两种切口开放复位内固定治疗跟骨骨折比较

[目的]探讨改良跗骨窦切口与传统L形切口对SandersⅢ、Ⅳ型跟骨骨折患者功能及术后并发症的影响。[方法]回顾性分析本院62例SandersⅢ、Ⅳ型跟骨骨折患者,根据手术方式分为改良跗骨窦切口组30例和传统外侧L形切口组32例,记录手术时间、出血量、骨愈合时间术后早晚期并发症发生率,对比术前、术后12个月B?hler角及Gissane角及Maryland足部功能评分。[结果]跗骨窦组切口长度及术后早期并发症发生率低于L形切口组(P0.05),两手术时间、术中出血量、骨折愈合时间及足部功能评分及术后12个月影像学参数差异均无统计学意义(P0.05)。[结论]改良跗骨窦切口与传统外侧L形切口均可有效改善SandersⅢ、Ⅳ跟骨骨折患者足部功能,相对于后者,前者具有手术切口小及术后并发症低的优势。     

跟外侧动脉损伤与跟骨骨折术后皮瓣坏死的关系(附11例报告)

目的 研究跟外侧动脉损伤与跟骨骨折术后皮瓣坏死的关系,为手术切口的改良提供依据.方法 收治跟骨骨折手术后皮瓣坏死11例,对于术中已经明确跟外侧动脉损伤的病例,术后观察皮瓣血运;就诊时已经发生皮瓣坏死的病例再次手术修复时,术前超声多普勒血管仪探测跟外侧动脉血流:术中对跟外侧动脉及伴行神经进行显微解剖,确认其损伤情况.结果 11例中,10例跟外侧动脉完全断裂,1例跟外侧动脉闭塞,8例腓肠神经终末支损伤.结论 跟骨骨折外侧"L"形切口术后皮瓣坏死与跟外侧动脉损伤有直接的关系.     

改良外侧切口治疗跟骨关节内骨折

[目的]探讨跟骨外侧改良切口治疗跟骨关节内骨折的疗效。[方法]比较跟骨外侧常规切口和改良切口,对手术时间、骨折愈合时间、切口并发症发生率做统计学处理。[结果]两者切口并发症发生率差异有统计学意义。[结论]改良外侧切口术后皮缘坏死率降低,值得推广。     

小切口与“L”型切口治疗跟骨骨折疗效及并发症的对比研究

[目的]对比研究跟骨骨折在小切口和"L"型切口术后疗效及并发症。[方法]2007年10月～2011年6月间,本院收治跟骨骨折病例71例,其中SandersⅡ型41例,Ⅲ型30例,分为小切口组(A组)和"L型"切口组(B组),A组SandersⅡ型21例,B组SandersⅡ型20例,A、B组SandersⅢ型各15例。小切口手术方法采用直视下复位距下关节,撬拨复位,观察跟骨长度、宽度、高度、Bolher角及Gissane角,螺钉固定;"L"型切口手术方法采用标准AO切口,直接复位距下关节面,植骨加钢板固定。术后随访评分参照美国骨科足与踝关节协会的足踝临床后足评分系统(AOFAS)。[结果]平均随访时间35个月(18～68个月),术后两组间Bolher角及Gissane角均无显著性差异(P>0.05),两组较术前有明显好转(P<0.05)。SandersⅡ型跟骨骨折A组AOFAS后足平均评分(88.3±7.6)分,高于B组(81.4±5.3)分,具有统计学差异(P<0.05)。SandersⅢ型跟骨骨折A组与B组无统计学差异(P>0.05)。SandersⅢ型跟骨骨折术后AOFAS评分(74.4±6.7)分,低于SandersⅡ型跟骨骨折评分(84.6±4.3)分,且具有统计学差异(P<0.05)。采用小切口术后并发症为皮肤浅表感染1例换药后恢复。"L"型切口术后6例出现深部感染,其中2例形成慢性跟骨骨髓炎,4例局部转移皮瓣后治愈。[结论]SandersⅡ型跟骨骨折采用小切口术后疗效优于"L型"切口,而SandersⅢ型跟骨骨折术后疗效与手术切口及方式无关。     

改良外侧L切口加植骨锁定钢板内固定治疗跟骨关节内骨折

目的探讨改良外侧L切口加植骨锁定钢板内固定治疗跟骨关节内骨折的疗效。方法对44例(52足)跟骨骨折行改良外侧L切口加植骨结合锁定钢板治疗。结果随访8~39个月,术后Maryland足部评分系统评分优31例,良9例,一般4例,优良率90.9%,无皮瓣坏死。结论改良外侧L切口加植骨锁定钢板内固定是治疗跟骨关节内骨折的有效方法。     

