肝移植术后并发桥脑中央髓鞘溶解症三例

目的 总结肝移植术后并发桥脑中央髓鞘溶解症(CPM)的诊治体会.方法 3例肝移植受者术后并发CPM,术前血清Na+明显偏低,分别为124 mmol/L、I 19 mmol/L和119 mmol/L,术后出现自主言语较少、自主动作变缓慢、吐词不清、昏迷等症状,经头颅磁共振(MRI)检查,例1主要表现为闭锁综合征,例2、3主要表现为昏迷.例I采取静脉给予大剂量丙种球蛋白治疗,例2采取高压氧治疗,例3未能进行针对性治疗.结果 3例患者术后均出现血钠快速升高,幅度达22～34mmol/L.例1术后随访3个月,基本恢复正常,但行动反应仍迟缓,肝功能正常.例2术后随访6个月,患者仍呈昏迷状态,肝功能良好.例3术后意识障碍逐渐加重,后死于肺部感染.结论CPM是肝移植术后的严重并发症,尚无有效的治疗方法 ,患者的预后差.     

体外静脉转流技术对肝移植患者术后早期肾功能的影响

肾功能损害甚至肾功能衰竭是肝移植术后常见的并发症。肝移植术中采用体外静脉．静脉转流技术(veno-venous bypass，V-VB)对患者肾脏功能的保护作用仍然存在争议。故本研究回顾性分析我院行原位肝移植手术病人104例，探讨采用体外静脉．静脉转流技术对肝移植术后早期肾功能的影响。     

肝移植术后桥脑中央髓鞘溶解症5例报告

目的探讨肝移植术后并发桥脑中央髓鞘溶解症(central pontine myelinolysis,CPM)的诊断和治疗。方法回顾性分析5例肝移植后并发CPM的临床资料和治疗经过。结果5例CPM患者均为男性,平均年龄49岁。原发病为慢性重症肝炎4例,原发性肝细胞癌1例,其中3例并发Ⅲ～Ⅳ度肝性脑病,3例并发严重肺部感染。CPM发生于术后4～13 d,平均发生时间为术后7 d,临床表现主要为闭锁综合征、肢体痉挛性瘫痪、缄默等。术前有明显低钠血症患者4例,发病时他克莫司血药浓度正常者4例,明显增高者1例。5例患者均经头颅磁共振成像检查诊断为CPM。采取病因治疗和对症处理相结合的治疗措施,重点防治并发症,其中两例由于早期合并水电解质、酸碱平衡紊乱,给予持续的肾脏替代治疗(continuous renal replacement therapy,CRRT)。本组患者3例死亡,2例存活,但均存在神经系统损害。结论肝移植后并发CPM的原因是多方面的,预后差,尚无有效的治疗方法,早期发现并积极防治并发症是降低病死率的主要措施。     

成人活体肝移植术后肝静脉狭窄的诊断与介入治疗:2例报道并文献复习

肝静脉狭窄是肝移植术后的一种严重并发症,在活体肝移植术后发生率较高。本文通过回顾性分析2例成人活体肝移植术后肝静脉狭窄患者的相关资料,结合国内外相关文献,探讨肝移植术后肝静脉狭窄的诊断方法及介入治疗效果。经皮肝静脉造影术可确诊肝静脉流出道梗阻,经皮经肝球囊、支架成形术是治疗活体肝移植术后早期肝静脉狭窄的一种安全、简便、有效的方法。     

肝移植后并发桥脑中央髓鞘溶解症三例

目的总结肝移植后并发桥脑中央髓鞘溶解症(CPM)的诊治体会。方法回顾性分析3例肝移植后并发CPM的临床资料。结果例1于术后第18d出现定向障碍、四肢抽搐,随之昏迷,症状出现前后血电解质在正常范围;例2于术后第6d出现昏迷,有明显的低钠血症;例3于术后第7d出现意识模糊、被害妄想,随之昏迷,症状出现前后血电解质在正常范围。3例患者均经头颅磁共振检查诊断为CPM,虽经积极治疗,但最后均死亡。结论肝移植后并发CPM的原因是多方面的,其预后差,病死率高;磁共振是诊断CPM的首选方法。     

肝移植术后并发桥脑中央髓鞘溶解症三例

肝移植术后并发桥脑中央髓鞘溶解症(CPM)的发病率约为5%～10%,明显高于一般人群(0.16%～5.8%)[1,2].其发病原因复杂,治疗棘手,死亡率高[3].我院肝移植中心自2003年4月至2008年1月,共进行同种原位肝移植术115例次.其中3例患者术后并发CPM,发病率为2.6%(3/115).3例患者经治疗后,好转1例,死亡2例.现报道如下.     

原位肝移植术后早期肾功能损害的原因分析

肝移植患者术后肾功能异常是其常见而严重的并发症,是影响该类患者预后的重要因素[1]。本研究通过回顾性分析62例非静脉-静脉转流下原位肝移植病例的临床资料,以筛选出肝移植术后影响早期肾功能的危险因素,为进一步指导肝移植术的麻醉管理提供参考。     

附加腔静脉成形的背驮式原位肝移植术

目的　探讨腔静脉成形术在背驮式原位肝移植中的应用价值及在防止移植肝流出道阻塞并发症中的作用。方法　 3例终末期肝病病人选为肝移植受者。供肝的下腔静脉及受体的肝后下腔静脉 (包括肝静脉 )均作了成形术 ,在单独股 -腋静脉转流术下行改良背驮式肝移植术。结果　 3例病人术中均较平稳 ,手术时间和无肝期缩短 ,出血量减少 ,术后肝功能恢复快 ,恢复顺利 ,无并发症发生。结论　腔静脉成形术可防止背驮式肝移植肝静脉流出道阻塞 ,术中对受体的血流动力学干扰小 ,并可缩短无肝期和减少腔静脉梗阻并发症的发生。     

肝移植术后脑桥中央髓鞘溶解症四例诊治

目的 探讨肝移植术后并发脑桥中央髓鞘溶解症(central pontine myelinolysis)的原因及诊治体会.方法 回顾性分析4例肝移植术后并发CPM患者的临床资料和诊治经过.结果 4例患者中有两例存在手术前后24 h内血钠明显升高史,另2例术后血钠无明显升高.分别于术后9、7、5、10 d发病,分别以头痛、面瘫、失语、双侧瞳孔不等大为首发症状.均经头颅磁共振(MRI)确诊为CPM,予对症支持、激素、血浆置换等治疗后1例痊愈,1例死亡,另2例遗留面瘫、肌力减弱、构音障碍等后遗症.结论 肝移植是CPM的高危因素,围手术期多种病理生理因素促使其发生发展,应以预防为主.其临床表现多样.提高临床警惕和反复的MRI检查是CPM早期诊断的关键.     

活体肝移植肝静脉流出道狭窄的诊断与治疗

肝静脉流出道狭窄是肝移植术后较为罕见的并发症,在活体肝移植中发生率为2％～4％。2006年6月至2010年5月,解放军总医院2例接受右肝活体肝移植的患者术后出现肝静脉流出道狭窄,接受保守治疗或介入球囊扩张成形术治疗。术后疗效显示：保守治疗肝静脉流出道狭窄具有一定的风险性;而介入肝静脉造影、球囊扩张以及金属支架置入能有效诊断和治疗肝静脉流出道狭窄。     

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.