trochanters assures both normal muscle tension and force vectors for hip rotation while avoiding extracapsular impingement on the pel-vis during physiologic joint motion. Adequate acetabular coverage, proper acetabular and proximal femoral version and 15° of external tibial torsion, results in a stable base to support the torso over the limb with a foot-forward gait during single leg stance.Hip dysplasia with a located, or subluxed, femoroacetabular joint is associated with inap-propriate development of either the acetabulum, proximal femur or both. Either alone or in combi-nations, the resulting pathomorphologies cause damage to the labrum/chondrolabral junction and articular cartilage, leading to premature degener-ation of the hip joint [4–8]. Acetabular under- coverage of the femoral head produces instability of the femoroacetabular joint. In addition to dam-aging intracapsular structures of the hip, intra-capsular/extracapsular impingement of the femur on the acetabulum or pelvis causes restricted motion and pain [10]. During ambulation, hip dysplasia may result in excessive stress on the labrum and/or chondrolabral junction (Fig.5.2), abnormal abductor muscle tension (with gait dis-turbance), and malalignment of the limb leading to distal joint patholo

gies. With these in mind, surgical approaches have been designed to pre-serve the hip joint, addressing the pathological mechanical problems presented by these pro-cesses. The goals of hip joint preservation sur-gery is to restore stable acetabular coverage of the femoral head and achieve a near normal range of motion, without femoral acetabular/pelvic impingement. Proximal femoral dysplasia may occur from primary developmental pathologies, such as proximal femoral focal deciency, coxa valga/vara or excessive version. It can also develop secondarily, from diseases such as Legg- Calve- Perthes disease, slipped capital femoral epiphysis or avascular necrosis. These conditions are presented in detail in other chapters. Acetabular dysplasia may occur primarily from failure of development or secondarily from improper loading by the proximal femur. The morphologic characteristics are dependent upon the stage of acetabular development at the time of insult.Acetabular development (Fig.5.3) is a dynamic process of endochondral ossication involving the cartilaginous anlage that includes two essential growth centers: the triradiate abcd Fig. 5.1 Prevailing theory of osteoarthritis of the hip. Mechanical pathology leads to labral pathology and hip osteoarthritis. (a) Radiographs of a mildly dysplastic hip in 34-year old female with right hip pain (white arrow rep-resents position of patient chondrolabral junction). (b, c) Years of improper loading of the hip results in tearing of the labrum or the chondrolabral junction (yellow arrow). (d) Progression of the tear, or increased pathologic load-ing leads to arthritis of the femoral head or the acetabulum (red arrow) 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86 87 88 89 90 91 92 93 94 95 96 97 98 99 100 101 102 103 104 105 106 107 108 109 110 111 112 113 114 115 116 117 cartilage and the acetabular epiphysis (os acetab-uli) [11–13]. During the rst 4 years of life the majority of acetabular development occurs via biomechanical molding, with sequential ossica-tion of the acetabular cartilaginous anlage and radial growth of the acetabulum (by the triradiate cartilage). The shape of the acetabular cartilagi-nous anlage is primarily inuenced through direct contact (articulation) with the femoral head. The femoral head must be stably reduced in the true acetabulum for optimal acetabular growth and development. The cartilaginous anlage is considerably plastic during the cartilaginous phase and becomes much less plastic later on, following vascular invasion and subsequent ossi-cation. The triradiate cartilage is responsible for growth of acetabular width, which must match the growth of the femoral epiphysis. In a normal hip, the majority of the cartilaginous anlage has ossied by 4years of age [12, 13]. After 4years of age, triradiate cartilage growth continues to widen the developing acetabulum to accommo-date a larger proximal femoral epiphysis [12, 13]. Triradiate cartilage growth is typically complete by 12years of age in girls and 14years of age in boys [12, 13]. Starting around age 4years, and continuing to skeletal maturity, an increase in acetabular depth occurs secondary to growth of the acetabular epiphysis. This growth is essential in provi

ding adequate coverage of a hip in response to the increased size of the femoral epiphysis [12, 13].Acetabular dysplasia can therefore be broken down to three categories: (1) improper shape and/or delay in ossication of the cartilaginous anlage, (2) damage to the triradiate cartilage, or (3) prob-lems of shape and/or delayed ossication of the acetabular epiphysis. Problems of shape and/or delay in ossication of the cartilaginous anlage occur early in life. As the cartilaginous anlage is considerably plastic, malformation most com-monly occurs as a result of eccentric loading of the proximal femur. This results in an altered hip cen-ter which is typically superiorly migrated, observed as a “break in Shelton’s line” on a weight bearing AP pelvis with femoral version neutral-ized (Fig.5.4). Severe subluxation may cause more signicant morphologic changes to the carti-laginous anlage and resemble a dislocated hip on radiographs. Additionally, inappropriate biome-chanical loading may also delay the vascular inva-sion and ossication of the cartilaginous anlage which is observed as an abnormal acetabular index (AI) (Fig.5.5). Although the cartilaginous anlage has a signicant capacity to remodel, it cannot do so without restoration of the appropriate hip cen-ter. Additionally, there is no evidence that once an anlage has undergone a morphologic change in the hip center (broken Shelton’s line) that it is capable of restoring its normal shape, and hip center, AU3 ab cd Fig. 5.2 Micro-instability of the dysplastic hip damages the chondrolabral junction. Hip dysplasia with a located, or subluxed, femoroacetabular joint refers to inappropri-ate development of either the acetabulum, proximal femur and or both. (a) Angle arrows represent insufcient lateral center edge angle (LCEA) of the ossifying acetabular epiphysis. (b) The resulting pathomorphologies leads to micro-instability of the femoroacetabular joint during daily activities. (c) This instability ultimately leads to damage of the (c) labrum/chondrolabral junction (red arrow) or even (d) fracture of the acetabular epiphysis (red arrow). Ultimately, this damage leads to premature degen-eration of the hip joint 118 119 120 121 122 123 124 125 126 127 128 129 130 131 132 133 134 135 136 137 138 139 140 141 142 143 144 145 146 147 148 149 150 151 152 153 154 155 156 157 158 159 160 161 162 163 164 165 166 167 168 169 170 171 172 173 174 175 176 177 abce d Fig. 5.3 The dynamic process of acetabular develop-ment. (a) Acetabular development is a dynamic process of endochondral ossication that occurs through the carti-laginous anlage that includes two essential growth cen-ters: the triradiate cartilage and the acetabular epiphysis (os acetabuli). (b) During the rst 4 years of life, the greater majority of acetabular development occurs through the biomechanical molding and sequential ossication of the acetabular cartilaginous anlage (big blue arrows) and the radial growth of the acetabulum by the triradiate carti-lage (small blue arrows). The triradiate cartilage is respon-sible for growth of acetabular width, which must match the growth of the femoral epiphysis. (c) After 4years of age, triradiate cartilage growth continues to widen the developing acetabulum to accommodate a larger proximal f

emoral epiphysis. Starting around the age of 4 and con-tinuing to skeletal maturity, an increase in acetabular depth occurs secondary to growth of the acetabular epiph-ysis. (d) Triradiate cartilage growth is typically complete by 12years of age in girls and 14years of age in boys, around which time the acetabular epiphysis initiates its ossication. (e) At skeletal maturity, the acetabular epiph-ysis is completely ossied and acetabular development is complete abcdef Fig. 5.4 Deformation of the cartilaginous anlage. Problems of shape and/or delay in ossication of the carti-laginous anlage occur early in life. As the cartilaginous anlage is considerably plastic, malformation most com-monly occurs from eccentric loading of the proximal femur. In this case an 8-month old female (a) with a dislocated hip observed by (b) radiographs with an ossication center in the superior lateral quadrant dened by Hilgenreiner’s line (white dashed line) and Perkin’s line (yellow dashed line). (c) The patient undergoes successful closed reduction with (d) restoration of the ossication center to the inferior medial quadrant of Hilgenreiner’s and Perkin’s line. At this point, although delayed in its ossication, the cartilaginous anlage observed in (c) is sufcient to maintain hip congru-ity. (e) As the child grows, if the acetabular anlage fails to ossify and deform, the hip will migrate superior lateral without dislocation. (f) This migration is observed on a standing radiograph with migration of the ossication cen-ter back towards the superior lateral quadrant formed by Hilgenreiner and Perkin’s lines, a break in Shenton’s line and increased acetabular index (AI) as compared to the contralateral side. Together, these pathologic changes in the anlage results in an altered hip center, which has not been demonstrated to spontaneously recover without surgical intervention. Delay in ossication of the acetabular cartilaginous anlage, observed as a delay in acetabular index normalization, may also occur in idiopathic cases without morpho-logic change in the anlage. Additionally, if left uncorrected, the acetabular anlage shape and the resultant position of the acetabular epiphysis and labrum, may result in an intra-articular deformity with dual hip centers that present few reconstruc-tive possibilities other than salvage procedures (Fig.5.6). Conditions affecting triradiate cartilage growth are typically caused by trauma, infection, cancer or iatrogenic (secondary to surgery) [15]. Abnormal triradiate cartilage growth often results a bc Fig. 5.5 Acetabular index. The acetabular index (a) mea-sures the ossication of the cartilaginous anlage. The nor-mal values per age are presented in Table5.1. In a normally forming hip (left hip and c), the ossication of the anlage results in an index of 20° by the age of 3. This maintains the hip center in the appropriate position (yel-low arrow c). With pathologic development (right hip and b) the anlage may deform leading to a delay in ossication and migration of the hip center laterally (yellow arrow b) abc Fig. 5.6 Severe deformation of the cartilaginous anlage in untreated dysplasia. Although the cartilaginous anlage has a signicant capacity to remodel, it cannot do so with-out restoration o

f the appropriate hip center. Severe defor-mity of an untreated subluxed, but not dislocated, hip often leads to permanent deformity of the vital developing structures of the hip. Radiographs (a), MRI (b) and draw-ing (c) of a 10-year-old boy demonstrates a subluxed hip with lateral migration and break in Shenton’s line. This migration places the labrum (yellow arrow) cartilaginous epiphysis at the junction with the labrum (red arrow) in a biomechanically unfavorable position to function. Additionally, the pathologic forces deform and delay the ossication of the cartilaginous anlage (blue arrow) 178 179 180 181 182 183 184 185 186 187 188 189 190 191 in the development of a severe pincer type acetab-ulum. Fortunately, likely secondary to the robust blood supply of the pelvis, premature triradiate cartilage arrest is rare. There are few reports of successfully restoring the normal development of a failed triradiate growth center. Problems of shape or delayed ossication of the acetabular epiphysis occur closer to skeletal maturity. They typically present radiographically as an insufcient anterior or lateral center edge angle radiographically or by MRI.Failure of both cartilaginous growth and ossication of the anterior and lateral acetabular epiphysis accounts for the majority of late-pre-senting acetabular dysplasia (Fig.5.7). Primary acetabular dysplasia occurs typically in females, the etiology is unknown.The main principle in the treatment of acetab-ular dysplasia involves maintaining hip joint reduction to provide an optimum environment for acetabular and femoral head development. Intervention should be considered to alter an adverse natural history of pathologic acetabular cartilaginous anlage, triradiate cartilage and ace-tabular epiphysis. abc Fig. 5.7 Late pathology of the acetabular epiphysis: Problems of development, shape or delay of ossication of the acetabular epiphysis occur close to skeletal matu-rity. They typically present radiographically as an insuf-cient anterior or lateral center edge angle (a) radiographically or (b) by MRI. Failure of both cartilagi-nous growth (red arrow) and ossication (blue arrow) of the anterior and lateral acetabular epiphysis accounts for the majority of late-presenting acetabular dysplasia. These developmental conditions lead to improper loading of the labrum (yellow arrow) and chondrolabral junctionAU4 Acetabular dysplasia can occur from either: (1) improper shape and/or delay in ossica-tion of the cartilaginous anlage, (2) damage to the triradiate cartilage, or (3) problems of shape and/or delayed ossication of the acetabular epiphysis. Essential Pathophysiology Leading to Early Hip Degeneration• Primary Dysplasia (conferred by devel-opmental pathology): –Acetabular dysplasia (e.g. failure of ossication of the acetabular carti-laginous anlage or epiphysis) –Proximal femoral dysplasia (e.g. congenital femoral deciency, coxa vara/valga, excessive femoral ante/retro-version)• Secondary Dysplasia (conferred by other diseases): –Perthes disease (or other avascular necrosis) with resulting coxa magna, 192 193 194 195 196 197 198 199 200 201 202 203 204 205 206 207 208 209 210 211 212 213 214 215 Natural HistoryThe lack of femoral head coverage exists along a spectrum; from under-cover

