Circulatory and vascular changes in the hip following traumatic hip dislocation.

An experimental study of the extraosseous and intraosseous vascular and circulatory changes following traumatic hip dislocation in dogs and rabbits is reported. The observations were made by dissection, angiography and histology following posterior dislocation and reduction at varying intervals. Traumatic dislocation of the hip causes extraosseous circulatory disturbance in the hip resulting in intraosseous circulatory deficiency in the femoral head. The sites of the vascular lesions are the extraosseous branches of the femoral circumflex arteries and their extraosseous branches of the epiphyseal and metaphyseal arteries and the retinacular artery of the circulus vasculosus articularis. The types of the vascular damage are irreversible tear of the minority of vessels along the ruptured capsule and teres ligament, and the compression, traction and spasm of the majority of intact vessels which are reversible by early reduction. In prolonged dislocation the circulatory disturbance persists or worsens due to additional pathological changes such as posttraumatic inflammatory changes, fixed deformity in the dislocated position, thrombosis, fibrosis and occlusion of vessels which may eventually cause an ischemic necrosis of the femoral head. Early reduction within several hours after dislocation restores nearly normal regional anatomy and relieves vessels from compression, traction or spasm and restores extra and intraosseous circulation. It also prevents or minimizes thrombosis, fibrosis and occlusion of vessels and avascular necrosis of the femoral head.     

Segmental vascular changes in the femoral head in children and adults

The segmental nature of the avascular involvement of the femoral head in both children and adults is similar. Avascular necrosis may be wrongly interpreted from roentgenograms in infancy, irregular ossification may be due to altered stress on the femoral head. The segment involved in Legg-Perthes' disease is superior and lateral to the fovea in an area supplied by a branch of the lateral epiphyseal artery. Secondary changes occur due to the separation of the dead segment from the living bone. Theron demonstrated the vascular interruption with micro-injection techniques in both child and adult. Finite analysis of the femoral head revealed the distortion of the computer model at the site of the branches of the lateral epiphyseal artery. Trauma with vascular interruption within the femoral head appears to explain the avascular segment.     

介入治疗股骨头缺血性坏死及疗效评价

自1995年8月-1997年6月作者采用经旋股内、外动脉超选插管溶通术治疗股骨头缺血性坏死65例(76侧),经6个月—20个月随访,并采用血管造影和股骨头缺血性坏死疗效百分法评价判定,优良率84.3％,血管造影显示治疗后血管计数较治疗前增多(p<0.02)静脉回流改善。此方法适用于各种类型的患者,可减轻临床症状,提高生活质量。     

股骨头缺血性坏死骨质含量与VEGF、bFGF、BMP-2 mRNA表达的相关性研究

目的坏死骨的血管再生及骨修复能力与VEGF、bFGF与BMP-2多种生长因子关系密切,通过观察股骨颈骨折、创伤性及非创伤性股骨头缺血性坏死(avascular necrosis of femoral head,ANFH)的股骨头局部上述因子的表达变化,并与其组织病理学的骨质含量指标进行相关性分析,为进一步探讨ANFH的发病机制及临床针对不同病因进行个性化治疗提供实验依据。方法取59例人工全髋关节置换术患者自愿捐赠的股骨头标本进行观察。创伤性ANFH 22例(A组),Ficat分期:Ⅲ期13例,Ⅳ期9例。非创伤性ANFH 19例(B组),Ficat分期:Ⅲ期11例,Ⅳ期8例;其中激素性10例,酒精性7例,原因不明2例。新鲜股骨颈骨折18例(C组)。3组患者性别、年龄等一般资料比较,差异均无统计学意义(P>0.05)。采用双能X线骨密度仪测量股骨头负重区骨密度;大体观察组织病理学改变,HE染色光镜及扫描电镜下观察其病理变化,计算空骨陷窝百分比及骨小梁面积百分比,并采用原位杂交技术分别对其VEGF、bFGF、BMP-2 mRNA表达进行检测。结果 A、B组骨密度均低于C组,B组低于A组,组间差异均有统计学意义(P<0.05)。A、B组股骨头形态不规则,光镜下见坏死区骨小梁稀疏、不完整,有大量空骨陷窝;健存区A组有较多纤维组织增生,B组髓腔内脂肪细胞增生、肥大。扫描电镜示A、B组大多骨细胞脂肪变性、坏死,骨基质内见脂肪细胞增生。C组均呈正常股骨头结构。A、B组空骨陷窝百分比均高于C组,骨小梁面积百分比均低于C组,差异均有统计学意义(P<0.05);A、B组间仅空骨陷窝百分比差异有统计学意义(P<0.05)。A组与B组VEGF、BMP-2、bFGF mRNA阳性染色面积百分比及吸光度(A)值均明显低于C组(P<0.05);A组BMP-2、bFGF mRNA两指标均较B组高(P<0.05),但VEGF mRNA A、B组间差异无统计学意义(P>0.05)。上述各因子表达强度与骨密度、骨小梁面积百分比成正相关,而与空骨陷窝百分比成负相关。结论创伤性ANFH的股骨头修复能力强于非创伤性ANFH,创伤性与非创伤性ANFH股骨头局部VEGF、bFGF、BMP-2 mRNA表达均降低。     

