適用疾?。后y關節(jié)疾病截骨術后，如DDH，髖關節(jié)脫位，兒童股骨頭壞死，髖內翻，頭骺滑脫等練習時機：術前練習，拆除石膏褲后的健側訓練，術后截骨處愈合可以下地后的患側訓練（或遵醫(yī)囑）禁 忌：截骨處未愈合時禁練患側 等其他不宜

適用疾病：髖關節(jié)疾病截骨術后，如DDH，髖關節(jié)脫位，兒童股骨頭壞死，髖內翻，頭骺滑脫等練習時機：術前練習，拆除石膏褲后的健側訓練，術后截骨處愈合可以下地后的患側訓練（或遵醫(yī)囑）禁 忌：截骨處未愈合時禁練患側 等其他不宜

適用疾?。后y關節(jié)疾病截骨術后，如DDH，髖關節(jié)脫位，兒童股骨頭壞死，髖內翻，頭骺滑脫等練習時機：術前練習，拆除石膏褲后的健側訓練，術后截骨處愈合可以下地后的患側訓練（或遵醫(yī)囑）禁 忌：截骨處未愈合時禁練患側 等其他不宜

適用疾?。后y關節(jié)疾病截骨術后，如DDH，髖關節(jié)脫位，兒童股骨頭壞死，髖內翻，頭骺滑脫等練習時機：術前練習，拆除石膏褲后的健側訓練，術后截骨處愈合可以下地后的患側訓練（或遵醫(yī)囑）禁 忌：截骨處未愈合時禁練患側 等其他不宜

適用疾?。后y關節(jié)疾病截骨術后，如DDH，髖關節(jié)脫位，兒童股骨頭壞死，髖內翻，頭骺滑脫等練習時機：術前練習，拆除石膏褲后的健側訓練，術后截骨處愈合可以下地后的患側訓練（或遵醫(yī)囑）禁 忌：截骨處未愈合時禁練患側 等其他不宜

適用疾?。后y關節(jié)疾病截骨術后，如DDH，髖關節(jié)脫位，兒童股骨頭壞死，髖內翻，頭骺滑脫等練習時機：術前練習，術后截骨處愈合可以下地后（或遵醫(yī)囑）禁 忌：截骨處未愈合時禁練，腦癱患兒無法保持平衡等其他不宜