age leading to improper joint loading and subluxation to over- coverage resulting in femoroacetabular impinge-ment (FAI) [16–18]. Both morphologies predispose the hip to damage of the labrum/chon-drolabral junction and articular cartilage; potenti-ating the premature development of OA [10, 16, 18–22]. Nevertheless, the factors which predis-pose certain hips to eventual degenerative change remain uncertain [23, 24]. Early in life, the fate of a congenital hip dislocation has been well docu-mented. However, the natural history of acetabu-lar dysplasia in the pediatric and young adult patient remains largely undescribed; with the exception of a few studies that have formed the basis of surgical indications for hip preservation [18, 24–28]. Understanding how acetabular mor-phological characteristics affect the rate of degenerative change in the hip has substantial implications for prognostic assessment and joint preservation patient selection at all ages [29]. The natural history of acetabular dysplasia with sub-luxation is clear; degenerative joint disease will develop in all patients, usually in the third to fourth decade of life [25, 27, 28]. Additionally, as LCEA decreases, subluxation increases [25]. The natural history of untreated adults with dysplasia is more difcult to predict because patients com-pensate well and present with dysplasia only as an incidental nding on radiographs or if they have symptoms. However, there is good evidence that dysplasia alone, particularly in females, leads to degenerative joint disease in adults [1, 25, 27, 28]. The question of when hip dysplasia patients will become symptomatic in the absence of treatment was evaluated by Hartolakidis etal. In their series of 202 dysplastic hips, the average age for onset of symptoms was 34.5years. In patients with a low and high dislocation, pain from degenerative arthritis asso-ciated with a false acetabulum started at an aver-age of 32.5 and 31.2years, respectively. If there was no false acetabulum, pain onset did not occur until 46.4years, and was mostly secondary to muscle fatigue [30].The natural history of hip dysplasia and sub-luxation in untreated adults can be extrapolated to residual dysplasia and subluxation after treat-ment in the pediatric patient [1, 27, 28]. In a study of 152 pediatric hips treated with closed reduc-tion and followed for 31years, the authors reported that dysplastic hips often went on to subluxation and the development of degenerative joint disease [27]. The cause of degenerative changes in dysplastic hips is probably mechani-cal in nature and related to increased contact stress, especially to the labrum/chondrolabral junction, leading to damages articular cartilage over time. There is a clear association between excessive contact stress and late degenerative joint diseases for other abnormal anatomical morphologies, such as genu varum and genu val-gum. This same association seems to occur in dysplastic hips with relation to the development of degenerative joint disease at long-term follow- up [31, 32].Untreated severe dysplasia of the hip fre-quently leads to osteoarthrosis [14, 25, 31, 33, 34]. While there is no debate that severe dyspla-sia of the hip should be treated operatively, objec-tive criteria on which to base the treatment of mild and

moderate dysplasia was not available until the mid-1990s and continues to be rened as we learn more about the natural history. Therefore, operative treatment for residual dys-plasia of the hip after skeletal maturity assumes that the dysplasia, if left untreated, will lead to secondary osteoarthrosis of the hip [14, 16, with late symptomatic impingement and acetabular dysplasia (variable) –Slipped capital femoral epiphysis (SCFE) associated with metaphyseal CAM deformity and femoroacetabu-lar impingement –Neuromuscular acetabular dysplasia and coxa valga occurring secondary to spasticity, muscle imbalance, etc. (e.g. cerebral palsy; Charcot-Marie tooth peripheral neuropathy). 216 217 218 219 220 221 222 223 224 225 226 227 228 229 230 231 232 233 234 235 236 237 238 239 240 241 242 243 244 245 246 247 248 249 250 251 252 253 254 255 256 257 258 259 260 261 262 263 264 265 266 267 268 269 270 271 272 273 274 275 276 277 278 279 280 281 282 283 284 285 286 287 288 289 290 291 292 293 294 295 35–41]. Without long-term studies with matched pairs and clearly dened parameters of dysplasia, the natural history of what is now often consid-ered an operative indication may never be real-ized. In an attempt to provide objective parameters to follow the natural history of acetabular dyspla-sia, Murphy and colleagues rst dened the dys-plastic acetabulum using CT to assess the morphological differences between two matched cohorts of females with mean age 20years [42]. In their study, the rst cohort all went on to pelvic osteotomies for symptomatic dysplasia and the control group was obtained from patients who had CT scans obtained for alternate pelvic pathol-ogies. Comparing the cohorts, acetabular ante-version was consistent (mean, 20°) and abduction was moderately increased in the dysplastic group (mean 62° vs. 53° in controls). The most signi-cant difference was in the mean lateral center edge angle with the normal hips measuring 31° and the dysplastic hips measuring 6°. This reduc-tion in femoral head lateral coverage was shown to be part of a more global acetabular deciency in the dysplastic hip. The normal acetabular vol-ume equated to a hemisphere while the dysplastic only measured one third of a sphere.Operative treatment for residual dysplasia of the hip after skeletal maturity assumes that the dysplasia, if left untreated, will lead to second-ary osteoarthrosis of the hip.From these objective determinates, Murphy etal. [43] then published the rst signicant nat-ural history study of the skeletally mature dys-plastic hip. This study retrospectively evaluated 286 young patients with previous unilateral THA for dysplasia and focused on the contralateral non-operated hip. Ultimately, 115 of the patients developed severe OA in the contralateral hip by 65years of age. These patients also had statisti-cally greater derangement of all measured radio-graphic features of dysplasia; including lateral center edge angle (LCEA), acetabular index of depth to width (D/W), vertical distance, lateral distance, peak-to-edge distance, femoral extru-sion distance and acetabular index (AI). Key ndings were that no patient in whom the hip functioned well until age 65 had a LCEA D/W 8%,;&#x 54.;耀AI 15°, femoral head uncovering 8%,;&#x 54.;耀31

% or a peak-to-edge distance of 0mm. While they clearly showed that for patients, whom have a hip replacement for dysplasia in one hip, severe OA will inevitably develop in the contralateral hip if the aforementioned acetabular criteria are not met. However, this investigation lacked a true non-operated control group but did have a com-parison group (171pts) without progression of OA over the same timeframe. Unfortunately, a major limitation to the study was that a substan-tial portion of the patients that progressed to OA had evidence of mild OA at the time of inclusion thus the outcomes are to some degree measure-ments of secondary OA progression [43].Further confounding our understanding of the natural history of acetabular dysplasia, patients often have additional pathologies. For example, many patients have combined acetabular dyspla-sia with FAI.It is not clear to what extent FAI impacts hip dysplasia and the development of OA.Bardakos etal. showed that mild to moder-ate OA in hips with a pistol-grip CAM deformity does not progress rapidly in all patients, with one-third of their patients taking at least 10 years to manifest signs of OA with some never showing radiologic signs [24]. Further analysis found two important variables associated with those that did progress; the height of the trochanter relative to the center of the femoral head and the presence of acetabular retroversion. Their conclusion was that a hip with cam impingement is not always destined for end-stage arthritic degeneration [24]. Other studies have found even larger percentages of asymptomatic patients with cam deformity that do not progress to OA.In the study by Hartolakidis etal., 82.3% of asymptomatic hips with a CAM deformity remained free of OA for a mean of 18.5years [26]. Clearly the role of FAI in the natural history of hip dysplasia requires more study to determine which hips are at higher risk of progression.Recently, Wyles etal. published the most comprehensive study of the natural history of OA in patients with hip dysplasia [18]. Similar to Murphy etal., they retrospectively studied 172 young patients (mean, 47years-old) that had undergone unilateral total hip arthroplasty (THA). While the Murphy etal. study contained 296 297 298 299 300 301 302 303 304 305 306 307 308 309 310 311 312 313 314 315 316 317 318 319 320 321 322 323 324 325 326 327 328 329 330 331 332 333 334 335 336 337 338 339 340 341 342 343 344 345 346 347 348 349 350 351 352 353 354 355 356 357 358 359 360 361 362 363 364 365 366 367 368 369 370 371 372 373 374 375 376 377 378 379 380 381 382 383 384 385 386 387 388 389 390 391 patients with advanced Tönnis grades, all patients in the Wyles etal. study had a Tönnis grade 0 grade for the contralateral hip. These hips were given a structural diagnosis of acetab-ular dysplasia (48 patients), FAI (74 patients) and normal (40 patients) and were evaluated for OA progression. At a mean follow-up of 20years, 35 patients underwent contralateral THA; 16 (33%) with acetabular dysplasia, 13 (18%) with FAI and 6 (15%) patients with nor-mal morphology. They showed degenerative changes progressed more rapidly in the acetabu-lar dysplasia group with an increased probability of undergoing a THA at 10- and 20-year follow-up com

pared to the FAI and normal morphology cohorts. FAI was similar to structurally normal hips in terms of progression to THA but patient with a CAM deformity and concomitant acetab-ular dysplasia developed OA more rapidly. From their data they created 10- and 20-year prognos-tic tables predictive of osteoarthritic progression (by Tönnis grade) based on the structural diag-nosis and initial Tönnis grade. Furthermore, based on their continuous multistate Markov models, they proposed the following new thresh-olds for an increased risk for OA progression and thus an indication for hip preservation sur-�gery: femoral head lateralization 8mm, femo-ral head extrusion inde�x 0.20, acetabular depth to width index Tönnis %° ; nd ;.7;angle 8°. A major limitation of this study is that all patients underwent an index THA and thus the ndings cannot be directly correlated to highly active patients. EpidemiologyAcetabular dysplasia is one of the most common causes of pre-arthritic hip pain, hip dysfunction, and secondary OA [1, 2, 4, 44]. The infantile form of acetabular dysplasia is considered a multifacto-rial disease with genetic, ethnic and environmen-tal risk factors [45, 46]. The intrauterine environmental associations include decreased uterine size with rst-born children and breech presentation, both of which restrict fetal leg mobility. The incidence of breech birth is 2–4% in the general population but 17–23% among patients with infantile hip dysplasia [45, 47]. The left hip is more commonly affected because of its fetal position adducted against the sacrum [48]. Although no genetic locus has been identied, a hereditary component of developmental dysplasia of the hip (DDH) is strongly supported on the basis of increased risk in patients with a positive family history and varying rates by ethnicity. Extremely low rates of DDH are seen in the African populations [49, 50] with the African Bantu having an incidence of essentially zero [51]. Much higher rates have been reported in Native Americans [52] and the Sami in Norway [53]. DDH is much more common in females but the exact cause is uncertain; one theory being increased joint laxity during the neonatal period secondary to increased female sensitivity to the maternal hormone relaxin [11, 54]. Another is that females are twice as likely as males to be born breech [9, 54].The prevalence of asymptomatic dysplasia in the general population varies with ethnicity. Caucasians have a 3–4% prevalence of hip dys-plasia, with females having a higher prevalence than males [55–60]. Inoue etal. showed the prev-alence in men and women respectively to be 5.1% and 11.6% for the Japanese and 1.7% and 5.6% for the French [56]. Another study by Lau etal. found the prevalence of dysplasia (CEA25°) to be similar between Chinese and British men at 4.5% and 3.6% respectively, how-ever the same cohort showed a 50% reduction in OA prevalence in the Chinese group (5.4% vs. 11.0%) [58]. It was not clear why the Chinese Acetabular dysplasia can be classied into mild, moderate and severe forms using several well-established measure-ments. However, its diagnosis and natu-ral history are complicated by the effects of acetabular and proximal femoral ver-sion as well as FAI.While the progres-sion to OA in s

evere dysplasia is clear, surgical indications in mild and moder-ate forms continue to be rened. 392 393 394 395 396 397 398 399 400 401 402 403 404 405 406 407 408 409 410 411 412 413 414 415 416 417 418 419 420 421 422 423 424 425 426 427 428 429 430 431 432 433 434 435 436 437 438 439 440 441 442 443 444 445 446 447 448 449 450 451 452 453 454 455 456 457 458 459 460 461 462 463 464 465 466 467 468 469 470 471 group did not progress to radiographic OA at the same rate. A recent study by Engesaeter etal. looked at 2081 Norwegians (mean age, 19years) and found the prevalence of a Wiberg center- edge- angle (CEA) less than 20° to be 3.3% (4.3% in women and 2.4% in men) [61]. If the Wiberg CEA threshold was increased to less than 25°, 20% (23% in women and 16% in men) of the cohort had hip dysplasia [61]. This further con-rmed the higher prevalence of hip dysplasia in Norway and agreed with previous Nordic Arthroplasty Registry ndings [62, 63]. Although the percentage of patients with dysplasia who will ultimately progress to end-stage OA is unknown, it has been documented that 25–50% of primary hip OA is due to acetabular dysplasia [30, 34, 64].Despite the plethora of studies investigating risk factors for infantile hip dysplasia, there is a scarcity of literature describing patient demo-graphics and disease epidemiology for adoles-cent and adult patients, with most data coming from single surgeon series reporting on symp-tomatic acetabular dysplasia [16, 65–68]. In a series of 337 patients undergoing total hip arthro-plasty, Clohisy etal. found that 48% less than age 50 had acetabular dysplasia as the predisposing factor for their OA [69]. A recent large multi- center study by Sankar etal. looked at disease epidemiology and patient demographics in dys-plastic patients treated with a periacetabular oste-otomy (PAO) in 950 consecutive patients [44]. They demonstrated that symptomatic acetabular dysplasia starts 1–3years before surgical inter-vention and occurs predominantly in young (average 25.3years), female, Caucasian patients with a normal BMI (average 24.6). These nd-ings are consistent with other reports in the litera-ture [70–73]. The same study found baseline functional scores to be mean modied Harris Hip Score (mHHS) of 61.8 and a mean UCLA activ-ity score of 6.6. The mean mHHS is slightly lower than published elsewhere (61.8 vs. 66–70) [71, 74] but the mean UCLA activity score is comparable with other authors [75].Lee etal. further evaluated the differences in symptomatic hip dysplasia treated with PAO based on when the diagnosis was rst obtained: infancy, adolescence or adulthood [54]. They found demographic differences between patients diagnosed with hip dysplasia in infancy versus adolescence/adulthood. There were more females with left hip involvement and breech presentation in the infant/DDH population while bilateral dis-ease (61% vs. 45%) was more common in the adolescent population. The same study also looked and f�amily history and found that 50% of all respondents had a family history of hip dis-ease with �40% being rst order relatives. rst order relatives of adolescent/adult diagnosed patients had a twofold increase in incidence of hip replacement by age 65 compared to infant/DDH &#