螺旋CT评价股骨颈骨折后股骨头血运的临床研究

目的探讨应用64排螺旋CT薄层增强扫描技术,观察股骨颈骨折后股骨头血液循环的变化,从而为预测股骨颈骨折后股骨头缺血性坏死提供影像学依据。方法选择2007年9月至2009年12月收治的30例股骨颈骨折患者。术前行双侧髋关节64排螺旋CT薄层增强扫描,健侧髋关节设为自身对照组。观察旋股内侧动脉、旋股外侧动脉、支持带动脉,测量双侧上述血管的管径和长度,计算比较血管容积。结果 GardenⅢ型股骨颈骨折患侧旋股内侧动脉、旋股外侧动脉以及头下型、基底型股骨颈骨折患侧旋股外侧动脉血管容积较健侧明显降低,差异具有统计学意义（GardenⅢ型旋股内侧动脉t=-2.379,P〈0.05;GardenⅢ型旋股外侧动脉t=-3.052,P〈0.05;头下型旋股外侧动脉t=-2.578,P〈0.05;基底型旋股外侧动脉t=-7.908,P〈0.05）。GardenⅠ型、GardenⅡ型以及经颈型骨折双侧血管容积比较,差异无统计学意义。GardenⅠ型、GardenⅡ型、GardenⅢ型股骨颈骨折3组间对比,各组患侧血管容积差异无统计学意义。头下型、经颈型、基底型股骨颈骨折3组间对比,各组患侧血管容积之间差异无统计学意义。支持带动脉因CT分辨率不足未能完全显示。结论股骨颈骨折可改变旋股内侧动脉和旋股外侧动脉血管容积,从而影响股骨头的血液循环状态,是股骨颈骨折后发生股骨头缺血坏死的病理基础之一。64排螺旋CT薄层增强扫描技术是一种直接、实时、无创的观察股骨头血液循环的方法,对评价股骨头血运,预测股骨颈骨折预后及选择治疗方案有一定的参考价值。由于CT分辨率不足,不能清晰显示及测量支持带动脉的血管容积,使其临床应用价值受到一定的局限。     

Micro Perfusion and Quantitative Analysis of the Femoral Head Intraosseous Artery

The present study investigates the feasibility of micro perfusion of femoral head specimens from femoral neck fracture patients by the inferior retinacular arteries and performing intraosseous artery quantitative analysis of the femoral head. Twelve femoral neck fracture patients who had undergone conventional hip replacement surgery were included in this study. Femoral head specimen arteries were first dissected and exposed and then perfused by the inferior retinacular arteries and all the femoral heads underwent micro‐CT scanning. After micro‐CT scanning, a digital 3‐D model was reconstructed to quantify the femoral head intraosseous arteries for comparison with a normal femoral head. The artery length density, artery volume density, and artery length/volume ratio were calculated separately and compared with normal femoral head parameters. Micro‐CT scanning displayed the epiphyseal arterial network structure and their fine vascular branches in all 12 femoral neck fractures. Blood was supplied from the inferior retinacular artery to the epiphyseal arterial network then to all the fine blood vessels within the femoral head. No statistical differences were observed in femoral heads’ intraosseous artery length densities or volume densities between the normal and femoral neck fracture specimens, while the artery length/volume ratio showed a statistical difference, and the ratio increased from 19 to 46. Micro perfusion of the femoral head by the inferior retinacular arteries is possible and can present the epiphyseal network and their fine arterial branches in pathologic conditions to provide a morphological basis for the study of femoral head disease.     

