早期扩髓髓内钉固定治疗合并胸部损伤的股骨干骨折

目的探讨合并胸部损伤的股骨干骨折早期扩髓及髓内钉固定是否增加并发症及死亡率. 方法采用回顾性对比分析,依据下列标准选择病例(1) 年龄在17～65岁;(2) 必须有胸部损伤[简明损伤定级(AIS)≥2], 且损伤严重度评分(ISS)≥16;(3) 住院时间≥48 h;(4) 病史中无明显影响全身状况的疾病, 如糖尿病, 慢性心、肺、肾功能不全等;(5) 有股骨干骨折, 且进行了扩髓髓内钉固定, 不含钢板、外固定支架或牵引及石膏固定者.并按受伤至手术时间划分为两组, A组为<24 h手术者(早期扩髓组), B组为≥24 h手术者(延期扩髓组),将两组间合并伤情况、ISS、住院时间、ICU时间、并发症、死亡及合并休克情况进行比较. 结果有96例符合上述标准, 其中A组57例, B组39例,经统计学处理, 两组间仅在股骨开放性骨折发生率(A组53%,B组31%,χ2=4.496, P<0.05)、合并休克率(A组51%, B组28%,χ2=4.895, P<0.05 )及住院时间[A组为(17.5±6.5)d, B组为(31.5±9.5)d,t=8.599, P<0.001]上差异有显著性意义和非常显著性意义, 而两组并发症发生率和死亡率等方面比较, 差异无显著性意义(P>0.05). 结论在合并胸部损伤的股骨干骨折中,只要能控制休克,保证生命体征平稳,对股骨干骨折行早期扩髓髓内钉固定不增加患者的并发症发生率及死亡率,并可促进患者早日康复,缩短住院时间.     

急性颈脊髓损伤并发抗利尿激素分泌异常综合征的诊断和治疗

目的探讨急性颈脊髓损伤并发抗利尿激素分泌异常综合征的临床特点、诊断和治疗方法。方法回顾性分析8例急性颈脊髓损伤并发抗利尿激素分泌异常综合征患者的临床资料。脊髓损伤分级:FrankelA级5例,B级3例;损伤节段:C4～53例,C5～63例,C6～72例。8例于受伤后3～7d行骨折椎体次全切除椎管减压、自体髂骨植骨融合及颈椎前路钢板内固定术。3例于术前,5例于术后3～7d发生低钠血症,所有患者低钠血症发生后第2～10d确诊SIADH,根据血钠水平,采用控制每日水量、补钠进行治疗。结果7例经10～21d治愈,血钠平均恢复至138(135～142)mmol/L,血浆渗透压、尿渗透压、尿钠均正常;1例C4骨折、FrankelA级者,因截瘫平面上升并发呼吸衰竭死亡。结论急性颈脊髓损伤并发抗利尿激素分泌异常综合征的发病机制与治疗措施不同于普通低钠血症,早期正确的诊治能降低患者病残率和死亡率,严格控制入液量及补钠为主要治疗方法。     

转录因子Egr-1在失血性休克复苏后肝脏损伤中的作用

目的研究转录因子Egr-1在失血性休克复苏（HS/R）后肝脏损伤中的作用.方法利用Egr-1野生型（WT）和基因封闭型（KO）小鼠复制失血性休克复苏模型.取肝组织,RT-PCR法测定肝组织中TNF-α、IL-6、G-CSF、ICAM-1 mRNA的表达变化.通过检测肝组织中MPO的含量、血清ALT水平和组织学检查,评估肝脏炎症细胞浸润和损伤程度.结果失血性休克2.5 h＋复苏4 h后,Egr-1 KO小鼠肝组织中TNF-α、IL-6、G-CSF、ICAM-1 mRNA的表达水平明显低于Egr-1WT组;Egr-1 KO组失血性休克复苏后肝组织炎性浸润和损伤程度减轻,表现为血清ALT水平低,肝组织中MPO含量低,病理损伤轻.结论本实验结果表明转录因子Egr-1参与了失血性休克复苏后肝脏炎症反应基因表达的调节,在失血性休克复苏后的肝脏损伤中起一定的作用.     