31;rst order relatives (50% vs. 22%). However, rst order family members of infant/DDH patients were four times more likely to have DDH themselves (59% vs. 16%).“Rates of acetabular dysplasia vary widely by gender and cultural origin with several well accepted patient characteristics being predictive of increased risk during infancy. Once a dysplastic hip is present, whether that hip will become symptomatic is directly related to the necessity of treat-ment. Severity of dislocation and family history along with cultural origin again inuence that symptomatology. The peri-acetabular osteotomy is commonly employed for younger ()-atic patients while a total hip replacement is indicated for older patients @yo;&#x sym;&#xptom;(40yo) with Tönnis 2 changes or greater”. Clinical PresentationYoung children with hip dysplasia with or with-out subluxation typically do not present with any complaints of hip pain or any apparent functional limitations. More likely, children in the rst 6–8years of life will have relatively normal hip function despite radiographic evidence of notable hip dysplasia. However, with growth and increased body mass during and post puberty, older children and adolescents with acetabular 472 473 474 475 476 477 478 479 480 481 482 483 484 485 486 487 488 489 490 491 492 493 494 495 496 497 498 499 500 501 502 503 504 505 506 507 508 509 510 511 512 513 514 515 516 517 518 519 520 521 522 523 524 525 526 527 528 529 530 531 532 533 534 535 536 537 538 539 540 541 542 543 544 545 546 547 548 549 550 551 552 553 554 555 556 557 558 559 560 561 562 deciency will variably become symptomatic, particularly in the presence of hip joint sublux-ation. Signs include functional hip joint associ-ated fatigue and often a subtle, though progressive, gluteus medius weakness limp (Trendelenburg). This early onset weight bearing pain typically is located laterally (trochanteric) and occurs sec-ondary to chronic gluteus medius fatigue. Later, anterolateral groin pain secondary to chondro-labral strain and or injury variably develops. In these relatively older patients, groin pain is characteristically described as an anterior hip centered discomfort often with catching or snap-ping. Groin pain typically occurs with hip motion such as in pivoting, twisting, running, when aris-ing from a sitting position, and on initiating walking.On physical examination, the gait of most of the younger children will appear to be normal. On careful observation of older children and or adolescents, there may be an abductor limp and/or a positive Trendelenburg sign on single leg stance examination. The hip abductors may be weak on resistance testing. Passive hip range of motion is initially normal and often increased in all planes, secondary to both relative joint laxity and a variably decient anterolateral acetabulum. Later as the hip disease progresses, range of motion can become restricted, associated with the onset of painful impingement at the acetabu-lar chondrolabral junction. ImagingHip joint dysplasia in the child occurs secondary to abnormal growth of either the acetabulum, femoral head, or both, in a non-dislocated hip joint. The shape of the acetabular anlage and its functional capacity to support weight bearing is evaluated with a standing anterior posterior (AP) radiograph

. Typically the acetabular development will be decient anterolaterally. In addition, the absence (or presence) of hip joint subluxation (i.e. Shenton’s line intact or not) is assessed. The contour of the anterior and posterior edges of the proximal femurs are visualized on the supine frog lateral radiographs. In older children and adolescents, further visualization of the anterior acetabulum can be seen with the standing false prole lateral radiograph [4]. Persistent hip sub-luxation after the age of 6 years portends a guarded prognosis for maximal acetabular devel-opment for any given hip dysplasia [9]. If sublux-ation is noted on the standing AP pelvic radiograph, a functional view (AP with hip abducted and internally rotated) is obtained to assess if the femoral head positionally reduces back into the true acetabulum. Knowing that positional reduction of femoral head subluxation is possible, is very helpful in the preoperative planning of joint reconstruction surgery.Normative values for acetabular index (AI) (Coleman 1968; Tönnis 1976), lateral center angle (LCEA) [4, 34], Tonnis sourcil angle [4, 14] are helpful in decision-making and are summarized in Tables 5.1 and 5.2. We also assess the anterior CEA [4, 14] in our older patients. The acetabular tear drop morphology can be useful in assessing acetabular development in late infancy/early AU5 Essential Imaging• Plain radiographs: For measurement of AI, LCEA, Tonnis sourcil angle, tear-drop morphology, and femoral deformity• MRI: Used on occasion to assess devel-opment of the cartilaginous acetabulum and/or version• MRI arthrogram (MRA): For assess-ment of chondrolabral integrity in adolescents• CT: For either assessment of version (femoral and acetabular) or for concom-itant FAITable 5.1 Suggested acetabular index (AI) guideline values [14] AgeAcetabular index136 563 564 565 566 567 568 569 570 571 572 573 574 575 576 577 578 579 580 581 582 583 584 585 586 587 588 589 590 591 592 593 594 595 596 597 598 599 600 601 602 603 604 605 606 607 608 609 610 611 612 613 614 615 616 617 618 619 620 621 622 623 624 625 626 627 628 629 t1.1 t1.2 t1.3 t1.4 t1.5 t1.6 childhood (Albinana etal. 1996; Smith etal. 1997). Similarly, Shenton’s line, intact or not, is very important in decision making, with chronic subluxation always being a concern for a guarded prognosis [9]. Non-operative Management Childhood (4–10Years Old)If sufcient femoral head coverage is present and the child is asymptomatic, one may observe until there is evidence of failure to improve radio-graphically or until pain develops (Chap. 4, Developmental Dysplasia of the Hip in Young Children). Deferring operative treatment after age 6years (with or without symptoms) is not indicated if hip is subluxated and/or there is per-sistent acetabular dysplasia in girls 8years or boys 9years. Older Child (11Years/Adolescent)Observe if asymptomatic, but it is essential to fol-low at least annually. Prognosis relatively guarded in proportion to degree of subluxation and/or acetabular dysplasia. Operative Management Essential Surgical Techniques inChildhood (4–10Years Old)Direct surgical correction of acetabular dysplasia can be broken into three different types: (1) ace-tabuloplasty, (2) redirectional osteotomies, and

(3) salvage procedures (Fig.5.8). The decision as to which procedure is most appropriate in attempting to achieve correction of a specic acetabular dysplasia is dictated by the principal deciency of development (acetabular anlage, tri-radiate cartilage or acetabular epiphysis), the age of the patient, and whether the hip is completely reduced. Currently, the incomplete acetabulo-plasties [76–80] have become the most popular surgical approach in the correction of residual dysplasia in the skeletal immature pelvis () AcetabuloplastyPathologic shape or delay of the acetabular car-tilaginous anlage is often characterized by an acetabulum with a relatively larger arc of curva-ture then of the femoral epiphysis (Fig.5.4). The intent of the acetabuloplasty is to correct the pathological increased slope of the superior anterolateral acetabulum (Fig.5.9). Correcting the acetabular insufciency (abnormal shape) without damaging the triradiate cartilage redi-rects the hip center to its natural location, reduc-ing femoral head subluxation. These acetabular osteotomies compress the cartilaginous anlage AU6 AU8 Table 5.2 Lateral center-edge angle (LCEA) guideline values at skeletal maturity LCEANormal30Minimum25Poor prognosis Non-operative Pitfalls• Inappropriate continued observation in childhood despite subluxation and or lack of progressive improvement in ace-tabular development (AI) and femoral head coverage (LCEA)• Loss of opportunity in younger patients (years of age) of correcting dysplasia with simpler procedures (acetabuloplasty and/or Salter innomi-nate osteotomy)• Failure to continue essential radio-graphic and clinical monitoring for min-imally or asymptomatic adolescents/young adults with hips at risk (acetabu-lar dysplasia and subluxation) 630 631 632 633 634 635 636 637 638 639 640 641 642 643 644 645 646 647 648 649 650 651 652 653 654 655 656 657 658 659 660 661 662 663 664 665 666 667 668 669 670 671 672 673 674 675 676 677 678 679 680 681 682 t2.1 t2.2 t2.3 t2.4 t2.5 t2.6 which restores endochondral ossication pro-viding needed support for functional loading (Fig.5.10). Acetabuloplasty is best indicated in conditions with remaining acetabular cartilagi-nous anlage, a relatively capacious acetabulum and or subluxation. Alternatively, satisfactory correction can be achieved with a single innomi-nate (Salter) osteotomy. If the femoral head is relatively large, the Salter redirectional osteot-omy can be the preferred technique in attempt-ing to correct acetabular dysplasia in a younger child. Following surgical correction of acetabu-lar dysplasia, an intraoperative arthrogram can be very helpful in assessing femoral head cover-age achieved, both laterally and anteriorly (Fig.5.11).“Success is often judged by a radio-graphically noting a reduction of the acetabular index, a medialized hip cen-ter, (from abnormally lateral to more normally medial), and a restored Shenton’s line. It is important to be aware of the extent of the acetabular car-tilaginous anlage when performing an acetabuloplasty in the correction of ace-tabular dysplasia. Over correction is very possible which can potentiate late occur-ring femoral acetabular impingement”. Surgical Technique: Pemberton Acetabuloplasty (Figs.5.9–5.11)With the patient positi

oned supine on the operat-ing room table, a small circular roll is placed behind the buttock in back of the affected extrem-ity. The approach to the hip and pelvis is made through a skin excision located lateral to and par-alleling the iliac crest extending a couple of cen-timeters distal to the anterior superior iliac spine. Using the electrocautery, subcutaneous aps are raised both medially and laterally to the super-cial fascia. The fascia overlying the tensor fascia lata muscle is incised longitudinally and dissec-tion directed medially over the tensor and under the sartorius, which protects the lateral femoral cutaneous nerve lying just under the sartorius fas-cia. Dissection is continued bluntly until the lat-eral aspect of the rectus femoris tendon and muscle are identied. The external oblique mus- Acetabuloplasty abc RedirectionalSalvage Fig. 5.8 Types of acetabular corrective surgeries: Direct surgical correction of acetabular dysplasia can be broken into three different types: (a) acetabuloplasty, such as the Pemberton osteotomy shown here (b) redirectional oste-otomies, such as the periacetabular osteotomy (PAO) shown here and (c) salvage procedures, such as the ace-tabular shelf procedure shown hereAU7 683 684 685 686 687 688 689 690 691 692 693 694 695 696 697 698 699 700 701 702 703 704 705 706 707 708 709 710 711 712 713 714 715 716 717 718 719 720 721 722 723 724 725 726 727 728 729 cle is reected of the iliac apophysis from lateral to medial, exposing the apophyseal cartilage which is sharply divided in half from anterior to posterior so as to achieve exposure of the ilium.The lateral ilium is subperiosteally exposed to the palpable edge of the acetabulum then posteri-orly down to the lateral entrance of the sciatic notch (which can be probed with blunt dissecting instrument). The lateral iliac cut is made rst. The course of the osteotomy begins anteriorly, mid distance between the anterior superior iliac spine (ASIS) and the anterior inferior iliac spine (AIIS), and extends in a posterior direction. The anterior and lateral line of the cut should be made at least 1½cm proximal to the edge of the acetab-ulum. The cut is initiated with a straight narrow osteotome extending in a posterior direction then with a narrow curved osteotome around the ace-tabulum toward the triradiate cartilage. The C-arm is brought in across from the surgeon and the hip joint and posterior column are visualized with 45° iliac oblique view. As monitored with the C-arm, the course and extent of the curved osteotomy can be precisely located one half way between the acetabulum and the medial edge of the posterior column. abcd Fig. 5.9 Acetabuloplasty: (a) Pathologic shape or 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 insufciency 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 arr

ow). (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) 730 731 732 733 734 735 736 737 738 739 740 741 742 743 744 745 746 747 748 749 750 751 752 753 754 755 abcdef Fig. 5.10 Restoration of hip development after an acetabu-loplasty: (a, b) Patient from Fig.5.4 with pathologic carti-laginous anlage (black arrow on drawing and yellow arrow on radiographs). (c, d) A Pemberton type osteotomy restores Shenton’s line and the proper position of the chondrolabral junction, however, note that initially the cartilaginous anlage still appears under-ossied (yellow arrow) as indicated by an increased acetabular anlage at age 2. (e, f) Four years later, at age 6, the anlage has ossied and the hip position has been maintained without iatrogenic over-coverage of the hip badcfe Fig. 5.11 Measuring correction during an acetabulo-plasty: (a) Correction of acetabular anlage under-coverage is often monitored by an arthrogram in order to visualize restoration of proper position of the chondrolabral junc-tion (black arrow and “thorn”). (b) The gap between the iliac fragments is lled with an allograft (white arrow) and typically inherently stable after graft insertionAU9 The medial ilium is subperiosteally exposed to and beyond the brim of the pelvis; incising the periosteum facilitates this exposure. A small straight osteotome is then directed through the lateral cut in a medial direction and is visualized cutting through the most anterior 2–3cm of the medial wall of the ilium. A transverse cut potenti-ates anterior coverage and a more oblique cut (medial cut made more distal than lateral) greater lateral coverage. The medial cut is continued with a curved osteotome, extending over the pel-vic brim, towards but not through the triradiate cartilage, monitored with the C-arm [15]. At this point the osteotomy will be near complete.“As the two fragments are separated with a laminar spreader, displacement of the typical oblique cut (from proximal lateral to distal medial) of the acetabular frag-ment allows for marked improvement in lateral and anterior femoral head coverage”.Improved femoral head coverage is moni-tored by the C-arm using both an AP and false prole lateral views. In the younger child, femo-ral head coverage is provided by both the bony acetabulum and by the cartilage anlage. An arthrogram can be very helpful showing the true extent of combined bone and cartilage head cov-erage (Fig.5.11). Correction achieved should be correlated with range of motion and adjusted to assure there is 90–95° of passive hip exion fol-lowing turning down the acetabular fragment. The gap between the fragments is lled with a structural allograft which is typically inherently stable after graft impaction. Optionally, if needed to assure graft stability, a small K-wire may be used in smaller children and/or a 3.5mm cortical screw in older children, inserted in an antegrade direction starting in the proximal iliac crest and directed across the osteotomy (through the bone graft) and into the ilium medially, just short of the roof of the acetabulum. Bilateral Pemberton osteotomies can be performed if needed. In patients with either excessive femoral antever-sion and or