Metachondromatosis and avascular necrosis of the femoral head: a radiographic and histologic correlation

We report the case histories, radiographic and computed tomographic studies, and histologic findings of two children with metachondromatosis who developed avascular necrosis (AVN) of the femoral ossific nucleus. The first was a 9-year-old boy with involvement of both femoral heads; the second was an 8-year-old girl with involvement of her right femoral head. The changes were associated with either exostoses or enchondromalike lesions of the femoral neck. Interference with the integrity of the lateral epiphyseal vessels by these lesions would explain the avascular changes that occurred. The findings in these cases and other reports associating AVN with skeletal dysplasia should encourage treating physicians to analyze carefully a sudden increase in hip pain or rapid radiographic development of femoral head collapse in a child with a skeletal dysplasia. Recognition of true AVN, in contrast to the gradual evolution of head shape change in typical skeletal dysplasia, may change treatment recommendations and prognosis.     

干细胞移植改善股骨头坏死缺血状态122例临床观察

目的探讨经动脉自体骨髓干细胞（BMSC）和外周血干细胞（PBSC）移植改善股骨头坏死缺血状态的临床疗效。方法2004年7月至2006年12月对122例（211髋）成人缺血性股骨头坏死（ANFH）患者施行自体BMSC或PBSC移植治疗,按国际分期标准（ARCO）分期,设自身前后对照方法进行疗效观察。BMSC组90例和PBSC组32例在DSA下行股骨头供血动脉干细胞移植术,移植后第3、6、12、24个月进行髋关节Harris评分做疗效评价,6个月复查股骨头供血动脉造影观察血管新生情况。每间隔6个月复查影像学变化。结果122例患者随访3～24个月（平均10．2个月）,髋关节疼痛缓解104例（85．1％）,关节功能改善76例（62．0％）,90例（73．9％）行走间距延长。干细胞移植术后6个月,15例患者股骨头供血动脉造影检查见供血动脉较移植前明显增多、增粗,血流速度增快;12～24个月20例股骨头区可见骨质病变获得改善。结论经动脉自体BMSC和PBSC移植方法简便,安全有效,对缺血性股骨头无再次损伤,患者依从性好,是治疗缺血性股骨头坏死的一种新途径。     

单侧穿刺介入治疗股骨头缺血性坏死

目的评价股骨头缺血坏死介入治疗的疗效及方法。方法对48例股骨头缺血坏死患者共70个股骨头采用seldinger技术单侧穿刺股动脉插管,造影观察血液供应情况后,超选择进入到股骨头营养血管如旋股内、外侧动脉,注入溶栓药物、扩血管药物及改善微循环药物,术后再次造影观察对比股骨头供血改变情况,并行治疗前后临床表现与影像学表现对比研究。结果治疗前后血管造影对照显示治疗后血管增多,股骨头染色增强,疼痛症状及关节功能明显改善,影像检查显示骨质不同程度修复。结论股骨头缺血坏死介入治疗是安全有效的方法,能改善重建股骨头局部微循环,促进修复。     

特发性股骨头缺血坏死的病理变化及发病机制探讨

目的：观察特发性股骨头缺血坏死（ANFH）的病理变化，探讨脂肪栓子及微血栓，分坏死原因。方法：34个特发性ANFH的股骨头，采用苏木素－伊红、脂肪、微血栓和弹力纤维染色方法，光镜下观察股骨头内各部位的坏死和修复情况，确定脂肪栓子和微血栓的形态和分布状态。结果：坏死股骨头内骨髓细胞减少，脂肪组织增多，脂肪细胞肥大。血管中有大量脂肪栓子和微血栓，19个股骨头内发现脂肪栓子，21个发现微血栓，在1例中显示骨髓内脂肪滴正从静脉破裂口进入静脉内。结论：脂肪栓塞是ANFH的重要原因，骨髓脂肪滴进入血管可能起动了ANFH并维持其发展。     

