不同方法治疗老年股骨粗隆间骨折的临床疗效评估

目的 对比分析不同方法治疗老年股骨粗隆间骨折的临床疗效及其安全性.方法 对128例股骨粗隆间骨折分别应用PFNA、DHS、Gamma钉内固定及人工股骨头置换术治疗.结果 127例获随访3～24个月,平均16个月.人工股骨头置换组在切口长度、手术时间、出血量等方面与PFNA、Gamma钉组差异有统计学意义(P＜0.05),髓内固定组创伤小、手术时间短、出血量少,与DHS组差异无统计学意义(P＞0.05).结论 PFNA、DHS、Gamma钉内固定术及人工股骨头置换术均是治疗老年股骨粗隆间骨折的有效方法,对高龄患者行人工股骨头置换术可早期下地活动,减少严重卧床并发症.     

不同手术方法治疗老年股骨粗隆间骨折疗效分析

目的比较动力髋螺钉(DHS)、解剖型锁定钛板(LCP)内固定和加长柄双极人工股骨头置换术治疗老年股骨粗隆间骨折的疗效。方法 454例老年股骨粗隆间骨折采用DHS内固定182例,LCP内固定201例,人工股骨头置换71例。结果 DHS、LCP、人工股骨头置换组手术时间相当,差异无统计学意义(P>0.05);内固定组(DHS、LCP组)术中出血量、卧床时间相当,差异无统计学意义(P>0.05),但术中出血量少于人工股骨头置换组,卧床时间明显长于人工股骨头置换组,差异均有统计学意义(P<0.05);末次随访Harris评分优良率DHS组明显低于LCP、人工股骨头置换组,差异均有统计学意义(P<0.05)。结论 LCP是治疗老年股骨粗隆间骨折比较理想的内固定方式,人工股骨头置换术也是一种正确的选择,但适用于75岁以上不稳定且合并重度骨质疏松骨折。     

股骨头置换与DHS内固定术治疗老年人股骨粗隆间粉碎性骨折的前瞻性对比研究

目的 前瞻性研究比较人工股骨头置换术与DHS内固定治疗老年股骨粗隆间粉碎性骨折的预后.评价加长骨水泥型股骨柄股骨头置换治疗股骨粗隆间粉碎性骨折的效果.方法 自2001年12月～2007年12月,共收治老年股骨粗隆间粉碎性骨折109例,男59例,女50例,年龄70～94岁,平均80.7岁.随机选择股骨头置换或DHS内固定,人工股骨头置换术48例(置换组),DHS内固定61例(内固定组).骨折类型按Evens分型:Ⅲ型54例,Ⅳ型45例,Ⅴ型10例.随访时比较两组治疗方法的住院天数、术中X线暴露次数、手术时间、出血量、术后卧床时间、并发症发生率、髋关节功能、日常生活能力和Barthel生活质量指数.结果 本组87例得到随访,时间3个月～5年,平均15.7个月,内固定失效后有2例行人工股骨头置换术治疗.内固定组在术中出血量方面有优势外,置换组在住院天数、术中X线暴露次数、术后卧床时间、并发症发生率、髋关节功能、Barthel生活质量指数等方面与内固定组比较有显著优势(P<0.05).结论 人工股骨头置换术疗效较好,生活质量较高,可以成为治疗老年股骨粗隆间粉碎性骨折的主要方法.     

四种手术方法治疗老年股骨粗隆间骨折的疗效研究

目的 探讨4种不同的手术方法治疗老年股骨粗隆间骨折的疗效。方法 回顾性分析2005年1月至2013年12月间在本组接受手术治疗的132例老年股骨粗隆间骨折患者,其中动力髋螺钉(DHS)组41例,股骨近端防旋髓内钉(PFNA)组35例,Gamma钉组30例,人工股骨头置换术组26例。对其手术时间、手术出血量、术后下地负重时间、患髋功能恢复及术后并发症等作比较分析。结果 132例患者中127例获得随访(DHS组38例,PFNA组33例,Gamma钉组30例,人工股骨头置换术组26例),随访时间12~72个月,平均28.4个月。人工股骨头置换术在手术后下地负重时间短于其他3组(P<0.01);PFNA手术时间、术中出血量少于其他3组(P<0.01);1年后患髋功能4组无统计学差异(P>0.05)。结论 DHS、PFNA、Gamma钉和人工股骨头置换术4种手术方法均能有效治疗老年股骨粗隆间骨折。PFNA更适合于更需要短手术时间的手术耐受力差的患者;人工股骨头置换术适合于更需要早期活动以减少并发症的患者。     