患有雙髖Perthes病兒童的臨床結果和預后因素：對40名兒童進行5年的前瞻性研究北京大學人民醫(yī)院骨關節(jié)科陶可譯者：陶可（北京大學人民醫(yī)院骨關節(jié)科）摘要：目的：本研究目的是闡述非手術治療、雙髖Perthes病的病程，并確定放射學和臨床結果的具體預后因素。患者和方法：我們確定了40名平均年齡為5.9歲（1.8至13.5歲）的兒童，這些兒童均納入我們這項對雙髖Perthes病進行非手術性治療的多中心、前瞻性研究中，這包括了挪威所有在1996年至2000年5年內被診斷出患有Perthes病的兒童。所有兒童都進行了五年的隨訪。髖關節(jié)病變嚴重程度按照Catterall分類法進行分類。一種改良的Stulberg三組分類被用作臨床結果的評價，其中，球形股骨頭被定義為優(yōu)良，橢圓形頭被定義為尚可，扁平狀股骨頭被定義為差。結果：23名兒童可見雙髖Perthes病，同時17名兒童在隨訪中出現雙髖Perthes病。后一組第二側髖關節(jié)發(fā)病平均延遲1.9年（0.3至5.5年）。五年放射學結果中，30髖優(yōu)良（39%），25髖尚可（33%）和21髖差（28%）。預后不良的最強預測因素是范圍大于50%的股骨頭壞死，比值比（OR）為19.6和確診時年齡=6歲（OR 3.3）。結果差的其他危險因素是疾病發(fā)病的時間，即前后連續(xù)發(fā)生雙髖Perthes病的兒童比同時發(fā)生雙髖Perthes病的兒童風險更高（p = 0.021，卡方檢驗）。一側髖關節(jié)確診Perthes病后，有5%的機會對側髖關節(jié)會出現Perthes病。結論：上述結果表明，我們需要區(qū)分同時發(fā)病的兒童和前后連續(xù)發(fā)生雙髖Perthes病的兒童，因為預后結果可能不同。之前尚無研究對此進行闡述。雙髖同時出現Perthes病兒童的臨床結果與之前我們研究的一系列單髖患有Perthes病的兒童相似，而前后連續(xù)發(fā)生雙髖Perthes病的兒童預后較差。對孩子和父母需要注意的是，一側髖關節(jié)出現Perthes病，對側髖患病風險增加。文獻出處：O Wiig, S Huhnstock, T Terjesen, A H Pripp, S Svenningsen. The Outcome and Prognostic Factors in Children With Bilateral Perthes' Disease: A Prospective Study of 40 Children With Follow-Up Over Five Years. Bone Joint J, 2016 Apr;98-B(4):569-75.The Outcome and Prognostic Factors in Children With Bilateral Perthes' Disease: A Prospective Study of 40 Children With Follow-Up Over Five YearsAbstractAims: The aims of this study were to describe the course of non-operatively managed, bilateral Perthes' disease, and to determine specific prognostic factors for the radiographic and clinical outcome. Patients and methods: We identified 40 children with a mean age of 5.9 years (1.8 to 13.5), who were managed non-operatively for bilateral Perthes' disease from our prospective, multicentre study of this condition, which included all children in Norway who were diagnosed with Perthes' disease in the five-year period between 1996 and 2000. All children were followed up for five years. The hips were classified according to the Catterall classification. A modified three-group Stulberg classification was used as an outcome measure, with a spherical femoral head being defined as a good outcome, an oval head as fair, and a flat femoral head as a poor outcome. Results: Concurrent, simultaneous bilateral Perthes' disease was seen in 23 children and 17 had the sequential onset of bilateral disease. The mean delay in onset for the second hip in the latter group was 1.9 years (0.3 to 5.5). The five-year radiographic outcome was good in 30 (39%), fair in 25 (33%) and poor in 21 (28%) of the hips. The strongest predictors of poor outcome were > 50% necrosis of the femoral head, with odds ratio (OR) 19.6, and age at diagnosis > 6 years (OR 3.3). Other risk factors for poor outcome were the timing of the onset of disease, where children with the sequential onset of bilateral disease had a higher risk than those with the concurrent onset of bilateral disease (p = 0.021, chi-squared test). Following a diagnosis of Perthes' disease in one hip, there was a 5% chance of developing it in the contralateral hip.Conclusion: These results imply that we need to distinguish between children with concurrent onset and those with sequential onset of bilateral Perthes' disease, as the outcomes may be different. This has not been previously described. Children with concurrent onset of bilateral disease had a similar outcome to our previous series of those with unilateral disease, whereas children with sequential onset of bilateral disease had a worse prognosis. The increased risk of developing Perthes' disease in the contralateral hip in those with unilateral disease is important information for the child and parents. Anteroposterior and Lauenstein radiograph projections of the hips of a 3.5 year old boy with the concurrent onset of bilateral Perthes disease, at the time of diagnosis (a). The right hip was classified as Catterall I, the left as Catterall IV. And (b); five years after diagnosis. The right hip was classified as spherical (Stulberg 1) and the left hip as oval (Stulberg 3)圖1. 在確診時，一個3.5歲男孩的髖關節(jié)前后位和Lauenstein位X線片，發(fā)現雙髖Perthes?。╝）右髖被歸類為Catterall I型，左髖為Catterall IV型；（b）確診5年后右髖被歸類為球形（Stulberg 1型），左髖被歸類為橢圓形（Stulberg 3型）Anteroposterior and Lauenstein radiograph projections of the hips of a 4.5 years old boy with the sequential onset of bilateral Perthes disease, at the time of diagnosis (a) The left hip was classified as Catterall group III. And (b); six months later. The right hip is now also affected, in the initial phase of the disease and classified as Catterall IV when in the fragmentation phase. And (c); When aged ten years with both hips classified as oval (Stulberg 3).。圖2. 在確診時，一個4.5歲男孩的髖關節(jié)前后位和Lauenstein位X線片，提示前后連續(xù)發(fā)生雙髖Perthes?。╝）左髖被歸類為Catterall III型；（b）6個月后，右髖也受到影響，在疾病的早期并分類為Catterall IV型，碎片階段；和（c）10歲，雙側髖關節(jié)分類為橢圓形（Stulberg 3型）。