coxa valga deformity, a proximal redirectional femoral osteotomy can be concom-itantly performed. The anteriorly prominent spike of bone on the acetabulum fragment is subperiosteally exposed and resected. The apophyseal cartilage is securely repaired with interrupted #1 absorbable sutures, the tensor-sartorius facia reapproximated and the external oblique muscle reattached just lateral to the apophyseal cartilage with running #1 absorb-able sutures. The subcutaneous and skin tissues are closed with absorbable sutures. To protect the osteotomy in children less than 4years of age, a one and half spica cast is placed. In older patients, an abduction pillow is used for 6 weeks. Typically, healing of the osteotomy is sufcient to allow weight bearing as tolerated at 6–8weeks post operatively. Pelvic Redirectional OsteotomiesA pelvic redirectional osteotomy can be single innominate (childhood) or triple pelvic (adoles-cents/young adults) both being effective in cor-recting pathological acetabular insufciency. Salter [39] pioneered operative pelvic redirec-tional osteotomy correction of congenital acetab-ular deciency [39, 81]. The single horizontal osteotomy through the ilium allows for a consid-erable anterolateral acetabular redirection around the relatively exible pubic symphysis.“In years past, the Salter osteotomy was the procedure of choice in younger chil-dren. It is now used less frequently given the current popularity of acetabuloplas-ties. However, the Salter osteotomy is still the preferred surgical approach in the correction of residual acetabular dyspla-sia in the very young child (yrs of age) in which there is relatively little sublux-ation and an arc of curvature of the ace-tabulum that is quite similar to the corresponding arc of curvature of the femoral head”. Surgical Technique: Single Innominate (Salter) Pelvic OsteotomyThe patient positioning and initial exposure to the ilium is as described above for performing the Pemberton acetabuloplasty. Following division 756 757 758 759 760 761 762 763 764 765 766 767 768 769 770 771 772 773 774 775 776 777 778 779 780 781 782 783 784 785 786 787 788 789 790 791 792 793 794 795 796 797 798 799 800 801 802 803 804 805 806 807 808 809 810 811 812 813 814 815 816 817 818 819 820 821 822 823 824 825 826 827 828 829 830 831 832 833 834 835 836 837 838 839 840 841 842 843 844 845 846 of the iliac apophysis, both tables of the ilium are dissected subperiosteally until the sciatic notch is encountered, both medially and laterally. Care is taken to avoid penetrating the periosteum as the sciatic notch is dissected subperiosteally. A small curved clamp, such as a Satinsky, is used to pass a # 1 Vicryl suture through the sciatic notch which is then tied to a Gigli saw, so that the saw then carefully passed through the sciatic notch. Crego or similar retractors are inserted into the sciatic notch medially and laterally in order to protect the adjacent soft tissues. An oscillating saw is used to cut the ilium beginning just distal to the ASIS and directed towards the sciatic notch, terminating about 1cm anterior to it. The Gigli saw is then used to complete the iliac oste-otomy so that an angle is created between the posteriorly directed saw cut and the anteriorly directed Gigli cut. Creating such an angle wil

l assist in stabilizing the rotated acetabular frag-ment against the ilium. The ischiopubic fragment is grasped with a pointed bone forceps just ante-rior to the sciatic notch osteotomy which effec-tively helps rotate the acetabulum anteriorly in order to improve anterior and lateral coverage of the femoral epiphysis. The prominent anterior extension of the acetabular fragment is osteoto-mized (which will be a tricortical bone graft wedge) to be impacted into the gap between the ilium and the acetabular fragment. The osteot-omy is transxed with two threaded Kirschner wires inserted antegrade under AP uoroscopy, just proximal to the triradiate cartilage. The sta-bility of the osteotomy is assessed manually. The C-arm, with or without a concomitant arthro-gram, is used to assure that satisfactory femoral head coverage has been achieved.Repair of the split apophyseal cartilage is achieved securely with interrupted absorbable sutures. The threaded Kirschner wires are then cut about 1cm proud from the iliac repaired apophysis in order to facilitate easier removal. Closure of the tensor—Sartorius fascia, reattach-ment of the external oblique muscle and subcuta-neous and skin tissues is as previously described for the Pemberton acetabuloplasty. Following wound dressing application, a single-leg hip spica is applied. The patient is followed up in approximately 2 weeks for clinical and radio-graphic assessment. The cast is removed at 6 weeks post-operatively and ambulation initiated with a walker until healing is conrmed radiographically. Essential Surgical Techniques inChildhoo�d (11Years Old toYoung Adults) Addressing Pathology Subsequent toOssication oftheAcetabular AnlageOnce the acetabular cartilaginous anlage has completely ossied and if the triradiate cartilage is still biologically active, a triple innominate osteotomy should be considered when attempting to achieve satisfactory mobility of the acetabular fragment and, in turn, adequate redirection and correction of acetabular dysplasia (Fig.5.12). For older children and young adolescents, especially those with signicant remaining triradiate growth, greater acetabular mobility is desirable/necessary so as to achieve optimal hip joint sta-bility not only laterally but also anteriorly and posteriorly as needed [14, 76, 77, 82, 83]. With the triple innominate redirectional osteotomy, the surgeon can satisfactorily mobilize the acetabular fragment in attempting to achieve redirection of the acetabulum and optimal hip joint stability.In the younger child, the surgical exposure during triple innominate osteotomy is extra- periosteal, an essential modication so as to not injure the triradiate cartilage and to facilitate greater mobility with less stress on xation devices. This technique allows for optimal ace-tabular redirection (achieving desirable acetabu-lar version) in restoring hip stability; particularly for the younger child with global deciency (e.g. Down syndrome, Spina Bida). Surgical Technique: Triple Innominate Osteotomy (Fig.5.12)The patient is positioned supine on a at radiolu-cent table. A roll is placed behind the contralat-eral knee in order to maintain hip exion, which helps both to ex the pelvis and to atten t

he 847 848 849 850 851 852 853 854 855 856 857 858 859 860 861 862 863 864 865 866 867 868 869 870 871 872 873 874 875 876 877 878 879 880 881 882 883 884 885 886 887 888 889 890 891 892 893 894 895 896 897 898 899 900 901 902 903 904 905 906 907 908 909 910 911 912 913 914 915 916 917 918 919 920 921 922 923 924 925 926 927 928 929 930 931 932 933 934 935 936 937 938 lumbar lordosis. The initial approach for the tri-ple innominate is as previously described for the Pemberton Acetabuloplasty. Following exposure of the ilium, the interval between the tensor and sartorius is identied. Dissection then proceeds within this interval proximal to the brim of the pelvis. The lateral iliac apophysis is then reected and the lateral ilium dissected subperiosteally until the sciatic notch is identied. The sciatic notch is also identied medially. The subsequent dissection involves an extraperiosteal exposure of the ischium and pubis while visualizing and pro-tecting the obturator nerve within the retroperito-neum. In order to accomplish this exposure, the fascia of the iliacus is released from the rectus tendon and the hip is exed in order to relax the iliacus and psoas muscles. This relaxation allows identication of the iliopectineal bursa just medial to the AIIS with blunt dissection medially to expose the pubis. A double-pronged Hohmann retractor is then inserted into the superior pubic ramus medially to retract the iliopsoas while maintaining the hip in exion to protect the fem-oral nerve. The interval between the psoas tendon sheath and the hip capsule is developed by open-ing the iliopectineal bursa medial to the hip cap-sule in order to access the ischium. Next, with the hip still held in exion, the iliacus muscle is gen-tly separated from the periosteum of the ilium so that the iliopectineal fascia can be exposed at the attachment to the iliopectineal line. In order to access the retroperitoneum and to protect the obturator nerve, the fascia is then incised and released from the iliopectineal line. The golden coloured retroperitoneal fat is exposed, and the obturator vein and nerve are carefully identied and protected by packing a Ray-Tec sponge extraperiosteally along the quadrilateral surface of the acetabulum. The pubic periosteum can be incised and the remaining iliopectineal fascia released from the iliopectineal line. The true pel-vis is then exposed extraperiosteally from the ischial tuberosity to the iliopectineal line.The pubic osteotomy is performed medial to the pubic limb of the triradiate cartilage using a Gigli saw. In older children the pubis can be dis-sected subperiosteally; however, in younger chil-dren the periosteum is cut with the osteotomy. The anterior pubic periosteum is incised and the root of the pubis carefully dissected subperiosteally using a right-angled clamp. The obturator nerve is pro-tected during this part of the procedure. Alternatively, the entire pubic root can be exposed extraperiosteally. A #1 Vicryl suture is passed through the obturator foramen and used to pass a Gigli saw. The root of the pubis is protected either in an extra- or sub-periosteal fashion and a trans-verse pubic osteotomy performed using the Gigli saw. Care is taken to orient the osteotomy as per-pendicular as possible to the long axis of the

pubis.“To achieve maximal mobility of the ace-tabular fragment in children and adoles-cents, it is very helpful to cut the surrounding periosteum to effectively mobilize the superior pubic ramus frag-ments after the osteotomy”. abc Fig. 5.12 Triple innominate osteotomy. A 9-year-old male (bone age, 7years) with a history of viral transverse myelitis secondary to chemotherapy who is functionally a mild diplegic. He is a community ambulator (GMFCS II) with AFO braces and presented with gait deterioration and pain with insufcient lateral and superior coverage of the left hip (a). The patient underwent a triple innominate osteotomy (b, 3months post-operatively). (c) Two-years later, after hardware removal, the patient had restoration of coverage, increased function and resolution of pain 939 940 941 942 943 944 945 946 947 948 949 950 951 952 953 954 955 956 957 958 959 960 961 962 963 964 965 966 967 968 969 970 971 972 973 974 975 976 977 978 979 980 981 982 983 984 985 986 987 988 989 990 991 992 993 994 995 996 997 998 999 1000 1001 1002 1003 1004 Next the ischial osteotomy is performed using a Ganz osteotome that is passed between the ilio-pectineal bursa and the hip capsule and posi-tioned at the level of the infracotyloid groove. Using both a 50° cephalad and oblique radio-graphic (C-arm) guidance, the medial and lateral cortices of the ischium are osteotomized com-pletely, terminating just distal to the ischial spine. The osteotome as visualized on the 50° cephalad view is rotated back and forth in the transverse anatomic plane in order to conrm that the ischium is completely cut. Similar to the pubic cut, the ischial periosteum is cut simulta-neously while performing the osteotomy. AP uoroscopy is used to select the line of the intended iliac osteotomy sufciently proximal to the acetabulum to allow for later stabilization with screws and/or threaded guide wires. A #1 Vicryl suture is passed through the sciatic notch and used to pass a Gigli saw. The adjacent soft tissue are protected with Hohmann retractors. An oscillating saw is used to divide the ilium from anterior to posterior aiming slightly in a caudal direction and terminating approximately 1cm anterior to the iliopectineal line. The Gigli saw that has been passed through the sciatic notch is used to complete the iliac osteotomy in order to create a small cephalad directed angle into which the rotated acetabulum can be stabi-lized. To redirect and control the position of the acetabulum, a 4mm Schanz screw is inserted into the supra-acetabular ilium and a pointed bone clamp applied to the root of the pubis. The acetabulum is redirected such that the sourcil is oriented horizontally and the anterior- posterior acetabular walls are balanced appropriately across the femoral head (i.e. no “crossover” sign). Provisional xation is obtained using 2mm Kirschner wires and an intraoperative radiographs obtained to conrm appropriate reorientation of the acetabulum. On occasion, an intraoperative arthrogram is performed to con-rm that the hip is well reduced. The “thorn sign” is used to identify lateral coverage of the head of the femur and overall rotation of the ace-tabulum. The provisional xation is then removed and replaced with cortical screws or Steinmann pins. The anteri

or extension of the acetabular fragment is osteotomized and used as a tricortical graft within the supra-acetabular ilium. The graft is transxed with one anterior cortical iliac screw. The hip range of motion is assessed for impingement.Closure is performed in a layered fashion. If the anterior superior iliac spine has been osteoto-mized, it is reattached with intraosseous O-Vicryl. Repair of the iliac apophysis, closure of the tensor- sartorius interval, reattachment of the external oblique, subcutaneous and skin closure are as previously described. Typically, xation is sufcient to obviate the need for spica casting, patients are mobilized as appropriate on post- operative day #1. Neurologically disabled chil-dren are, as necessary, immobilized in an abduction pillow. Surgical Technique: Ganz Periacetabular Osteotomy (PAO) (Figs.5.13, 5.14, 5.15, and5.16)If the triradiate cartilage appears to be closing or is closed, performing a periacetabular osteotomy (Ganz) achieves both maximal mobility and the potential to redirect the acetabulum into the desired location (Fig.5.12) [5, 8, 16, 84]. The patient is positioned supine on a radiolucent table. The skin excision again parallels the iliac crest laterally and extends more distally down onto the thigh. Exposure is as described for the Pemberton acetabuloplasty, as is the initial ilio- femoral dissection. When reecting the external oblique muscle from lateral to medial in a skele-tally mature patient, the apophysis will be ossi-ed, so the tissue plane is between the external oblique and the periosteum of the iliac crest.Next, the medial ilium is subperiosteally exposed and an interval is developed between the sartorius and rectus tendon. The ASIS (with the attached sartorius muscle) is osteotomized through an approximately 3cm oblique cut in a lateral to medial, proximal to distal direction. The interval between the sartorius and the attached ASIS medially and the rectus muscle/tendon complex laterally is developed. Deeper to this, the same interval is further developed between the rectus laterally and the iliacus, ilio-capsularis, and iliopsoas muscles medially. With 1005 1006 1007 1008 1009 1010 1011 1012 1013 1014 1015 1016 1017 1018 1019 1020 1021 1022 1023 1024 1025 1026 1027 1028 1029 1030 1031 1032 1033 1034 1035 1036 1037 1038 1039 1040 1041 1042 1043 1044 1045 1046 1047 1048 1049 1050 1051 1052 1053 1054 1055 1056 1057 1058 1059 1060 1061 1062 1063 1064 1065 1066 1067 1068 1069 1070 1071 1072 1073 1074 1075 1076 1077 1078 1079 1080 1081 1082 1083 1084 1085 1086 1087 1088 1089 1090 1091 1092 1093 1094 1095 1096 1097 1098 1099 the hip slightly exed, the dissection extends in a posterior direction medial to the hip capsule and lateral to the psoas tendon. A long large Mayo type sutures is essential in expanding this interval around the hip capsule posteriorly down to the ischium inferior to the acetabulum. The anterior, medial and lateral cortical surface of the ischium is palpated with the scissors tip. This interval is developed so as to allow for pas-sage of rst a hip skid (if possible), then the Ganz angled osteotome inserted down to the ischium with the hip skid protecting the sur-rounding soft tissues. The ischial cut starts in the infracotyloid groove just inferior to the ace-