改良外侧切口钢板内固定治疗跟骨关节内骨折

[目的]探讨改良外侧切口治疗跟骨关节内骨折的临床疗效.[方法]采用回顾性研究,自2006年1月～ 2009年1月,对88足跟骨关节内骨折采用手术治疗,其中48足采用传统跟骨外侧“L”形切口,40足采用改良外侧切口.对两者手术时间、切口长度、术后Bohler角、切口并发症发生率及AOFAS评分做统计学处理.[结果]两者手术时间、切口长度及切口并发症发生率比较P＜0.05,有统计学意义,术后Bohler角及AOFAS评分P＞0.05,无统计学意义.[结论]改良外侧切口钢板固定治疗跟骨关节内骨折是一种有效的方法,术后并发症少.     

改良微创切口内固定治疗跟骨骨折的疗效

目的 探讨改良微创切口内固定治疗跟骨骨折的临床疗效.方法 将23例跟骨骨折患者根据手术切口不同分为传统组(采用传统外侧L形切口内固定治疗,12例)和改良组(采用改良微创切口内固定治疗,11例).记录两组手术时间、切口总长度、术中出血量及术后切口并发症情况,采用AOFAS踝-后足评分标准评价临床疗效.结果 患者均获得随访...     

改良经跗骨窦小切口复位钢板内固定治疗跟骨骨折的效果观察

目的探讨改良经跗骨窦小切口复位钢板内固定治疗跟骨骨折的效果。方法选取2017-06—2019-02间在叶县人民医院接受切开复位钢板内固定术的76例跟骨骨折患者,将行传统外侧L形切口的患者作为传统组,将行改良经跗骨窦小切口的患者作为改良组,各38例。回顾性分析患者的临床资料。结果2组手术时间和并发症发生率差异无统计学意义(P>0.05)。改良组术中出血量、骨折愈合时间及患足功能优良率等指标,均优于传统组,差异均有统计学意义(P<0.05)。结论改良经跗骨窦小切口复位钢板内固定术治疗跟骨骨折,可减少术中出血,促进骨折愈合。     

跟骨外侧直切口解剖钢板内固定治疗跟骨关节内骨折

[目的]通过对跟骨外侧直切口治疗跟骨关节内骨折的疗效观察,探讨该手术方法的优势.[方法]1999年1月-2008年5月,对70例87足跟骨关节内骨折行手术治疗,采用跟骨外侧直切口,切口位于足背与足底皮肤移行部上方1 cm处,向前达跟骨前部近跟骰关节,向后达跟骨结节前方,腓肠外侧皮神经及腓骨长短肌腱被保护于近端皮瓣中并牵开,沿骨膜向上锐性剥离显露距下关节外侧,观察骨折情况及Gissane角的改变.将骨折复位,恢复距下关节解剖形态及足弓,克氏针临时固定,选择合适的可塑性跟骨解剖钛钢板自切口内置入并调整,C型臂X线机下观察位置良好,分别用松质骨螺钉经过跟骨板钉孔将跟骨距下关节后外侧骨折块与跟骨载距突、跟骨粗隆部及跟骨前部固定,骨缺损部植入自体或异体骨填充.[结果]70例87足全部获得随访,随访时间8～24个月,术后并发症发生率12.6%.根据Maryland足部评分标准,优良率86.2%.[结论]该手术创伤小,血运破坏少,术后并发症发生率低,是治疗跟骨骨折的一种有效方法.     

跟骨骨折内固定术后负压引流与传统引流切口愈合的临床观察

目的比较跟骨骨折切开复位内固定术后手雷式负压引流与传统引流后切口愈合情况。方法回顾性分析自2008-01—2012-12采用跟骨外侧L形切口行切开复位内固定治疗的跟骨骨折58例（64足）,术后采用手雷式负压引流31足,传统引流33足。结果 58例均获随访12-24个月,平均18个月。传统引流组术后28足切口一期愈合,5足出现创缘皮肤坏死,切口一期愈合率84.8%;负压引流组术后30足切口一期愈合,1足切口愈合不良,一期愈合率96.8%。结论跟骨骨折切开复位内固定术后使用手雷式负压引流较传统引流切口愈合情况较好。     

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.     