影响肝外伤手术死亡的危险因素分析

目的分析影响肝外伤手术死亡的危险因素,探讨其临床意义。方法根据AAST和ISS标准,回顾性分析90例肝外伤手术病例,对影响手术死亡的危险因素进行单因素比较和Logistic回归分析。结果死亡15例,其中Ⅲ级2例、Ⅳ级4例、Ⅴ级9例,总体手术死亡率17%。Ⅳ~Ⅴ级肝外伤手术方式的单因素比较提示:清创性肝切除术的相对危险度是0.73;而规则性肝切除术、肝静脉或肝后下腔静脉修补术相对危险度分别是1.32、1.52。Logistic回归分析提示:ISS分会和术中失血量是影响手术死亡率的2个独立因素。结论ISS分值、术中失出血量和手术方式是影响肝外伤手术死亡的3个重要因素,娴熟的手术技能和合理的手术方式可以减少术中出血量和降低手术死亡率。     

应用足底内侧皮瓣修复足跟部软组织缺损

目的探讨应用足底内侧皮瓣转移修复足跟部软组织缺损的临床疗效。方法应用足底内侧皮瓣转移修复15例深达跟骨的足跟部软组织缺损。结果15例皮瓣移植后均成活,术后随访3~12个月,所有皮瓣外形和感觉均恢复良好。结论足底内侧皮瓣修复足跟部深度软组织缺损效果较好。     

Extracellular signal regulated kinases 1/2 signal pathway and responses of astrocytes after diffuse brain injury

BACKGROUND: The treatment of diffuse brain injury during an acute period is focused on relieving degrees of secondary brain injury. Generation and development of pathological changes of secondary brain injury depend on signal conduction, so down-regulating over response of astrocyte through interfering a key link of signal conduction pathway may bring a new thinking for the treatment of diffuse brain injury. OBJECTIVE: To observe the effect of over activity of extracellular signal regulated kinases 1/2 (ERK1/2) signal pathway on the response of astrocyte during an acute period of diffuse brain injury. DESIGN: Completely randomized grouping and controlled animal study. SETTINGS: Department of Neurosurgery, the Third Affiliated Hospital, Nanchang University; Department of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology. MATERIALS: A total of 158 healthy male SD rats, of 11 weeks old, weighing 320–370 g, were provided by Experimental Animal Faulty, Tongji Medical College, Huazhong University of Science and Technology. Rabbit-anti-phosphorylated ERK1/2 (pERK1/2) polyclonal antibody was provided by R&D Company; rabbit-anti-glial fibrillary acidic protein (GFAP) polyclonal antibody, SP immunohistochemical kit and horseradish peroxidase (HRP)-labeled goat-anti-rabbit IgG by Santa Cruz Company; specific inhibitor U0126 of ERK1/2 signal pathway by Alexis Company. METHODS: The experiment was carried out in the Laboratory of Neurosurgery, Union Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology from September 2004 to March 2006. ① Detection of pERK1/2 expression: A total of 110 rats were randomly divided into sham operation group (n =5), model group (n =35), high-dosage U0126 group (n =35) and low-dosage U0126 group (n =35). Rats in the sham operation group were only treated with incision of epicranium and fixation of backup plate, but not hit. Rats in the model group were used to establish diffuse brain injury models based on Marmarou free falling body without drug intervention. Rats in the high- and low-dosage U0126 groups were injected into caudal vein with 0.1 and 0.05 mg/kg U0126, respectively, and then, rats were hit to establish injured models. Every 5 rats were collected from model, high- and low-dosage U0126 groups at 5, 30 minutes, 3, 12, 24, 72 hours and 7 days after diffuse brain injury to detect pERK1/2 expression in cortex of parietal lobe based on Western blot technique. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue: Another 48 rats were randomly divided into sham operation group (n =3), model group (n =15), high-dosage U0126 group (n =15) and low-dosage U0126 group (n =15). The intervention and administration were dealt as the same as those mentioned above. Every 3 rats were collected from model, high- and low-dosage U0126 groups at 30 minutes, 3, 12, 24 and 72 hours after model establishment to observe the distribution of pERK1/2 and postive GFAP cells in brain tissue which was cut from coronal section at Bregma –4.8 mm layer with immunohistochemical staining. MAIN OUTCOME MEASURES: pERK1/2 expression in cortex of parietal lobe and distribution of pERK1/2 and positive GFAP cells in brain tissues. RESULTS: ① pERK1/2 expression: After diffuse brain injury, pERK1/2 expression in cortex of parietal lobe was rapidly increased in the model group, reached at peak at 5 minutes and then decreased gradually. But the expression was still in a high level until the 72nd hour and fallen to the basic level on the 7th day. pERK1/2 level was lower in high- and low-dosage U0126 groups than that in model group at various time points (P < 0.01); meanwhile, pERK1/2 level was lower in high-dosage U0126 group than that in low-dosage U0126 group. The results showed that there was a certain dosage dependence on pERK1/2 expression. ② Distribution of pERK1/2 and positive GFAP cells in brain tissue: Positive expression of pERK1/2 lasted in brain tissue from 30 minutes to 72 hours after diffuse brain injury (P < 0.05). In addition, from 30 minutes to 3 hours, brown-yellow stained cells were mainly distributed in plasma, but rarely in nucleus. A lot of positive cells had tree-like apophysis, which was similar to neurons. With the time passing by, more and more nuclei manifested positive stains; moreover, nuclei mainly manifested positive staining until 24 hours after diffuse brain injury. Immune-positive pERK1/2 cells were widely distributed in brain tissue, especially mainly in binding site between deep cortex and cerebral white matter, and then in hippocampus. In addition, ependymal cell and vascular endothelial cells of choroids plexus also manifested strongly positive staining. As compared with model group, positive cells were decreased gradually in high- and low-dosage U0126 groups. However, number of positive cells was less in high-dosage U0126 group than that in low-dosage U0126 group. CONCLUSION: Diffuse brain injury strongly induces the activity of ERK1/2 signal pathway and response of astrocyte; in addition, U0126 can inhibit response of glial cells during an acute period, and the effect manifests dosage dependence.     