tabulum, extending the cut posteriorly around the acetabulum and then proximally, ending near the level of the base of the ischial spine. AP and 45° iliac oblique C-arm views are essential in assuring the correct placement of the osteo-tome. The medial ischial cortex is cut rst, in turn, the middle and lateral cuts are completed. The lateral cut will be shorter (cm), the abcd Fig. 5.13 Periacetabular osteotomy (PAO) Ischial Cuts: The ischium is partially cut (a) medially (b) centrally and (c) laterally in sequence. (d) The cuts should extend pos-teriorly to allow the nal posterior column cut (Fig.5.14) to connect 1100 1101 1102 1103 1104 1105 1106 1107 1108 1109 1110 1111 1112 1113 1114 1115 1116 1117 1118 1119 1120 1121 osteotome directed posteriorly and medially away from the adjacent sciatic nerve. The leg is externally rotated and a foot hand-held to detect any muscle contraction which might suggest sciatic nerve irritation.The second cut is an osteotomy of the superior pubic ramus. The medial ilium is subperiosteally exposed down to the pelvic brim medially then distally to the obturator foramen. Anteriorly, exposure is extended to and beyond the iliopec-tineal eminence onto the superior pelvic ramus. A pointed Homan type is driven into the most medial anterior ramus as a retractor for the ilio-psoas muscle and neurovascular bundle. Subperiosteal (Crego) type retractors are inserted around the ramus through the obturator foramen proximally (rst) and then distally, protecting the obturator nerve. The distal retractor should be abcd Fig. 5.14 Periacetabular osteotomy (PAO) Posterior Column Cuts: The nal cut of the PAO is to split the pos-terior column. It is important to complete this cut both medially (a, b) and laterally (c, d). (a) A “ag” osteotome can be used to follow the false and true pelvis for the medial cut while monitoring the position within the poste-rior column on the lateral view. (b) It should connect with the medial cut of the ischium (see Fig.5.13a). (c) A straight osteotome is used complete the cut—aligning the lateral edge with the lateral edge of the ischium (see Fig.5.13c) 1122 1123 1124 1125 1126 1127 1128 1129 1130 1131 1132 1133 1134 1135 1136 1137 1138 1139 slightly medial to the proximal retractor. The superior ramus osteotomy should slope from lat-eral to medial beginning at a point at least 1cm medial to the iliopectineal eminence to assure the hip joint is not entered during the completion of the osteotomy.“Palpating the adductor muscle for con-tracture when placing the Crego retrac-tors and/or cutting the superior pubic ramus helps to further protect the obtura-tor nerve”.To perform the iliac osteotomy followed by the posterior column osteotomy, further expo-sure is necessary. The quadrilateral plate is sub-periosteally exposed down to the sciatic notch and base of the ischial spine. A point is marked on the false pelvis just lateral to the brim of the pelvis which corresponds with the proximal extent of the sciatic notch. To further protect soft tissues, a sub- periosteal retractor is placed along the lateral wall of the ilium in line with the intended course of the iliac osteotomy. The ilium abcd Fig. 5.15 Periacetabular osteotomy (PAO) Correction: Once free, the acetabular fragment is repositioned to p

ro-vide anterior coverage (a) that permits 90° of hip exion (b). Additionally, (c) the fragment should be repositioned to provide signicant lateral coverage as judged by an AP radiograph. (d) An arthrogram can help judge the position of the un-ossied cartilaginous epiphysis and position of the labrum 1140 1141 1142 1143 1144 1145 1146 1147 1148 1149 1150 1151 1152 1153 1154 1155 1156 1157 1158 1159 1160 1161 is cut with a power saw to point marked (see above) on false pelvis.“The posterior column cut begins at the end of the iliac cut and extends distally to a point near or at the most proximal extent of the initial ischial cut (rst cut). The cut should be centered equal distance from the posterior edge of the acetabulum and the edge of the posterior column. The C-arm (45° iliac oblique view) is critical in monitoring the direction of the osteotomy. As the distal portions of the lateral cortex is osteotomized, care must be taken to min-imize injury to the sciatic nerve. The hip is extended, abducted and externally rotated and a hand is placed on the foot”.Having completed all osteotomies, a Shantz screw is inserted into the acetabular fragment just superior to the acetabulum and a T-handle chuck attached. The fragment is carefully mobilized which effectively completes the osteotomies, freeing the fragment from the surrounding intact periosteum. The T-handle is further secured to the acetabular fragment with a curved (lobster claw) bone fragment. Correction desired is typically achieved by adducting, medializing and anterior tilting (extending) of the acetabular fragment. Provisional xation is achieved with 3/32 K-wires.“Correction achieved is assessed with the C-arm. Adjustments are made so as to optimize coverage, medialization and ace-tabular version. The range of motion is assessed, exion to 90° and abduction to 30° should be present. If not, the correc-tion obtained should be decreased”.The acetabular fragment is secured with corti-cal screws, inserted in the same direction as the previously placed K-wires. Final correction is ab Fig. 5.16 Periacetabular osteotomy (PAO): (a) A 16-year-old female with signicant lateral and anterior under-coverage, pain but no labral tear or signs of arthritis underwent a PAO (Figs.5.13–5.16). (b) Two years later the osteotomy is well healed, note the restoration of Shenton’s line and hip center. The patient is now pain free returned to sport 1162 1163 1164 1165 1166 1167 1168 1169 1170 1171 1172 1173 1174 1175 1176 1177 1178 1179 1180 1181 1182 1183 1184 1185 1186 1187 1188 1189 1190 1191 1192 1193 1194 1195 1196 1197 1198 1199 again assessed by C-arm and hip motion again assessed. If internal rotation in 90° of exion is limited ()and a head-neck offset de-ciency is noted on pre-operative radiographs, an anterior arthrotomy is performed and an antero-lateral head-neck osteochondroplasty performed which typically allows for improved internal rota-tion in exion [85]. If opened, the capsule is closed. The ASIS and attached sartorius muscle are reattached with #5 permanent suture, placed through the drill holes in the ilium and around the base of the ASIS.The tensor/sartorius fascia is reapproximated and the external oblique muscle sutured to the soft tissue on the anterolateral edge of the ilium.

The subcutaneous and skin tissues are closed in layers. Patients are mobilized on post-operative day #1, and early weight bearing is encouraged for patients with good bone quality. Irreducible Hip JointFor those hips unable to achieve a concentric reduction, salvage procedures, rather than redi-rectional, are indicated. These involve either moving the ilium itself laterally (i.e. Chiari-type) [86–89] or augmenting extracapsular bone with a bone graft (i.e. shelf arthroplasty) to provide fem-oral head coverage [90, 91].“Importantly, for satisfactory outcome of either a pelvic redirectional osteotomy or an acetabuloplasty, it is essential that ana-tomical reduction of the femoral head into the true acetabulum is possible. In cases in which this is not possible, a salvage type procedure should be considered so as to provide extracapsular stability of the hip joint Fig. 5.17)”. Surgical Technique: Chiari OsteotomyThe approach for the Chiari osteotomy is quite similar as to the approach for Bernese PAO and or triple innominate osteotomy. Subperiosteal expo-sure of both the lateral and medial walls of the ilium is obtained. Medially, the subperiosteal dis-section extends to and beyond the brim of the pel-vis down to and into the sciatic notch, and distally to the base of the ischial spine. Laterally, the abductor muscle is detached from the iliac crest and subperiosteal dissection extended down to and into the sciatic notch. When exposing later-ally, subperiosteal exposure is carried as far dis-tally as possible. In some instances, this may include distally elevating proximally displaced lateral labral chondral tissues (distally, without violating the lateral capsule). Dissecting in the notch with a sponge facilitates exposure. The osteotomy begins anteriorly at a point half way between the ASIS and AIIS and extends posteri-orly (similar to the iliac cut of the previously described Ganz PAO) but extends across and through the posterior column, exiting at the sciatic notch. To both optimize the eventual displace-ment of the fragments and provide enhanced oste-otomy stabilization, the osteotomy should be angulated approximately 15° cephalad in the frontal plane. Completion of the osteotomy is per-formed with a power saw beginning anteriorly and extending towards the sciatic notch. Completion of osteotomy within the notch can be abc Fig. 5.17 Salvage procedure: Shelf Arthroplasty. (a) A patient with in incongruent femoral head and acetabulum underwent a shelf osteotomy (b). Two years later, the patient has healed the shelf and the extracapsular arthro-plasty has inuenced restoration of the hip shape (white arrow)AU10 1200 1201 1202 1203 1204 1205 1206 1207 1208 1209 1210 1211 1212 1213 1214 1215 1216 1217 1218 1219 1220 1221 1222 1223 1224 1225 1226 1227 1228 1229 1230 1231 1232 1233 1234 1235 1236 1237 1238 1239 1240 1241 1242 1243 1244 1245 1246 1247 1248 1249 1250 1251 1252 1253 1254 1255 1256 1257 1258 1259 1260 1261 1262 1263 1264 1265 achieved with a Gigli saw, cutting anteriorly and laterally out of the notch, or with an osteotome cutting into the notch. In doing so, medial and lat-eral large Hohmann retractors are subperiosteally placed in the notch, serving to protect the gluteal vessels and sciatic nerve.“Once completed, the distal fragment is displaced medially, which variably effe

cts improved superior capsular coverage by the osteotomy surface of the proximal fragment. Effort must be made to assure that sufcient displacement occurs but also that the distal fragment does not dis-place too posteriorly”.Improved lateral coverage can be augmented with insertion of a shelf augmentation, which also helps to minimize the variably occurring osseous offset between the two pelvic fragments. The osteotomy is transxed with K-wires (inserted proximal-distal/lateral-medial) in younger patients (years). For older patients, and/or when no cast immobilization is planned, the osteotomy is xated with large fragment (4.5mm) cortical screws and cast immobilization is not required.Typically, a capsulotomy is not performed. However, if there is considerable subluxation, performing an anterior capsulotomy can help minimize the extent of subsequent hip joint insta-bility. The capsulotomy is performed anteriorly, does not extend superolaterally, but correctly extends through the most medial capsule to the medial edge of the true acetabulum. This potenti-ates femoral head medialization which in turn makes it possible to perform a more distal Chiari osteotomy cut (which is desired). When repairing the capsulotomy, it is critical to achieve a very competent capsulorrhaphy as the capsule later serves as an interpositional arthroplasty, essential in performing a Chiari displacement osteotomy. The medial and lateral ilial soft tissues are securely repaired both to each other and to the iliac crest with #1 Vicryl suture. The tensor sarto-rius interval is closed and the external oblique is also reattached to the soft tissues just lateral to the iliac crest. The subcutaneous and skin tissues are closed in layers. In younger patients, hips are protected with an abduction pillow, and kept non-weightbearing for 5–6weeks. Younger patients are then mobilized as possible with protected weight bearing using a walker and/or crutches. Older patients whose osteotomies have been xed with cortical screws are mobilized as possible post operatively. Weight bearing is limited until early bone healing is pres-ent (6–8weeks) and then weight bearing is grad-ually increased. Surgical Technique: Shelf Arthroplasty (Figs.5.8 and5.17)Shelf arthroplasty can at times be very effective in the treatment of problematic hip joint sublux-ation secondary to various developmental hip joint pathologies, in older children and adoles-cents. The surgical approach in all cases includes rst achieving femoral head reduction and then providing stabilization of what often is a complex hip joint subluxation. For the shelf arthroplasty, it is desirable to use either a screw-plate or screw- washer stabilization of the shelf to optimize immediate post-operative early hip joint stabili-zation. The combination of surgical reduction as necessary and secured shelf arthroplasty has proven to be very effective for the patient with severe hip subluxation and deformity.“A relatively “xed” shelf provides imme-diate/early important stabilization follow-ing surgical reduction of the previously subluxated hip in patients with severe acetabular insufciency secondary to neuromuscular disorders such as cerebral palsy and Charcot-Marie-Tooth Disease. A surgically secured shelf also provides earl