采用经导管动脉栓塞术建立猪股骨头缺血性坏死模型

目的探讨经皮穿刺供血动脉栓塞建立猪股骨头缺血性坏死（ANFH）模型的可行性。方法健康杂种家猪20只,随机分为实验组和对照组,每组10只。实验组：采用经皮穿刺插管的方法经右侧股动脉插入5F Cobra导管至左侧股动脉,超选择性插入股骨头供血动脉,用长约500μm的真丝微粒栓塞供血动脉;对照组：仅行左侧髂总动脉造影,不行动脉栓塞。术后2周和4周分别行左侧髋关节X线摄片、CT和MR检查;第4周影像学检查结束后行病理学检查,观察细胞形态,并计算单位面积的骨小梁体积和空缺骨陷窝百分比,对两组影像学和病理学资料进行比较。结果栓塞术后2周,股骨头X线平片无明显异常表现;CT示髋部软组织肿胀,MRI显示髋关节腔内长T2信号。栓塞4周后,X线平片、CT和MRI示实验组股骨头典型缺血性坏死改变;对照组未见明显异常改变。组织病理学检查显示,实验组骨细胞核固缩、深染,骨细胞减少或消失;单位面积的空缺骨陷窝百分比增多,骨小梁体积减少,与对照组比较差异有统计学意义（P〈0.05）。结论采用经皮穿刺股骨头供血动脉栓塞可成功建立猪ANFH模型,并较好地模拟ANFH的临床病理过程。     

带血管蒂髂骨瓣移位治疗股骨颈骨折术后股骨头缺血性坏死

目的 探讨应用带血管蒂髂骨瓣移位治疗股骨颈骨折术后股骨头缺血性坏死(avascular necrosis of femoral head,ANFH)的疗效.方法 2002年6月-2006年12月,采用带血管蒂髂骨瓣移位治疗股骨颈骨折内固定术后ANFH 22例22髋.男18例,女4例;年龄28～48岁,平均37.5岁.左...     

特发性股骨头缺血坏死动脉病变与发病机制探讨

目的 观察特发性股骨头缺血坏死(ANFH)股骨头内的病理变化，分析小动脉损伤在发病机制中的作用。方法 持发性ANFH患者的股骨头共34个，采用苏木素—伊红(HE)染色、脂肪、微血栓和弹力纤维染色方法，观察股骨头内各部位的坏死和修复及小动脉损伤情况。结果 34个股骨头从头内到支持带中均有动脉损伤，小动脉较为普遍，内膜破坏、中膜变性和平滑肌细胞变性坏死，动脉中还出现管壁上的或骨髓内的变性坏死组织，还可见到破碎的小动脉。结论 小动脉损伤是ANFH的重要病理变化，在ANFH发病和发展中可能起到至关重要的作用。     

股骨颈骨折对局部血供的损伤及评估——解剖基础及其临床运用进展

股骨颈骨折内固定的稳定性可在很大程度上通过手术技巧及内固定排布和植入骨替代物等方法获得,但当前医疗技术水平尚无法完全逆转骨折产生的血供损伤。因此,在围手术期,全面评估股骨颈骨折后局部残余血供以避免医源性损伤成为了目前研究的热点。关于股骨颈骨外层面血供的解剖研究相对成熟,其运用主要涉及旋股内侧动脉和支持带动脉的评估,但不同损伤程度的预后需要进一步探索。当前,临床上尚无法直接观察到骨面的滋养孔,但可根据其分布的密集次序、进行合理的术前规划,尽可能保护残存血供,以避免后续股骨头坏死的发生。而骨内血供的解剖基础及临床研究主要聚焦于头颈结合区,以探究股骨头坏死的机制。但关于股骨颈的其它区域骨内血管分布及交联机制仍需要进一步探究。此外,后续研究可根据骨外血管走行、滋养孔分布及骨内血管网的特征建立完善的基于三层次结构综合的血供评估体系,用于辅助股骨颈骨折的治疗。     

股直肌骨瓣移植治疗股骨头缺血性坏死

自1992～1996年作者应用一种新的手术方法治疗股骨头无菌坏死病人26例,该手术方法包括彻底清除坏死骨组织,骨腔内打孔、髂骨骨髓移植和股直肌骨瓣移植,使骨缺血区重新建立血液循环并带入多种成骨效应细胞和骨诱导因素。其中20例病人随访1～4.5年效果满意。该手术可以有效预防坏死股骨头塌陷并可促进缺血区血液循环的形成及新骨再生。作者认为该手术尤其适用于股骨头缺血性坏死Ⅱ、Ⅲ期的患者。     

Methylprednisolone enhances contraction of porcine femoral head epiphyseal arteries