兒童股骨頭壞死，又稱Legg-Calvé-Perthes’ disease，簡稱Perthes’病，是兒童骨科主要髖關節(jié)疾病之一。多見于15歲以下兒童，發(fā)生率約0.4~32.0/100000。本病病因尚不明確，可能與以下因素有關：家族聚集性、基因突變：Miyamoto于2007年首次報道在一個日本家庭(12個成員)，家族聚集性的Perthes’病，表現為常染色體顯性遺傳病，主要是COL2A1基因突變，導致氨基酸序列改變，II型膠原異常，從而引發(fā)Perthes’病。國內蘇培強等學者于2010年報道在一個五代42人家族中也發(fā)現同樣基因位點突變導致的家族聚集性的Perthes’病。Miyamoto N, Matsuda T, Kitoh H, et al. A recurrent mutation in type II collagen gene causes Legg-Calvé-Perthes disease in a Japanese family[J]. Hum Genet, 2007, 121: 625-629.Su PQ, Zhang LM, Peng Y, et al. A histological and ultrastructural study of femoral head cartilage in a new type II collagenopathy[J]. Int Orthop, 2010, 34: 1333-1339.凝血功能異常：2001年，發(fā)表在世界頂級兒科學雜志Pediatric上的一項病例對照研究(55例患兒和56例對照組)表明Perthes’病患兒血漿蛋白C、蛋白S水平明顯降低，可能與靜脈血栓形成、靜脈高壓、低氧性骨壞死有關。2014年，一篇關于12項病例對照研究(824例患兒和2033對照組)的Meta分析中，進行血液高凝狀態(tài)遺傳因素(凝血因子V、凝血酶原II、亞甲基四氫葉酸還原酶)和LCPD的關系研究，發(fā)現凝血因子V突變，可導致抗活化蛋白C的裂解，增加靜脈血栓的風險，致使Perthes’病的發(fā)生風險增加近3倍。Eldridge J, Dilley A, Austin H, et al. The Role of Protein C, Protein S, and Resistance to Activated Protein C in Legg-Perthes Disease[J]. Pediatrics, 2001, 107: 1329.Woratanarat E, Thaveeratitharm C, Woratanarat T, et al. Meta-Analysis of Hypercoagulability Genetic Polymorphisms in Perthes Disease[J]. J Orthop Res, 2014, 32: 1-7.母親孕期吸煙、二手煙：2008年，發(fā)表在世界頂級兒科學雜志Pediatric上的一項隨機病例對照研究(852例患兒和4432例隨機對照組)表明母親孕期吸煙與Perthes’病的發(fā)生密切相關，大量吸煙增加Perthes’病的風險幾乎達到100%(劑量依賴性，≥10支)，增加Perthes’病風險可能與煙中有害物質如尼古丁等限制、損害股骨頭血管發(fā)育有關。2017年，發(fā)表在世界頂級骨科雜志JBJSB上的一項病例對照研究(149例患兒和146對照組)表明吸煙與Perthes’病發(fā)生密切相關，吸煙暴露越早，Perthes’病發(fā)生風險越高，可能與煙中有害物質損傷血管引起股骨頭動脈梗塞有關。Bahmanyar S, Montgomery SM, Weiss RJ, et al. Maternal Smoking During Pregnancy, Other Prenatal and Perinatal Factors, and the Risk of Legg-Calvé-Perthes Disease[J]. Pediatrics, 2008, 122: e459.Perry DC, Thomson C, Pope D, et al. A case control study to determine the association between Perthes’ disease and the recalled use of tobacco during pregnancy, and biological markers of current tobacco smoke exposure[J]. Bone Joint J, 2017, 99-B: 1102-8.肥胖、瘦素：2013年，一項回顧性研究(150例/172髖)發(fā)現Perthes’病患兒中，有16%病例超重，32%病例肥胖，肥胖在Perthes’病患兒中常見，且與修復期、愈合期推遲有關。2016年，一項病例對照研究(41例患兒和41例對照組)，Perthes’病組血漿瘦素水平明顯高于對照組，瘦素受體水平明顯低于對照組；研究表明瘦素水平與Perthes’病嚴重程度、療效密切相關，瘦素可能是通過骨重建和促血管生成參與Perthes’病的發(fā)生發(fā)展。Lee JH, Zhou L, Kwon KS, et al. Role of Leptin in Legg-Calve-Perthes Disease[J]. J Orthop Res, 2013, 31: 1605-1610.Neal DC, Moualeu A, Jo CH, et al. Prevalence of Obesity in Patients With Legg-Calvé-Perthes Disease[J]. J Am Acad Orthop Surg, 2016, 24: 660-665.