人工髋关节置换术与DHS内固定治疗高龄不稳定股骨粗隆间骨折的疗效对比

目的比较人工髋关节置换术与动力髋螺钉(DHS)内固定治疗高龄不稳定股骨粗隆间骨折的疗效。方法 121例高龄不稳定股骨粗隆间骨折中52例行人工髋关节置换术,69例采用DHS内固定。结果人工髋关节置换组手术时间、术中出血量、术后开始负重时间及术后并发症发生率上均明显小于DHS组,差异有统计学意义(P<0.05)。结论对于高龄不稳定股骨粗隆间骨折,除DHS内固定治疗外,人工髋关节置换术也是一种正确的选择。     

DHS内固定与组合式外固定架治疗高龄股骨粗隆间骨折的疗效分析

目的比较动力髋螺钉(DHS)内固定与组合式外固定架治疗高龄股骨粗隆间骨折的临床疗效。方法 64例高龄股骨粗隆间骨折采用DHS内固定41例(A组),组合式外固定架固定23例(B组)。结果 A、B组在术后卧床时间、骨折愈合时间和术后5个月Harris评分方面差异无统计学意义(P>0.05);但B组手术时间、术中出血量和术后住院时间少于A组。结论组合式外固定架治疗高龄股骨粗隆间骨折比DHS更有优势,具有操作简单、创伤小、固定稳定等优点。     

骨水泥型股骨头置换与DHS治疗高龄股骨粗隆间骨折的疗效观察

目的 通过分析骨水泥型人工股骨头置换术与DHS内固定术治疗高龄股骨粗隆间骨折的疗效,前瞻性评价骨水泥型人工股骨头置换术治疗高龄股骨粗隆间骨折的效果.方法 对59例高龄股骨粗隆间骨折,分别用人工股骨头置换术与DHS内固定术治疗.结果 58例得到平均1.5年的随访.两组患者术后并发症发生率比较差异有显著性意义(0.025相似文献   

下肢

双支撑骨柱移植术治疗股骨头坏死的远期疗效分析；MIPPO结合DHS治疗老年股骨粗隆间骨折；14例儿童股骨颈骨折疗效分析；DHS治疗股骨粗隆间骨折术后切割发生原因分析；人工股骨头置换与内固定治疗老年股骨转子间骨折疗效比较     

PFNA与人工股骨头置换术治疗高龄股骨粗隆间骨折的比较

目的探讨股骨近端防旋髓内钉(PFNA)与人工股骨头置换术治疗老年股骨粗隆间骨折的疗效。方法 68例老年股骨粗隆间骨折分别采用PFNA内固定(A组,37例)和人工股骨头置换术(B组,31例)治疗,对比两组手术时间、出血量及髋关节功能评分方面的疗效。结果两组手术时间差异无统计学意义(P>0.05);A组出血量、Harris功能评分少于B组,差异有统计学意义(P<0.05)。结论 PFNA内固定与人工股骨头置换术治疗高龄股骨粗隆间骨折各有优势,严格掌握手术适应证后均可以取得满意的疗效。     

人工股骨头置换与DHS治疗高龄股骨粗隆间骨折

目的通过比较分析人工股骨头置换术与DHS内固定术治疗高龄股骨粗隆间粉碎骨折的疗效及预后，前瞻性评价加长柄骨水泥型人工股骨头置换术治疗高龄股骨粗隆唰粉碎骨折的效果。方法1999年6月至2005年6月间我科收治高龄股骨粗隆间骨折120例患者，男67例。女j3例。年龄75～94岁，平均81．4岁。120例分别用人工股骨头置换术与DHS内固定术治疗，其中加长柄骨水泥型人工股骨头置换术50例，DHS内固定术70例。骨折类型按Evans分型。Ⅲ型58例。Ⅳ型62例。结果110例患者得到近期随访。平均随访时间1．5年．10例DHS内固定患者失访。DHS内固定组有6例手术失败后，均重新用加长柄骨水泥人工股骨头置换术治疗。加长柄骨水泥人工股骨头置换术50例．术后随访期间患者仅有1例并发肺部感染。其余疗效满意。术后并发症两组患者比较差异有显著性意义（P〈0．05）。结论人工股骨头置换术将成为治疗高龄股骨粗隆间不稳定骨折的主要方法。     

