CRRT加复合抗惊厥治疗重度毒鼠强中毒患者的护理

目的探讨重度毒鼠强中毒抢救的护理方法。方法采用连续肾脏替代治疗（CRRT）、地西泮和德巴金联合止痉、洗胃、保持呼吸道通畅、多参数生命体症监护等治疗、护理重度毒鼠强中毒。结果所有患者经联合抗惊厥治疗1h后，抽搐次数明显减少或消失，24h后病情明显好转，7例重度中毒患者成功获救，无1例死亡。结论CRRT加复合抗惊厥治疗毒鼠强中毒方法可靠，也是目前最有效的治疗手段，而科学的护理是保证治疗效果的关键。     

序贯性血液净化治疗重症毒鼠强中毒

目的观察血液净化治疗重症毒鼠强中毒患者的临床疗效和对预后的影响。方法11例重症毒鼠强中毒的患者人院后．除给予镇静、抗惊厥、冼胃、利尿、导泻、营养神经、支持等常规治疗外,并给予序贯性血液净化治疗。观察患者的临床症状、血压、脉搏、血清酶学变化。结果11例患者进行血液净化治疗,死亡1例,1例临床症状好转后自动出院．其余9例患者痊愈。结论及时有效的血液净化治疗可明显改善毒鼠强中毒患者的预后。     

血液灌流联合血液透析抢救重度乙草胺中毒15例

目的 观察反复血液灌流联合血液透析对重度乙草胺中毒的临床疗效.方法 2009年6月至2012年3月我院共收治重度乙草胺中毒患者15例,其中女13例,男2例,年龄20 ～ 52岁,平均年龄33岁,服用剂量从100～250 ml不等,临床表现为嗜睡、昏迷、胸闷、(噁)心、呕吐等.患者入院后除洗胃等一般治疗外,均给予血液灌流联合血液透析治疗,血液灌流每隔12h1次,每次持续2h,血液透析每隔24h1次,每次持续4h.结果 9例患者行血液灌流5次、血液透析3次后治愈,3例患者行血液灌流7次,血液透析4次后治愈,3例患者因中毒后12h以上才转至我院,仅行血液灌流联合血液透析1次即死亡.结论 血液灌流联合血液透析治疗能安全、有效地吸附清除体内残存的乙草胺及其代谢产物,从而减轻脏器损害,提高治疗成功率,但需反复多次使用.     

不同血液净化方式治疗急性中毒患者的疗效

目的比较不同血液净化方式在危重中毒患者治疗中的效果。方法将危重中毒患者104例按不同的血液净化方式分为连续性肾脏替代治疗联合血液灌流（CRRT＋HP）组和血液透析联合血液灌流（HD＋HP）组,测定2组患者治疗前、后的相关生化指标,比较2组治疗后的各项指标和病死率的差异。结果CRRT＋HP组患者治疗后血清肌酸激酶同工酶（CK-MB）、肌酸激酶（CK）、血肌酐（SCr）、天门冬氨酸氨基转移酶（AST）、丙氨酸氨基转移酶（ALT）水平,24h和48h后的急性生理学与慢性健康状况评分（APACHE）Ⅱ评分,住院天数及病死率均明显低于HD＋HP组（P〈0．05）。结论CRRT联合HP较HD联合HP更适合用于危重症患者的治疗,可能是改善危重中毒患者病情,降低患者病死率,提高患者预后的重要措施。     

地西泮联合二巯丙磺钠辅助治疗急性毒鼠强中毒患者的护理

对16例急性毒鼠强中毒患者在常规治疗基础上采用地西泮联合二巯丙磺钠治疗。结果痊愈12例,好转4例。提出早期彻底清除胃肠道内毒物、保持呼吸道通畅,联合使用地西泮、二巯丙磺钠控制抽搐,密切观察病情变化,加强心理护理是急性毒鼠强中毒抢救成功的关键。     

血液灌流联合血液透析治疗重度有机磷农药中毒40例临床分析

目的 分析血液灌流联合血液透析治疗重度有机磷农药中毒疗效和安全性.方法 回顾性分析2006年1月至2009年4月收治的40例重度有机磷农药中毒患者行血液灌流联合血液透析治疗的临床资料.结果 40例重度有机磷农药中毒患者行血液灌流联合血液透析治疗后,有36例痊愈,4例死亡.40例患者中有2例出现中间综合征,继续多次行血液灌流联合血液透析治疗后痊愈.40例患者中有1例患者因原有胃黏膜损伤而出现消化道出血.结论 血液灌流联合血液透析治疗重度有机磷农药中毒疗效可靠安全、能提高抢救成功率、减少中毒后遗症,且安全性好.     

血液灌流治疗急性中、重度毒鼠强中毒临床研究

我们观察和评价血液灌流对中、重度毒鼠强中毒治疗的疗效,报告如下。 资料与方法 1.资料:男44例,女20例,平均年龄(36±16)岁。服食至中毒发作时间为(48±21)min;其中重度中毒41例,中度中毒23例。 2.诊断标准:据病史、症状及体征,加上胃内容物或血液中测出毒鼠强成份。病情按常规分为轻、中、重三级。 3.治疗:常规治疗加血液灌流。 4.观测指标:血中毒鼠强浓度,临     

地西泮联合二巯丙磺钠辅助治疗急性毒鼠强中毒患者的护理

对16例急性毒鼠强中毒患者在常规治疗基础上采用地西泮联合二巯丙磺钠治疗。结果痊愈12例，好转4例。提出早期彻底清除胃肠道内毒物、保持呼吸道通畅，联合使用地西泮、二巯丙磺钠控制抽搐，密切观察痛情变化．加强心理护理是急性毒鼠强中毒抢救成功的关键。     

急性光气中毒45例的特点及治疗分析

目的探讨急性光气中毒的临床特点及治疗措施。方法采用笔者所在医院收治的45例急性光气中毒的病例资料,对临床表现及治疗措施进行综合性分析和总结。结果急性光气中毒的主要临床表现为胸闷、气短、咳嗽,重度中毒出现呼吸频速、发绀、泡沫痰等,1例出现多器官功能障碍综合征。轻中度中毒采取以糖皮质激素为主的综合治疗,重度中毒出现ARDS时予最佳PEEP机械通气,出现MODS时予CRRT治疗,45例患者均痊愈出院。结论急性光气中毒的临床表现主要引起呼吸系统损害,通过以糖皮质激素为主的综合治疗,取得明显疗效,机械通气及CRRT的应用,可提高重症患者的治愈率。     

高危出血患者无肝素抗凝连续性肾替代治疗的护理

目的 探讨高危出血患者无肝素抗凝连续肾替代治疗(CRRT)的护理.方法 对32例高危出血患者采用无肝素抗凝法行CRRT治疗120例次.治疗过程严密观察病情变化,保证血管通路通畅,严密监测动脉压、滤前压、静脉压及跨膜压的变化,预防感染等.结果 32例患者无1例出现透析相关性出血,透析器寿命4～35(9.3±3.7)h,经更换滤器及血管路后患者均顺利完成治疗.结论 高危出血患者行无肝素抗凝CRRT治疗,既能达到有效的抗凝效果,亦可减少抗凝剂引起的不良反应;有效的护理手段是完成治疗的保障.     

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.