y stability in the containment treat-ment of Perthes disease”.The procedure is performed with the patient positioned supine on a at radiolucent table with a small bump under the buttock and lower back. The hip and pelvis are exposed anteriorly through an iliofemoral approach identical to that described for the Pemberton Acetabuloplasty. If the femoral head is notably subluxated and a capsulotomy and capsulorrhaphy are to be performed, the rec-tus tendon is transected 1cm distal to insertion 1266 1267 1268 1269 1270 1271 1272 1273 1274 1275 1276 1277 1278 1279 1280 1281 1282 1283 1284 1285 1286 1287 1288 1289 1290 1291 1292 1293 1294 1295 1296 1297 1298 1299 1300 1301 1302 1303 1304 1305 1306 1307 1308 1309 1310 1311 1312 1313 1314 1315 1316 1317 1318 1319 1320 1321 1322 1323 1324 1325 1326 1327 1328 1329 1330 1331 1332 1333 1334 1335 1336 1337 1338 1339 1340 1341 1342 1343 1344 1345 1346 1347 1348 1349 1350 1351 1352 1353 1354 1355 1356 1357 1358 and the muscle complex reected distally to achieve complete capsular exposure. A near hori-zontal capsulotomy is performed, starting 1cm lateral to the acetabular rim sloping slightly from proximal lateral to distal medial. To facilitate essential medialization of the head into the true acetabulum, the capsulotomy must be extended to the medial rim of the acetabulum. Problematic musculotendinous and ligamentous contractures may preclude obtaining a satisfactory reduction of the femoral head into the true acetabulum and/or achieving satisfactory hip motion after reduc-tion. To deal with this, a proximal femoral oste-otomy (PFO) is designed as dictated by the patient pathology. Components of the PFO include shortening of the femur by ~1.5cm, rota-tion as indicated to correct excessive anteversion and increasing varus of neck shaft angle to better seat the femoral head into the acetabulum. The PFO is completed through a second incision using a standard lateral approach to the proximal femur. The timing of the PFO during the proce-dure is based on need. If femoral shortening is required then the PFO should be done prior to attempting open reduction.Once the head is reduced into the acetabulum and the capsulorrhaphy complete (if necessary), the shelf acetabuloplasty is performed. The anter-osuperior aspect of the acetabulum is located uti-lizing an AP uoroscopic image. A series of unicortical holes are made just above the acetab-ulum, using a 3.2mm drill through the outer table (2cm deep, directed 20° cephalad)“Starting anterior and moving posterior– just above and as close as possible to the superior acetabular– the shelf must ana-tomically about the hip capsule without penetrating into acetabular articular surface”.Once the line of drill holes is complete, they are connected from anterior to posterior using small curettes and dental burrs, directing the dis-section so the slot being created is immediately adjacent to the capsule and directed proximally. The trough should be deep enough to abut but not penetrate the inner table. After the trough is cre-ated, proceed in harvesting the outer table bone graft. An oscillating saw is used to cut off the top of the iliac crest (saved as a source of bone graft) and then a curved osteotome is used to cut three adjacent longitudinal Cortico-Cancellous strips f

rom the outer (or inner table). The strips should be made as long as possible, but be sure to leave enough intact. One should leave room in the dis-tal outer table to accommodate subsequent plate xation of the shelf. The total width of the com-bined strips should be roughly the length of the previously constructed trough. Depending on the volume of graft harvested, you may have to fash-ion additional corticocancellous strips from a tri-cortical allograft to augment both the thickness and width of the bony shelf.The shelf is constructed by laying the graft strips in the trough side-by-side starting posterior and moving anterior. Tamp each individual strip deep into the trough abutting immediately on the capsule. Use the initially obtained osteotomized top of the ilium (a tricortical autograft) to press t and backll the superior aspect of the trough and reinforce the shelf. The shelf will become more stable as the trough is tightly lled with graft reinforcing its superior surface. A Freer elevator is inserted between the shelf and the capsule and the C-arm is used to assess there is a tight t between shelf and capsule.To assure the shelf remains impacted against the capsule, the shelf is secured in place with either a plate and/or abutting screws. A small fragment (distal radius type) T-plate is appro-priately bent and secured with 2–3 bicortical screws through the ilium and 2 locking screws through the shelf. The plate is contoured and xated between the pelvis and graft so as to both hold the composite graft in-place and compress the shelf against the capsule. Alternatively stabilize the shelf by inserting two cortical screws abutting rmly against the proximal surface of the bony shelf in a blocking strategy (washers with points are essential in achieving secure screw head purchase on the lateral edges of the shelf).“Once the shelf arthroplasty has been secured. Final C-arm views include an AP (in abduction and adduction) and false prole lateral (in neutral extension and 1359 1360 1361 1362 1363 1364 1365 1366 1367 1368 1369 1370 1371 1372 1373 1374 1375 1376 1377 1378 1379 1380 1381 1382 1383 1384 1385 1386 1387 1388 1389 1390 1391 1392 1393 1394 1395 1396 1397 1398 1399 1400 1401 1402 1403 1404 1405 1406 1407 1408 1409 1410 1411 1412 1413 1414 1415 1416 1417 1418 1419 1420 1421 1422 1423 1424 1425 1426 1427 1428 1429 1430 1431 1432 1433 1434 1435 1436 1437 1438 1439 1440 1441 1442 1443 1444 1445 1446 1447 1448 1449 1450 1451 1452 1453 exion). Assess femoral head coverage and the desired immediate adjacent con-tact, with the capsule interposed between the head and the shelf. Also, hip motion should be conrmed, with exion to 90° and abduction to 25–30° mandatory so as to avoid impingement”.In closing the conjoined rectus tendon (if tran-sected in the approach) repaired with #1 Ethibond. Repair of the apophyseal cartilage, closure of the tensor-sartorius interval, and reattachment of the external oblique and subcutaneous and cutaneous is performed, as previously described. The patient is placed into an A-frame long leg cast bilaterally with the knees slightly exed. After 5–6weeks in the A-frame cast the patient is converted to an A-frame brace and three times daily range of motion exercises initiated. At 3months, the patie

nts can begin weightbearing based on X-ray evidence of graft incorporation, continuing with the A-frame brace at night. Classic PapersHarris WH.Etiology of OA of the hip. Instr Coume Lect 1986. Proposed that OA of the hip typically does not exist as a primary disease, a change in our thinking. Operative Pitfalls• Failure to use C-arm monitoring while performing an acetabuloplasty risks inadvertently extending the osteotome into the acetabulum and/or the bone graft into and through the tri-radiate cartilage.• Overcorrective anterolateral coverage, particularly when performing an acetab-uloplasty, risks later development of symptomatic FAI.• Inadequate xation risks a post- operative loss of reduction following Salter osteotomy; especially in a small pelvis.• Attempting to achieve improved cover-age with a pelvic procedure without rst obtaining satisfactory reduction of the femoral head into the true ace-tabulum risks persistent postoperative subluxation.• Exacerbating posterior deciency and the potential for early redislocation by overcorrection can occur with a combi-nation of acetabuloplasty (or single innominate osteotomy) and an overzeal-ous proximal femoral derotational oste-otomy that corrects for anteversion.• Attempting to correct global deciency associated with myelodysplasia or Down syndrome, with either an acetab-uloplasty or single innominate, may fail because of posterior acetabular de-ciency. In these cases, a triple innomi-nate osteotomy is typically necessary.• Lack of familiarity of the modication of the Smith Peterson approach neces-sary to achieve access to anterior ischial and superior pubic ramus will make it technically near impossible to safely complete either a triple innominate or PAO osteotomy.• Failure to complete the posterior col-umn osteotomy of an attempted Ganz PAO and mobilize the acetabulum frag-ment will limit achieving both satisfac-tory redirection and medialization of the acetabulum.• Failure to stabilize a triple innominate or Ganz PAO risks early post-operative loss of acetabular reorientation.• If a Chiari osteotomy is too proximal, relative to the joint capsule, the potential for improved stability provided to the femoral head is notably compromised.• Allowing excessive posterior displace-ment of the distal Chiari fragment risks injury to the sciatic nerve.• Failing to obtain intimate contact of the capsule and femoral head when per-forming a shelf arthroplasty minimizes any subsequent benecial supportive function of the shelf. 1454 1455 1456 1457 1458 1459 1460 1461 1462 1463 1464 1465 1466 1467 1468 1469 1470 1471 1472 1473 1474 1475 1476 1477 1478 1479 Klaue K.The acetabular rim syndrome. A clinical presentation of dysplasia of the hip J Bone Joint Surg Br 1991. Hip pathology that leads to damage to the labrum and/or chondrolat-eral junction is what typically leads to acetabular and femoral head arthritis.Ponsetti IV.Morphology of the acetabulum in congenital dislocation of the hip, gross, his-tological and roentgenographic studies. J Bone and Joint Am 1976. Detailed description of the cartilaginous anatomy of the acetabulum and its growth and development.Weinstein SL.Natural history of congenital hip dislocation (CDH) and hip dysplasia. Clin Orthop Relat Res 1987. Extensive description of th

e normal and abnormal radiological features of hip development and factors, most important in clinical outcome.Tonnis D.Congenital dysplasia and dislo-cation of the Hip in children and Adults. Springer 1987. The most informative/authorita-tive text on hip dysplasia (a “must” for hip acionados).Cooperman DR.Acetabulum dysplasia in the adult. Clin Orthop Relat Res. 1983. Documented that degenerative hip joint disease will eventually develop in all patients with hip subluxation.Wiberg G.Studies on dysplastic acetabular and congenital subluxation of the hip joint with special reference to the complication of OA.ACTA Chine Scandinavia 1939. Very early denitive description of radiographic acetabular deciency, what was felt to be normal and abnormal and its association with the development of OA.Salter RB.Innominate osteotomy in the treatment of congenital dislocation and sub-luxation of the hip. J Bone Joint Surg Br 1961. First publication of its kind describing a com-plete iliac pelvic osteotomy allowing for antero-lateral redirection of the congenitally decient acetabulum.Pemberton PA.Pericapsular osteotomy of the ilium for treatment of congenital sublux-ation and dislocation of the hip. J Bone Joint Am. 1965. Also a rst in the description of redirecting the acetabulum without making a complete cut through the entire ilium, i.e. “acetabuloplasty”.Wyles EC.The John Charnley Award: Redening the natural history of osteoarthri-tis in patients with hip dysplasia and impinge-ment. Clin Orthop Relat Res 2017. Comprehensive comparison in longitudinal study of frequency of total hip replacement necessary in patients with either FAI, dysplasia or normal morphology.Smith-Petersen MN.The Classic: Treatment of malum coxae senilis, old slipped upper femoral epiphysis, intra pelvic protru-sion of the acetabulum, and coxa plana by means of acetabuloplasty in 1936 (reprinted in Clin Orthop Relat Res 2009). Original descrip-tion on the technique of what is now the standard anterior approach to the pelvis and hip joint.Betz RR.Chiari pelvic osteotomy in chil-dren and young adults. J Bone Joint Surg Am 1988. Indications for and technique of perform-ing a Chiari osteotomy.Kuwajima SS.Comparison between Salter’s innominate osteotomy and augmented acetabuloplasty in the treatment of patients with severe Legg Calve-Perthes disease. J Pediatr Orthop B 2002. The author demon-strated the slot-secured shelf arthroplasty in the treatment of problematic Coxa Plana.Faciszewski T.Triple innominate osteotomy for acetabular dysplasia. J Pediatr Orthop 1993. Publication with a substantial number of patients (other than Steel’s original article) of successful treatment of residual dysplasia utiliz-ing the Steel triple innominate osteotomies.Ganz R.A new periacetabular osteotomy for the treatment of hip dysplasia. Technique and preliminary results. Clin Orthop Relat Res 1988. “The” article that introduced the Bernese PAO as an alternate to a triple innomi-nate or dial osteotomy in correcting acetabular dysplasia.Wells J.Intermediate-term hip survivor-ship and patient-reported outcomes of peri-acetabular osteotomy: The Washington University experience. J Bone Joint Surg Am 2018. Comprehensive review of both local, 1480 1481 1482 1483 148