多動癥(ADHD)：2013年，發(fā)表在世界頂級兒童骨科雜志JPO上一項病例對照研究(146例患兒和142例對照組)表明多動癥與Perthes’病密切相關，尤其是在對診斷2年時間內更加明顯，可能與多動癥發(fā)生股骨頭骨骺損傷風險增大。2014年，一項病例對照研究(4057例患兒和40570例對照組)表明多動癥與Perthes’病密切相關，可能與多動癥引起的股骨頭機械應力增高有關。Perry DC, Pope D, Bruce CE, et al. Hyperactivity and the Psychological Burden of Perthes Disease: A Case-Control Study[J]. J Pediatr Orthop, 2013, 33: 644-649.Hailer YD, Nilsson O. Legg-Calvé-Perthes disease and the risk of ADHD, depression, and mortality[J]. Acta Orthopaedica, 2014, 85 (5): 501-505.其他因素：如胰島素樣生長因子(IGF-1)通過影響股骨頭骨骺骨化延遲，強度減弱，血管易受壓缺血引發(fā)Perthes’?。话捉樗?6(IL-6)通過促進破骨細胞骨吸收和抑制成骨細胞骨形成引發(fā)Perthes’病；血管內皮生長因子(VEGF)、低氧誘導因子-1(HIF-1)通過影響血管長入引發(fā)Perthes’??；低出生體重(＜1500g)與Perthes’病存在相關性，可能與營養(yǎng)不良造成股骨頭血管發(fā)育、結構、功能缺陷所致的程序性易感性；滑膜炎，急性期股骨頭會出現一定的血流動力學改變，股骨頭壓力僅輕度增高，可在3周內恢復正常，絕大多數研究報道滑膜炎后出現Perthes’病的發(fā)生率不到1%~4%，兩者無明顯相關。Neidel J, Schnau E, Zander D, et al. Normal plasma levels of IGF binding protein in Perthes' disease. Follow-up of previous report[J]. Acta Orthop Scand,1993,64: 540-542.Grasemann H, Nicolai RD, Hauffa BP, et al. Skeletal immaturity, IGF-I and IGFBP-3 serum concentrations in Legg-Calvé-Perthes disease (skeletal immaturity, IGF-I and IGFBP-3 in LCPD)[J]. Klin Padiatr,1996,208: 339-343.Matsumoto T, Enomoto H, Takahashi K, et al. Decreased levels of IGF binding protein-3 in serum from children with Perthes' disease[J]. Acta Orthop Scand,1998,69: 125-128.Srzenti S, Spasovski V, Spasovski D, et al. Association of gene variants in TLR4 and IL-6 genes with Perthes disease[J]. Srp Arh Celok Lek,2014,142: 450-456Kamiya N, Yamaguchi R, Adapala NS, et al, Aruwajoye O, Drissi H, Kim HK. Legg-Calvé-Perthes disease produces chronic hip synovitis and elevation of interleukin-6 in the synovial fluid[J]. J Bone Miner Res,2015,30: 1009-1013Kim HK, Bian H, Aya-ay J, et al. Hypoxia and HIF-1alpha expression in the epiphyseal cartilage following ischemic injury to the immature femoral head[J]. Bone, 2009, 45: 280-288.Suehiro M, Hirano T, Shindo H. Osteonecrosis induced by standing in growing Wistar Kyoto rats[J]. J Orthop Sci, 2005, 10: 501-507.Lappina K, Kealeyb D, CosgroveaA, et al. Does low birthweight predispose to Perthes’ disease? Perthes’ disease in twins[J]. J Pediatr Orthop B, 2003,12:307-310.總之，兒童股骨頭壞死(Perthes’病)病因不明，目前認為是遺傳因素（如COL2A1基因、eNOS基因、肥胖基因等）和環(huán)境因素（如母親孕期吸煙、二手煙等）等多因素綜合作用導致。一旦存在上述危險因素，臨床表現為膝關節(jié)或髖關節(jié)疼痛、跛行，家長應高度警惕，嚴禁患兒負重站立和行走，及早帶患兒找兒童骨科?？漆t(yī)生評估處理，以免造成不可挽救的嚴重后果。