杭州健康女性定量骨超声测定原发性骨质疏松

目的 评价杭州健康女性骨超声速度(SOS)值随增龄减少和骨质疏松患病率，建立杭州地区女性骨超声速度值参考数据库。方法 定量超声法测定1208例杭州地区健康女性桡骨远端(RAD)，第3指骨近节(PLX)，第V跖骨(MTR)和胫骨中段(TIB)的超声速度值。结果 RAD、PLX、MTR和TIBSOS峰值(Peak of SOS)均出现在40-45岁，TJB的SOS峰值出现在35—40岁，此后随年龄增长而下降。绝经后妇女在绝经后早期和晚期各有1个SOS快速减少期，前见于桡骨近端，平均年减少率为2．4％，后见于胫骨中段，平均年减少率为1．8％。各部位骨SOS累积减少率随年龄增长而增加，到85岁4部位累积减少为13％-18％。60岁以后骨质疏松性症(OP)检出率为45％-70％，OP检出率以桡骨远端最高，60-70岁平均为67％，第3指骨近端次之约50％，胫骨中段最低为36％；75岁以后分别为70％，65％和45％。结论 全身各部位骨超声速度值到达峰值的年龄不同，峰值也各有差异。绝经后妇女骨超声速度值随年龄增加减少较快，应予激素和补钙治疗，桡骨远端为本地区SOS检测和OP检出的敏感部位。     

Importance of echocardiography in prognosis of surgical outcomes in cholecystitis in elderly patients

The authors propose to use more often echocardiography (EchoCG) in examination of elderly (over 60 years) of age patients with cholecystitis that permits to increase surgical activity to 92.4%. Left ventricular ejection fraction is the most informative. When this fraction is lower than 45% surgery must be recommended on vital indications only. EchoCG was used in 155 patients with cholecystitis, 131 of them were operated. 2 (1.52%) patients died due to acute cardio-vascular insufficiency and pulmonary artery thromboembolism.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

目的 评价脊髓胶质细胞在小鼠骨癌痛形成中的作用.方法 健康雄性C3H/He小鼠40只,周龄8～10周,体重18～22 g,随机分为4组(n=10):假手术组(S组)、骨癌痛组(B组)、PBS组(P组)和米诺环素组(M组).S组跟骨骨髓腔内注射PBS 10 μl;余3组跟骨骨髓腔内注射含2×105个骨纤维肉瘤细胞的PBS 10 μl制备骨癌痛模型,于造模前即刻开始PBS组鞘内注射PBS 5μl,M组鞘内注射米诺环素(用PBS溶解为0.2 mmol/L)5μl,1次/d,连续11 d.于造模前1 d、造模后即刻、3、5、7、9、11 d时测定机械痛阈;于造模后3、7、9、11 d机械痛阈测定结束后测定冷痛阈.痛阈测定结束后处死小鼠,取脊髓组织,测定神经胶质纤维酸性蛋白(GFAP)和CD11b的表达水平.结果 与S组比较,B组和P组造模后3-11 d时、M组造模后3、5 d时机械痛阈升高,B组、P组和M组造模后7～11 d时冷痛阈升高,脊髓CD11b和GFAP表达上调(P<0.05).与B组比较,M组造模后3-11 d时机械痛阈降低,造模后7-11 d时冷痛阈降低,脊髓CD11b和GFAP表达下调(P<0.05).结论 脊髓胶质细胞(星形胶质细胞和小胶质细胞)的激活参与了小鼠骨癌痛的形成.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.     

脊髓胶质细胞在小鼠骨癌痛形成中的作用

Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.