4 1485 1486 1487 1488 1489 1490 1491 1492 1493 1494 1495 1496 1497 1498 1499 1500 1501 1502 1503 1504 1505 1506 1507 1508 1509 1510 1511 1512 1513 1514 1515 1516 1517 1518 1519 1520 1521 1522 1523 1524 1525 1526 1527 1528 1529 1530 1531 1532 1533 1534 1535 1536 1537 1538 1539 1540 1541 1542 1543 1544 1545 1546 1547 1548 1549 1550 1551 1552 1553 1554 1555 1556 1557 1558 1559 1560 1561 1562 1563 1564 1565 1566 1567 1568 1569 1570 1571 1572 1573 national and international outcomes to date of treatment of acetabular dysplasia with the Bernese (Ganz) PAO. Key EvidenceThe indications for performing either a pelvic redirectional osteotomy or an acetabuloplasty in attempting to correct acetabular dysplasia are dependent upon age and cause of the dysplasia. In the young child (during development of the cartilaginous anlage), indications for surgical correction are dependent on the functional capacity of the acetabulum to support weight bearing and hip range of motion. For these patients, radiographic evidence of acetabular underdevelopment and subluxation/instability (i.e. break in Shenton’s line) or symptomatic dysplasia (pain or feeling of instability) is a clear indication for surgical intervention [9]. Given the predictable remodeling potential of the cartilaginous anlage, patients do very well following properly performed interventions [39, 76, 77]. In relatively older patients (following near complete development/ossication of the cartilaginous anlage), the indications are some-what less clear for the surgical correction of residual acetabular dysplasia (Fig.5.18). There is a paucity of both natural history and properly controlled interventional studies of hip dysplasia in this age group. In these more mature hips, there will be less potential remodeling following joint preserving surgery. Precise repositioning of the acetabulum is more critical in assuring satis-factory long-term outcome [8, 76, 77]. Most sur-geons consider symptoms of dysplasia (pain, feeling of instability, and limping), a positive Trendelenburg sign on exam and radiographic evidence of subluxation as indications for cor-rective surgery in these more skeletally mature patients. Outcomes of surgical connection of acetabular dysplasia have been very favorable, with a reported 95% 15 year survival rate [92–95]. Younger patients and the preoperative absence of arthritis were predictors of poten-tially better outcomes. The status of the labral chondral complex and/or head-neck prominence as predictors of outcome is less clear. While techniques have been developed that make it possible to correct both labral chondral pathol-ogy and head-neck junction abnormalities abc Fig. 5.18 Current indications of the PAO: Indications for correction of insufcient lateral (black arrow) or anterior coverage (a) are continually evolving. Current evidence supports correction of a symptomatic under-covered (see Table5.1 for values) hip. Current evidence also supports replacement, not preservation, of a (c) symptomatic dys-plasia with a labral tear (red arrow) and osteoarthritis (green arrow). However, evidence is less clear as to the outcome of correcting incidentally discovered, asymp-tomatic dysplasia (a). Additionally, with the advent of combined arthroscopy, it is unknown if labral repair is required when addressing dysplas

ia, or, how much a tear is too signicant to warrant surgical correction of both the labrum and dysplasia in favor of replacementAU11 1574 1575 1576 1577 1578 1579 1580 1581 1582 1583 1584 1585 1586 1587 1588 1589 1590 1591 1592 1593 1594 1595 1596 1597 1598 1599 1600 1601 1602 1603 1604 1605 1606 1607 1608 1609 1610 1611 1612 1613 1614 1615 1616 1617 1618 1619 1620 1621 1622 concomitant with acetabular reorientation, clini-cal studies are still ongoing in attempting to show how effective these adjacent procedures are (or are not) in further improving the outcome of ace-tabular reorientation joint preserving surgery. References 1. Harris WH.Etiology of osteoarthritis of the hip. Clin Orthop Relat Res. 1986;(213):20–33. 2. Aronson J.Osteoarthritis of the young adult hip: etiol-ogy and treatment. Instr Course Lect. 1986;35:119–28. 3. Klaue K, Durnin CW, Ganz R.The acetabular rim syndrome. A clinical presentation of dysplasia of the hip. J Bone Joint Surg Br. 1991;73(3):423–9. 4. Clohisy JC, Beaule PE, O’Malley A, Safran MR, Schoenecker P.AOA symposium. Hip disease in the young adult: current concepts of etiology and surgical treatment. J Bone Joint Surg Am. 2008;90(10):2267–81. 5. Leunig M, Siebenrock KA, Ganz R.Rationale of periacetabular osteotomy and background work. Instr Course Lect. 2001;50:229–38. 6. Nepple JJ, Byrd JW, Siebenrock KA, Prather H, Clohisy JC.Overview of treatment options, clinical results, and controversies in the management of femo-roacetabular impingement. J Am Acad Orthop Surg. 2013;21(Suppl 1):S53–8. 7. Schoenecker PL, Clohisy JC, Millis MB, Wenger DR.Surgical management of the problematic hip in adolescent and young adult patients. J Am Acad Orthop Surg. 2011;19(5):275–86. 8. Siebenrock KA, Leunig M, Ganz R.Periacetabular osteotomy: the Bernese experience. Instr Course Lect. 2001;50:239–45. 9. Weinstein SL.Natural history of congenital hip dis-location (CDH) and hip dysplasia. Clin Orthop Relat Res. 1987;(225):62–76. 10. Beck M, Kalhor M, Leunig M, Ganz R.Hip morphol-ogy inuences the pattern of damage to the acetabular cartilage: femoroacetabular impingement as a cause of early osteoarthritis of the hip. J Bone Joint Surg Br. 2005;87(7):1012–8. 11. Aronsson DD, Goldberg MJ, Kling TF Jr, Roy DR.Developmental dysplasia of the hip. Pediatrics. 1994;94(2 Pt 1):201–8. 12. Ponseti IV.Growth and development of the acetabu-lum in the normal child. Anatomical, histological, and roentgenographic studies. J Bone Joint Surg Am. 1978a;60(5):575–85. 13. Ponseti IV.Morphology of the acetabulum in con-genital dislocation of the hip. Gross, histological and roentgenographic studies. J Bone Joint Surg Am. 1978b;60(5):586–99. 14. Tonnis D.Congenital dysplasia and dislocation of the hip in children and adults. NewYork: Springer; 1987. 15. Leet AI, Mackenzie WG, Szoke G, Harcke HT.Injury to the growth plate after Pemberton osteotomy. J Bone Joint Surg Am. 1999;81(2):169–76. 16. Ganz R, Klaue K, Vinh TS, Mast JW.A new periace-tabular osteotomy for the treatment of hip dysplasias. Technique and preliminary results. Clin Orthop Relat Res. 1988;(232):26–36. 17. Parvizi J, Leunig M, Ganz R.Femoroacetabular impingement. J Am Acad Orthop Surg. 2007; 15(9):561–70.AU12 Take Home Message• In the las

t few decades, both our under-standing of what leads to hip joint arthri-tis secondary to acetabular dysplasia and the ability to surgically correct it has changed the practice of our hip surgery.• It is essential to be knowledgeable of the development of the hip and the pro-cesses by which it can fail when select-ing a surgical approach in the correction of residual acetabular dysplasia.• Having an understanding of both the normal and abnormal growth of the ace-tabulum helps in both the need for tim-ing of and choosing the optimal surgical technique in correcting acetabular deciency.• Further observation is indicated for younger children (less than 7years old) with a progressive decrease of the ace-tabular index, an intact Shelton’s line, normal hip motion and no limp.• Further observation is not indicated for older children (7years and older) with an unchanging acetabular index, break in Shelton’s line, and a positive Trendelenburg sign. Rather, appropriate surgical correction should be considered.• For skeletally mature patients, surgical correction of residual acetabular dyspla-sia is selectively performed typically only for symptomatic patients.• The clinical and radiographic goals at skeletal maturity, whether by natural his-tory or following surgical intervention, include: lateral and anterior CEA of 25°, less than 20% of the femoral head later-ally uncovered, a “stable” hip (i.e. Tonnis angle s line intact) and, most importantly, a congruent hip with satisfactory range of motion. 1623 1624 1625 1626 1627 1628 1629 1630 1631 1632 1633 1634 1635 1636 1637 1638 1639 1640 1641 1642 1643 1644 1645 1646 1647 1648 1649 1650 1651 1652 1653 1654 1655 1656 1657 1658 1659 1660 1661 1662 1663 1664 1665 1666 1667 1668 1669 1670 1671 1672 1673 1674 1675 1676 1677 1678 1679 1680 1681 1682 1683 1684 1685 1686 18. Wyles CC, Heidenreich MJ, Jeng J, Larson DR, Trousdale RT, Sierra RJ.The John Charnley Award: redening the natural history of OA in patients with hip dysplasia and impingement. Clin Orthop Relat Res. 2017;475(2):336–50. 19. Chegini S, Beck M, Ferguson SJ.The effects of impingement and dysplasia on stress distribu-tions in the hip joint during sitting and walk-ing: a finite element analysis. J Orthop Res. 2009;27(2):195–201. 20. Ecker TM, Tannast M, Puls M, Siebenrock KA, Murphy SB.Pathomorphologic alterations predict presence or absence of hip osteoarthrosis. Clin Orthop Relat Res. 2007;465:46–52. 21. Ganz R, Parvizi J, Beck M, Leunig M, Notzli H, Siebenrock KA.Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clin Orthop Relat Res. 2003;(417):112–20. 22. Smith-Petersen MN.The classic: Treatment of malum coxae senilis, old slipped upper femoral epiphysis, intrapelvic protrusion of the acetabulum, and coxa plana by means of acetabuloplasty. 1936. Clin Orthop Relat Res. 2009;467(3):608–15. 23. Allen D, Beaule PE, Ramadan O, Doucette S.Prevalence of associated deformities and hip pain in patients with cam-type femoroacetabular impinge-ment. J Bone Joint Surg Br. 2009;91(5):589–94. 24. Bardakos NV, Villar RN.Predictors of progression of osteoarthritis in femoroacetabular impingement: a radiological study with a minimum of ten years follow- up. J Bone Joint Surg Br. 2009;91(2):162–9. 25. Cooperman DR, Wallensten R, Stulb

erg SD.Acetabular dysplasia in the adult. Clin Orthop Relat Res. 1983;(175):79–85. 26. Hartolakidis G, Bardakos NV, Babis GC, Georgiades G.An examination of the association between dif-ferent morphotypes of femoroacetabular impinge-ment in asymptomatic subjects and the development of osteoarthritis of the hip. J Bone Joint Surg Br. 2011;93(5):580–6. 27. Malvitz TA, Weinstein SL.Closed reduction for con-genital dysplasia of the hip. Functional and radio-graphic results after an average of thirty years. J Bone Joint Surg Am. 1994;76(12):1777–92. 28. Schwend RM, Pratt WB, Fultz J.Untreated acetabular dysplasia of the hip in the Navajo. A 34 year case series followup. Clin Orthop Relat Res. 1999;(364):108–16. 29. Sierra RJ, Trousdale RT, Ganz R, Leunig M.Hip dis-ease in the young, active patient: evaluation and non-arthroplasty surgical options. J Am Acad Orthop Surg. 2008;16(12):689–703. 30. Hartolakidis G, Karachalios T, Stamos KG.Epidemiology, demographics, and natural his-tory of congenital hip disease in adults. Orthopedics. 2000;23(8):823–7. 31. Hadley NA, Brown TD, Weinstein SL.The effects of contact pressure elevations and aseptic necrosis on the long-term outcome of congenital hip dislocation. J Orthop Res. 1990;8(4):504–13. 32. Maxian TA, Brown TD, Weinstein SL.Chronic stress tolerance levels for human articular cartilage: two nonuniform contact models applied to long-term fol-low- up of CDH.J Biomech. 1995;28(2):159–66. 33. Wedge JH, Wasylenko MJ.The natural history of con-genital dislocation of the hip: a critical review. Clin Orthop Relat Res. 1978;(137):154–62. 34. Wiberg G.Studies on dysplastic acetabula and congen-ital subluxation of the hip joint with special reference to the complication of OA.Acta Chir Scand. 1939;83:58. 35. Eppright R.Dial osteotomy of the acetabulum in the treatment of dysplasia of the hip. J Bone Joint Surg Am. 1975;57:212–5. 36. Millis MB, Murphy SB.Use of computed tomo-graphic reconstruction in planning osteotomies of the hip. Clin Orthop Relat Res. 1992;(274):154–9. 37. Muller ME.Intertrochanteric osteotomy: indication, preoperative planning, technique. In: Schatzker J, editor. The intertrochanteric osteotomy. NewYork: Springer; 1984. p.25–66. 38. Pauwels F.Biomechanics of the normal and diseased hip. In: Furlong R, Maquet P, editors. Theoretical foundation, technique and results of treatment an atlas. NewYork: Springer; 1976. p.136–43. 39. Salter RB.The classic. Innominate osteotomy in the treatment of congenital dislocation and sublux-ation of the hip by Robert B.Salter, J Bone Joint Surg (Brit) 43B:3:518, 1961. Clin Orthop Relat Res. 1978;(137):2–14. 40. Wagner H.Experiences with spherical acetabular osteotomy for the correction of the dysplastic acetab-ulum. In: Weil U, editor. Acetabular dysplasia prog-ress in orthopaedic surgery, vol. 2. Berlin, Heidelberg: Springer; 1978. p.131–45. 41. Wagner H.Osteotomies for congenital hip dislocation. In: The hip proceedings of the fourth open scientic meeting of the Hip Society. St Louis: Mosby; 1976. p.45–66. 42. Murphy SB, Kijewski PK, Millis MB, Harless A.Acetabular dysplasia in the adolescent and young adult. Clin Orthop Relat Res. 1990;(261):214–23. 43. Mu