周五上午出門診，安徽的小S回來復查，從兩年前孩子剛被診斷為“兒童股骨頭壞死”時全家的緊張不安到現在的談笑風生，很高興我們不僅僅為孩子提供了及時、恰當的治療，還盡量降低這樣病程長的疾病對家庭、孩子的心理方面不良影響。兒童股骨頭壞死，也叫Perthes病，和成年人的股骨頭壞死是完全兩種病。早期發(fā)現、及時恰當治療，利用好孩子神奇、強大的自我修復能力，治療效果會非常理想。6歲3個月男孩，走路跛行后拍片診斷“右側股骨頭壞死”，蛙式位片顯示股骨頭壞死范圍大、塌陷嚴重經過早期及時保守治療，恢復滿意，預計可達到S-2級結果，蛙式位片顯示股骨頭修復非常滿意

來自本中心公眾號“股骨頭壞死” 兒童髖部骨折很少發(fā)生，其大部分是由機動車事故或高處墜落的高能量創(chuàng)傷造成。但兒童髖部骨折的并發(fā)癥發(fā)生率高，包括骨折不愈合、髖內翻、骨骺早閉以及最嚴重的后果——股骨頭缺血性壞死（ON）。 兒童髖部骨折的 Delbet 分型 兒童發(fā)生股骨頭壞死在高能量創(chuàng)傷后引起的股骨頸骨折導致的股骨頭壞死并不稀奇！ Delbet 分型可以很好地預測兒童髖部骨折后股骨頭缺血性壞死。Delbet I 型或經骨骺的髖部骨折雖然并不常見，但其 ON 的發(fā)生率很高，甚至高達 100%！ 再來看這個III型的患者（男，7歲）：車禍傷，左側股骨干骨折+右側股骨頸骨折 24小時內行切開復位+內固定手術。 術后4年，雖然是24小時以內就行切開復位并行內固定治療，但是還是發(fā)生了股骨頭壞死： 兒童股骨頸骨折占小兒骨折的1％以下，但是股骨頭壞死是該骨折類型的破壞性并發(fā)癥之一。 那么兒童的股骨頸骨折的早期治療和延遲治療是否與股骨頭壞死發(fā)生率相關呢？ 國外2018年6月在線出版了這樣一篇文獻對這個問題進行了meta分析： https://doi.org/10.1007/s00264-018-3998-4 從1966年1月到2017年11月，通過搜索幾個數據庫（PubMed，Embase和Cochrane圖書館），用于比較早期（ 24小時）治療小兒股骨頸骨折的比較研究。并且分析了經歷早期治療與延遲治療，切開與閉合復位，移位與非移位以及不同Delbet分型股骨頸骨折的兒童之間與股骨頭壞死的關系。這篇文章發(fā)現不管切開或者閉合復位方法并沒有減少股骨頭壞死的發(fā)生率。 與延遲（> 24 h）治療相比，早期（