The pathomechanism of steroid-induced femoral head necrosis is thought to be disturbed femoral head blood flow. We hypothesize that methylprednisolone increases vasocontraction of femoral head epiphyseal arteries, thereby reducing femoral head blood flow. Nine immature female domestic pigs were randomly selected from a group of 18 to receive 24-hour methylprednisolone treatment, whereas the nine remaining pigs received the placebo control in a blinded fashion. After sacrifice, lateral epiphyseal artery segments from the femoral heads were mounted as ring preparations on a small vessel myograph. Isometric active tension was measured in relation to cumulating doses of the vasoconstrictors noradrenaline and endothelin-1, and the vasodilator bradykinin. Vasocontraction to noradrenaline was not altered by methylprednisolone. Bradykinin elicited a concentration-dependent vasodilation which was lower in the corticosteroid-treated vessels. Vasoconstriction to endothelin-1 was stronger in the corticosteroid-treated vessels. Our data indicate that methylprednisolone enhances contraction of femoral head lateral epiphyseal arteries and may decrease femoral head blood flow. To our knowledge, this pathomechanic factor in femoral head necrosis has not been described before.     

Deformation and vascular occlusion of the growing rat femoral head induced by mechanical stress

To investigate the effects of mechanical stress on the extent of deformation and decrease of the blood supply to the femoral head in the growing rat, we conducted a histological and microangiographic study, using a custom-made hip-joint loading device. Application of a 1-kg to 3-kg load to the hip joint caused compression not only of the articular cartilage but also of the growth plate of the femoral head. These changes were particularly prominent in the lateral portion of the femoral head. The compression also caused complete occlusion of the lateral epiphyseal arteries, representing the blood supply to the femoral head, at the point of penetration into the epiphyseal cartilage. Our results indicate that the sum of forces during mechanical load application to the hip joint in growing rats acts to deform the cartilage of the lateral side of the femoral head. Our results also indicate the presence of a mechanically weak point in the femoral head which may lead to occlusion of the lateral epiphyseal arteries. Received: November 15, 1999 / Accepted: March 17, 2000     

股骨头缺血坏死介入治疗及近期疗效

目的：探讨介入性治疗股骨头缺血坏死的近期疗效。方法：自2006年至2008年,对28例（男19例,女9例,年龄14～70岁,平均38岁）股骨头缺血坏死患者采用介入插管的方法,超选择进入到股骨头营养血管旋股内外侧动脉和闭孔动脉,造影观察其血液供给情况后,注入溶栓药物、扩血管药物及改善微循环药物,术后再次造影观察对比股骨头供血改变情况;治疗后12～36个月摄X线片观察股骨头骨密度改变情况;并分析其临床症状（疼痛及关节活动度）的改变情况。结果：28例患者治疗前后血管造影对照显示治疗后血管增多,股骨头染色增强,12～36个月后X线片显示病骨密度和形态逐渐恢复或接近正常者占97.2%（35/36）,患髋疼痛程度及关节活动度临床症状明显改善。结论：介入方法治疗股骨头缺血坏死是一种简便、无痛苦、安全、疗效可靠的治疗方法,能在临床上广泛应用。     

Avascular necrosis and the blood supply of the femoral head

Postmortem femoral artery perfusion revealed abnormalities in the femoral head pattern of vessels in steroid-treated renal transplant patients as compared with controls. Degenerative changes were found in some of the arteries and arterioles of the hip capsule and femoral head in the renal transplant patients. Two of these patients' femoral heads showed microfocal avascular necrosis. Although high-dose steroids were used in these patients, none had suffered clinically from hip disease while alive. These findings suggest the possibility that local arterial disease may be involved in the pathogenesis of avascular necrosis.     

Fracture of the femoral neck. II. Relative importance of primary vascular damage and surgical procedure for the development of necrosis of the femoral head

The opinion is widely held that interruption of the arterial flow through the retinacular arteries to the femoral head is the main cause of avascular necrosis after fracture of the neck. In this study the state of the vascular supply to the femoral head was assessed--prior to osteosynthesis--by means of intramedullary pressure measurements in the femoral head and neck in 72 patients with medial neck fractures. The patients were followed 2 or 3 years or until avascular necrosis became evident. The relative importance of primary avascularity and surgical technique for the development of necrosis suggests that damage to the retinacular arteries may not be the single decisive factor in the pathogenesis of femoral head necrosis. Proper fracture reduction with extensive contact between the cancellous bone surfaces and stable fixation seemed to be more important, probably because they offer the best possibilities for re-establishment of transosseous blood flow across the fracture site.