rphy SB, Ganz R, Muller ME.The prognosis in untreated dysplasia of the hip. A study of radiographic factors that predict the outcome. J Bone Joint Surg Am. 1995;77(7):985–9. 44. Sankar WN, Duncan ST, Baca GR, Beaule PE, Millis MB, Kim YJ, etal. Descriptive epidemiology of acetabular dysplasia: The Academic Network of Conservational Hip Outcomes Research (ANCHOR) periacetabular osteotomy. J Am Acad Orthop Surg. 2017;25(2):150–9. 45. Carter CO, Wilkinson JA.Genetic and environmental factors in the etiology of congenital dislocation of the hip. Clin Orthop Relat Res. 1964;33:119–28. 46. Weinstein SL, Mubarak SJ, Wenger DR.Developmental hip dysplasia and dislocation: Part I.Instr Course Lect. 2004;53:523–30. 47. Salter RB.Etiology, pathogenesis and possible pre-vention of congenital dislocation of the hip. Can Med Assoc J. 1968;98(20):933–45. 48. Dunn PM.Perinatal observations on the etiology of congenital dislocation of the hip. Clin Orthop Relat Res. 1976;(119):11–22. 1687 1688 1689 1690 1691 1692 1693 1694 1695 1696 1697 1698 1699 1700 1701 1702 1703 1704 1705 1706 1707 1708 1709 1710 1711 1712 1713 1714 1715 1716 1717 1718 1719 1720 1721 1722 1723 1724 1725 1726 1727 1728 1729 1730 1731 1732 1733 1734 1735 1736 1737 1738 1739 1740 1741 1742 1743 1744 1745 1746 1747 1748 1749 1750 1751 1752 1753 1754 1755 1756 1757 1758 1759 1760 1761 1762 1763 1764 1765 1766 1767 1768 1769 1770 1771 1772 1773 1774 1775 1776 1777 1778 1779 1780 1781 1782 1783 1784 1785 1786 1787 1788 1789 1790 1791 1792 1793 1794 1795 1796 1797 1798 1799 1800 1801 1802 1803 1804 1805 1806 1807 1808 49. Bialik V, Berant M. “Immunity” of Ethiopian Jews to developmental dysplasia of the hip: a pre-liminary sonographic study. J Pediatr Orthop B. 1997;6(4):253–4. 50. Roper A.Hip dysplasia in the African Bantu. J Bone Joint Surg Br. 1976;58(2):155–8. 51. Skirving AP, Scadden WJ.The African neonatal hip and its immunity from congenital dislocation. J Bone Joint Surg Br. 1979;61-B(3):339–41. 52. Rabin DL, Barnett CR, Arnold WD, Freiberger RH, Brooks G.Untreated congenital hip disease. A study of the epidemiology, natural history, and social aspects of the disease in a Navajo population. Am J Public Health Nations Health. 1965;55(Suppl):1–44. 53. Johnsen K, Goll R, Reikeras O.Acetabular dyspla-sia in the Sami population: a population study among Sami in north Norway. Int J Circumpolar Health. 2008;67(1):147–53. 54. Lee CB, Mata-Fink A, Millis MB, Kim YJ.Demographic differences in adolescent-diagnosed and adult-diagnosed acetabular dysplasia compared with infantile developmental dysplasia of the hip. J Pediatr Orthop. 2013;33(2):107–11. 55. Croft P, Cooper C, Wickham C, Coggon D.Osteoarthritis of the hip and acetabular dysplasia. Ann Rheum Dis. 1991;50(5):308–10. 56. Inoue K, Wicart P, Kawasaki T, Huang J, Ushiyama T, Hukuda S, etal. Prevalence of hip osteoarthritis and acetabular dysplasia in French and Japanese adults. Rheumatology (Oxford). 2000;39(7):745–8. 57. Jacobsen S, Sonne-Holm S, Soballe K, Gebuhr P, Lund B.Hip dysplasia and osteoarthrosis: a survey of 4151 subjects from the Osteoarthrosis Substudy of the Copenhagen City Heart Study. Acta Orthop. 2005;76(2):149–58. 58. Lau EM, Lin F, Lam D, Silman A, Croft P.Hip osteo-arthritis and dysplasia in

Chinese men. Ann Rheum Dis. 1995;54(12):965–9. 59. Lehmann HP, Hinton R, Morello P, Santoli J.Developmental dysplasia of the hip practice guideline: technical report. Committee on Quality Improvement, and Subcommittee on Developmental Dysplasia of the Hip. Pediatrics. 2000;105(4):E57. 60. Smith RW, Egger P, Coggon D, Cawley MI, Cooper C.Osteoarthritis of the hip joint and acetabular dyspla-sia in women. Ann Rheum Dis. 1995;54(3):179–81. 61. Engesaeter IO, Laborie LB, Lehmann TG, Fevang JM, Lie SA, Engesaeter LB, etal. Prevalence of radiographic ndings associated with hip dysplasia in a population-based cohort of 2081 19-year-old Norwegians. Bone Joint J. 2013;95-B(2):279–85. 62. Engesaeter LB, Engesaeter IO, Fenstad AM, Havelin LI, Karrholm J, Garellick G, etal. Low revision rate after total hip arthroplasty in patients with pediatric hip diseases. Acta Orthop. 2012;83(5):436–41. 63. Lohmander LS, Engesaeter LB, Herberts P, Ingvarsson T, Lucht U, Puolakka TJ.Standardized incidence rates of total hip replacement for primary hip osteoarthritis in the 5 Nordic countries: similarities and differences. Acta Orthop. 2006;77(5):733–40. 64. Murray RO.The etiology of primary osteoarthritis of the hip. Br J Radiol. 1965;38(455):810–24. 65. Crockarell J Jr, Trousdale RT, Cabanela ME, Berry DJ.Early experience and results with the periace-tabular osteotomy. The Mayo Clinic experience. Clin Orthop Relat Res. 1999;(363):45–53. 66. Peters CL, Erickson JA, Hines JL.Early results of the Bernese periacetabular osteotomy: the learning curve at an academic medical center. J Bone Joint Surg Am. 2006;88(9):1920–6. 67. Trousdale RT, Ekkernkamp A, Ganz R, Wallrichs SL.Periacetabular and intertrochanteric osteotomy for the treatment of osteoarthrosis in dysplastic hips. J Bone Joint Surg Am. 1995;77(1):73–85. 68. Trumble SJ, Mayo KA, Mast JW.The periacetabular osteotomy. Minimum 2 year followup in more than 100 hips. Clin Orthop Relat Res. 1999;(363):54–63. 69. Clohisy JC, Dobson MA, Robison JF, Warth LC, Zheng J, Liu SS, etal. Radiographic structural abnor-malities associated with premature, natural hip-joint failure. J Bone Joint Surg Am. 2011;93(Suppl 2):3–9. 70. Clohisy JC, Barrett SE, Gordon JE, Delgado ED, Schoenecker PL.Medial translation of the hip joint center associated with the Bernese periacetabular osteotomy. Iowa Orthop J. 2004;24:43–8. 71. Nunley RM, Prather H, Hunt D, Schoenecker PL, Clohisy JC.Clinical presentation of symptomatic acetabular dysplasia in skeletally mature patients. J Bone Joint Surg Am. 2011;93(Suppl 2):17–21. 72. Steppacher SD, Tannast M, Ganz R, Siebenrock KA.Mean 20-year followup of Bernese peri-acetabular osteotomy. Clin Orthop Relat Res. 2008;466(7):1633–44. 73. Troelsen A, Elmengaard B, Soballe K.Medium-term outcome of periacetabular osteotomy and predictors of conversion to total hip replacement. J Bone Joint Surg Am. 2009;91(9):2169–79. 74. Ito H, Tanino H, Yamanaka Y, Minami A, Matsuno T.Intermediate to long-term results of periace-tabular osteotomy in patients younger and older than forty years of age. J Bone Joint Surg Am. 2011;93(14):1347–54. 75. Novais EN, Heyworth B, Murray K, Johnson VM, Kim YJ, Millis MB.Physical activity level improves after periacetabular osteotomy for the tr

eatment of symptomatic hip dysplasia. Clin Orthop Relat Res. 2013;471(3):981–8. 76. Faciszewski T, Coleman SS, Biddulph G.Triple innominate osteotomy for acetabular dysplasia. J Pediatr Orthop. 1993a;13(4):426–30. 77. Faciszewski T, Kiefer GN, Coleman SS.Pemberton osteotomy for residual acetabular dysplasia in chil-dren who have congenital dislocation of the hip. J Bone Joint Surg Am. 1993b;75(5):643–9. 78. Gordon JE, Capelli AM, Strecker WB, Delgado ED, Schoenecker PL.Pemberton pelvic osteotomy and varus rotational osteotomy in the treatment of ace-tabular dysplasia in patients who have static encepha-lopathy. J Bone Joint Surg Am. 1996;78(12):1863–71. 1809 1810 1811 1812 1813 1814 1815 1816 1817 1818 1819 1820 1821 1822 1823 1824 1825 1826 1827 1828 1829 1830 1831 1832 1833 1834 1835 1836 1837 1838 1839 1840 1841 1842 1843 1844 1845 1846 1847 1848 1849 1850 1851 1852 1853 1854 1855 1856 1857 1858 1859 1860 1861 1862 1863 1864 1865 1866 1867 1868 1869 1870 1871 1872 1873 1874 1875 1876 1877 1878 1879 1880 1881 1882 1883 1884 1885 1886 1887 1888 1889 1890 1891 1892 1893 1894 1895 1896 1897 1898 1899 1900 1901 1902 1903 1904 1905 1906 1907 1908 1909 1910 1911 1912 1913 1914 1915 1916 1917 1918 1919 1920 1921 1922 1923 1924 1925 1926 1927 1928 79. Pemberton PA.Pericapsular osteotomy of the ilium for treatment of congenital subluxation and dislocation of the hip. J Bone Joint Surg Am. 1965;47:65–86. 80. Vedantam R, Capelli AM, Schoenecker PL.Pemberton osteotomy for the treatment of developmental dys-plasia of the hip in older children. J Pediatr Orthop. 1998;18(2):254–8. 81. Salter RB.Role of innominate osteotomy in the treatment of congenital dislocation and subluxation of the hip in the older child. J Bone Joint Surg Am. 1966;48(7):1413–39. 82. Rebello G, Zilkens C, Dudda M, Matheney T, Kim YJ.Triple pelvic osteotomy in complex hip dysplasia seen in neuromuscular and teratologic conditions. J Pediatr Orthop. 2009;29(6):527–34. 83. Steel HH.Triple osteotomy of the innominate bone. J Bone Joint Surg Am. 1973;55(2):343–50. 84. Clohisy JC, Barrett SE, Gordon JE, Delgado ED, Schoenecker PL.Periacetabular osteotomy in the treatment of severe acetabular dysplasia. Surgical technique. J Bone Joint Surg Am. 2006;88(Suppl 1 Pt 1):65–83. 85. Nassif NA, Schoenecker PL, Thorsness R, Clohisy JC.Periacetabular osteotomy and combined femoral head-neck junction osteochondroplasty: a minimum two-year follow-up cohort study. J Bone Joint Surg Am. 2012;94(21):1959–66. 86. Bailey TE Jr, Hall JE.Chiari medial displacement osteotomy. J Pediatr Orthop. 1985;5(6):635–41. 87. Betz RR, Kumar SJ, Palmer CT, MacEwen GD.Chiari pelvic osteotomy in children and young adults. J Bone Joint Surg Am. 1988;70(2):182–91. 88. Debnath UK, Guha AR, Karlakki S, Varghese J, Evans GA.Combined femoral and Chiari osteotomies for reconstruction of the painful subluxation or disloca-tion of the hip in cerebral palsy. A long-term outcome study. J Bone Joint Surg Br. 2006;88(10):1373–8. 89. Dietz FR, Knutson LM.Chiari pelvic osteotomy in cerebral palsy. J Pediatr Orthop. 1995;15(3):372–80. 90. Kuwajima SS, Crawford AH, Ishida A, Roy DR, Filho JL, Milani C.Comparison between Salter’s innomi-nate osteotomy and augmented acetabuloplasty in the treatment of patients wit

h severe Legg-Calve-Perthes disease. Analysis of 90 hips with special reference to roentgenographic sphericity and coverage of the fem-oral head. J Pediatr Orthop B. 2002;11(1):15–28. 91. Staheli LT, Chew DE.Slotted acetabular augmenta-tion in childhood and adolescence. J Pediatr Orthop. 1992;12(5):569–80. 92. Clohisy JC, Ackerman J, Baca G, Baty J, Beaule PE, Kim YJ, etal. Patient-reported outcomes of periacetabular osteotomy from the prospective ANCHOR cohort study. J Bone Joint Surg Am. 2017;99(1):33–41. 93. Lerch TD, Steppacher SD, Liechti EF, Tannast M, Siebenrock KA.One-third of hips after periacetabu-lar osteotomy survive 30 years with good clinical results, no progression of arthritis, or conversion to THA.Clin Orthop Relat Res. 2017;475(4):1154–68. 94. Wells J, Millis M, Kim YJ, Bulat E, Miller P, Matheney T.Survivorship of the Bernese periacetabular osteot-omy: what factors are associated with long-term fail-ure? Clin Orthop Relat Res. 2017;475(2):396–405. 95. Wells J, Schoenecker P, Duncan S, Goss CW, Thomason K, Clohisy JC.Intermediate-term hip survi-vorship and patient-reported outcomes of periacetabu-lar osteotomy: the Washington University experience. J Bone Joint Surg Am. 2018;100(3):218–25. 96. Weinstein SL, Mubarak SJ, Wenger DR.Fundamental concepts of developmental dysplasia of the hip. Instr Course Lect. 2014;63:299–305. 1929 1930 1931 1932 1933 1934 1935 1936 1937 1938 1939 1940 1941 1942 1943 1944 1945 1946 1947 1948 1949 1950 1951 1952 1953 1954 1955 1956 1957 1958 1959 1960 1961 1962 1963 1964 1965 1966 1967 1968 1969 1970 1971 1972 1973 1974 1975 1976 1977 1978 1979 1980 1981 1982 1983 1984 1985 1986 1987 1988 1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 Author QueriesChapter No.: 5 0004302441 QueriesDetails RequiredAuthor’s ResponseAU1Please check and conrm if the afliations are presented correctly.AU2As per reference style, name-date references have been changed to numbered references. Please check.AU3Ref. “Ponseti 1978” has been changed to “Ponseti 1978a, b” to match with the reference list. Please check here and in subsequent occurrences.AU4Part label (c) is present in the artwork but not mentioned in the caption of Fig. 5.7. Please check.AU5Refs. “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.AU6Ref. “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.AU7We have relabeled Fig. 5.8. Kindly check and provide better quality gures if any.AU8Please check the hierarchy of the section headings and conrm if correct.AU9Part labels (c–f) are present in the artwork but not mentioned in the caption of Fig. 5.11. Please check.AU10Part label (c) is present in the artwork but not mentioned in the caption of Fig. 5.17. Please check.AU11Part label (b) is present in the artwork but not mentioned in the caption of Fig. 5.18. Please check.AU12Reference “96” was not cited anywhere in the text. Please provide in text citation or delete the reference from the reference list. J. G. Schoenecker et al. Acetabular Dysplasia in