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。     

中脑导水管周围灰质小胶质细胞活化在大鼠神经病理性痛中的作用

目的 评价中脑导水管周围灰质小胶质细胞活化在大鼠神经病理性痛中的作用.方法 雄性SD大鼠176只,体重200 ～ 250 g,9周龄,采用随机数字法,将其分为4组:假手术组(S组,n=40)、神经病理性痛组(NP组,n=40)、生理盐水组(NS组,n=48)和米诺环素组(M组,n=48).NP组、NS组和M组采用慢性坐骨神经缩窄性损伤法制备大鼠神经病理性痛模型;S组仅暴露坐骨神经,而不结扎.术后第7天时,NS组和M组分别于中脑导水管周围灰质的腹外侧区注射生理盐水或米诺环素0.5μl.取8只大鼠,分别于术前1 d(T0)、术后第3天(T1)、第7天给药前30 min(T2)、第7天给药后30 min(T3)、第14天(T4)和第21天(T5)时测定机械痛阈.于T1-5时各处死8只大鼠,取脑组织,行小胶质细胞计数.结果 与S组比较,NP组、NS组和M组T1-5时机械痛阈降低,小胶质细胞计数升高(P＜0.05);NP组和NS组各时点机械痛阈和小胶质细胞计数差异无统计学意义(P＞0.05);与NP组和NS组比较,M组T3时机械痛阈升高,小胶质细胞计数降低(P＜0.05).结论 中脑导水管周围灰质小胶质细胞的活化参与了大鼠神经病理性痛中的形成与维持.     

沈阳男性髋部骨折多于女性原因探讨

为找出沈阳地区髋部骨折发生男性多于女性的原因，探索该病在不发达国家或地区的流行特点，我们再次通过查阅病例记录，对沈阳市１９９４年５０岁以上人口的部分髋部骨折病发生的原因进行了较详细的调查分析。共调查分析２６６髋部骨折病例，其中男１６３例，女１０３例。损伤原因记为单纯摔倒（滑倒或绊倒）、骑自行车摔倒、自行车撞倒、机动车事故和高位跌下（滚楼梯或从较高位置掉下）。结果表明：男女在髋部骨折伤因构成上有差别（Ｐ＝０．００４）。女性髋部骨折的大多数（７０％）是由单纯摔倒引起，而在男性则不足一半（４９％），即男性髋部骨折的一半以上不是由于单纯摔倒而是由各种意外事故造成的（Ｐ＝０．０００８）。在各种意外事故中，男性骑自行车摔倒引起骨折的频率（２８％）明显高于女性（１０％）。除了骑自行车摔倒外，男性由自行车撞倒和高位跌下引起骨折的频率稍高于女性，但无太大差别。机动车事故造成骨折的频率男女基本一致。此结果在一定的程度上说明，１９９４年沈阳５０岁以上的男性髋部骨折发病率高是由于男性发生的各种意外事故多，尤其是骑自行车引起的事故造成的。     

脊髓胶质细胞在大鼠炎性痛形成中的作用

目的 评价脊髓胶质细胞在大鼠炎性痛形成中的作用.方法 清洁Ⅱ级成年雄性SD大鼠,体重180～220 g,取蛛网膜下腔置管成功的大鼠65只,随机分为5组(n=13),生理盐水组(NS组):右后肢踝关节外侧皮下注射NS 50μl;炎性痛组(IP组):采用右后肢踝关节外侧皮下注射完全弗氏佐剂50μl的方法制备炎性痛模型;氟代柠檬酸组(FC组):经蛛网膜下腔导管注射FC 1 nmol/10 μl,15 min后右后肢踝关节外侧皮下注射NS 50 μl;NS+IP组:经蛛网膜下腔导管注射NS 10 μl,15 min后制备炎性痛模型;FC+IP组:经蛛网膜下腔导管注射FC 1 nmol/10 μ,15 min后制备炎性痛模型.于模型制备前2 d(T_0)、皮下注射药物前(T_1)和注射药物后2、4、6、8、10、12、24、26 h(T_(2～9))时测定机械缩足阈值(MWT)和热缩足潜伏期(TWL).皮下注射药物后8 h时采用免疫组化法测定脊髓背角星形胶质细胞标记物(GFAP)和小胶质细胞标记物(OX-42)的表达水平.结果 与NS组比较,IP组和NS+IP组T_(3～9)时MWT和TWL降低,FC+IP组T_(3～9)时MWT降低,T_(8,9)时TWL降低,IP组、NS+EP组和FC+EP组脊髓GFAP和OX-42的表达水平均上调(P<0.05);与IP组比较,FC组T_(3～9)时MWT和TWL升高,FC+IP组T_(3～7)时MWT和TWL升高,2组脊髓GFAP和OX-42的表达水平均下调(P<0.05或0.01).结论 脊髓胶质细胞的活化参与了大鼠炎性痛的形成.     

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.     

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.