KTQ质量认证体系在神经科ICU备用药品规范化管理中的应用

目的加强神经科ICU备用药品规范化管理,确保患者临床用药安全。方法采用KTQ认证体系中的PDCA质量管理方式对神经科ICU备用药品进行规范化管理。结果随着药品规范化管理的持续推进,病区药品检查得分逐月提高,护士对药品管理的满意率达96.30%~100%。结论通过对病区备用药品的规范化管理,有效地提高了病区备用药品的管理质量及临床用药的准确性,确保了临床用药安全。     

病区备用药品的安全管理

目的对病区备用药品进行有效的安全管理,堵塞药品管理漏洞,防范用药错误发生,保证患者用药安全。方法健全病区备用药品管理制度;加强药品安全管理知识培训;标识醒目并分类管理病区备用药品等。结果病区药品管理不良事件发生率较实施前显著下降(P0.05,P0.01)。结论加强病区备用药品的安全管理,能提升病区药品管理水平,降低药品不安全隐患,保障患者用药安全。     

病区备用药品的安全管理

目的对病区备用药品进行有效的安全管理,堵塞药品管理漏洞,防范用药错误发生,保证患者用药安全。方法健全病区备用药品管理制度;加强药品安全管理知识培训;标识醒目并分类管理病区备用药品等。结果病区药品管理不良事件发生率较实施前显著下降（P〈0.05,P〈0.01）。结论加强病区备用药品的安全管理,能提升病区药品管理水平,降低药品不安全隐患,保障患者用药安全。     

老年病房备用药品的集束化管理

目的探讨集束化管理方法提高老年病房备用药品管理水平的作用。方法对老年病房备用药品管理现状进行调查,分析药品管理中存在的问题,针对问题制定集束化管理策略方案并实施,包括确定老年科常备药和亚专科备药管理目录,加强特殊药品管理,统一制作药品标识,落实药物效期管理等。结果老年病房药品管理质控得分由实施前的(90.71±0.69)分提升至(95.00±1.52)分(P0.05)。结论运用集束化管理策略加强病区备用药品的规范管理,能提升病区药品管理水平,降低药品安全隐患,保障患者用药安全。     

外科病区高危药品的规范管理

目的规范病区高危药品管理方法,提高临床护理用药安全性。方法在病区成立专项小组,在专业药师的指导下制定病区高危药品目录,完善管理制度和使用流程,对护士实行高危药品知识培训。结果护士高危药品知识知晓率、医生满意率显著提高(P0.05,P0.01);临床使用高危药品的不良事件由管理前的11例次/年降至4例次/年。结论规范病区高危药品管理可有效降低高危药品风险,保障临床用药安全。     

应用“五常法”管理科室药品的体会

目的:探讨科室药品管理,提高工作效率及用药安全.方法:对应用“五常法”管理科室药品的经验进行总结.结果:通过应用“五常法”管理科室药品,提高了工作效率,确保了用药安全.     

药品失效表在病区抢救车药品管理中的应用

病区抢救车中备用药品是从病区药房、输液库房领回的药品,若管理或使用不当,将会造成不良后果.笔者在对药品进行管理的过程中发现,由于部分药品应用频次相对较低,经补充后的药品又因厂家、批号不同,有效期也不同,且药品因无原包装其有效期无法确定.为此,笔者设计制作了药品失效表,经临床应用效果满意,报告如下.     

病区药品管理中存在的问题及改进措施

目的 提高病区药品管理质量,保证用药安全.方法 针对我院病区药品管理中存在的药物混放、过期失效、标识不清、无专人管理、储存不当等问题.采取组织学习.掌握药品管理知识、建立有效期登记本、按照药品储存要求严格存放、专人管理,严格交班、固定基数,及时更新等管理改进措施.实施1年后评价效果.结果 改进管理措施后药物混放、过期失效、标识不清、无专人管理、储存不当5项问题发生率显著低于改进前(P＜0.05,P＜0.01).结论 针对性的改进措施可有效提高病区药品管理质量.     

病区药品管理中存在的问题及改进措施

目的提高病区药品管理质量，保证用药安全。方法针对我院病区药品管理中存在的药物混放、过期失效、标识不清、无专人管理、储存不当等问题。采取组织学习，掌握药品管理知识、建立有效期登记本、按照药品储存要求严格存放、专人管理，严格交班、固定基数，及时更新等管理改进措施，实施1年后评价效果。结果改进管理措施后药物混放、过期失效、标识不清、无专人管理、储存不当5项问题发生率显著低于改进前（P〈0．05，P〈0．01）。结论针对性的改进措施可有效提高病区药品管理质量。     

护理用药安全手册的制定及应用

目的 加强对临床药品的安全管理,确保患者用药安全.方法 成立用药安全管理组织,针对2011年医院41个护理单元上报用药不良事件及开展的用药安全专项检查存在的问题进行原因分析,确定护理用药安全手册制定的内容及人员分工和职责;用药安全手册内容包括各种用药安全管理组织及制度,收集临床多品多规、看似听似药品并拍成图片进行比对,将临床特殊用药药理知识以表格形式罗列;规范使用药物流程、组织培训与考核等.结果 手册应用后,护士对备用药品管理规范、高危药品管理制度、专科用药知识、药品不良反应上报流程及紧急处理知晓率显著提高(均P＜0.01),临床用药不良事件发生数下降.结论 该手册为护士临床用药安全提供了参照资料,起到临床用药指引作用,可有效提高护理人员用药安全管理能力及自身业务水平,降低工作危机及用药风险,减少用药不良事件,保障患者用药及生命安全.     

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。     

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.     

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.     

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。