急性重型脑损伤患者脑组织氧代谢监测及意义

目的　探讨对急性重型脑损伤患者行脑组织氧代谢监测的临床意义。　方法对2 8例急性重型脑损伤患者 (均在全麻下急诊行血肿清除术和 (或 )去骨瓣减压术 )术中及术后持续进行脑组织氧代谢监测 ,观察脑组织氧分压 (PbtO2 )、二氧化碳分压 (PbtCO2 )和pH值 (pHbt)的变化。　结果　 (1) 2 8例脑外伤患者在剪开硬脑膜后PbtO2 、pHbt分别从 (13± 4 )mmHg、(6 .96± 0 .15 )增加至 (2 1± 5 )mmHg、7.0 5± 0 .12 (P <0 .0 5 ) ,PbtCO2 从 (6 1± 6 )mmHg下降至 (5 3± 5 )mmHg(P <0 .0 5 )。(2 )其中 2 4例脑外伤患者在血肿清除后 ,PbtO2 、pHbt值分别从 (2 1± 4 )mmHg、7.0 5± 0 .11增加至 (2 8± 6 )mmHg、7.15± 0 .10 (P <0 .0 5 ) ,PbtCO2 从 (5 2± 6 )mmHg下降至 (4 5± 4 )mmHg(P <0 .0 5 )。 (3)PbtO2 <10mmHg持续 30min以上的患者预后差。　结论　 (1)脑组织氧代谢监测是一种安全、可靠的监测手段 ,能直接动态反映脑组织的病理生理变化 ,及时发现脑组织缺血缺氧 ,以指导治疗。 (2 )持续进行脑组织氧代谢监测可判断重型脑外伤患者的预后。     

大鼠脊髓缺血再灌流时脊髓神经元对躯体和内脏传入刺激的反应

５０只大鼠用乌拉坦麻醉，箭毒制动。通过阻断腹主动脉血流以模拟腰段脊髓的局部缺血和再灌流损伤，玻璃微电极记录Ｌ２节段脊髓单位放电（ＳＣＵＤｓ），观察缺血再灌流时脊髓神经元对腓神经刺激（ＰＮＶ），内脏大神经刺激（ＶＬＮＶ）及两者同时刺激（ＳＶ）的反应。结果在缺血前所记录的１３３个自发放电单位中，对３种刺激均产生兴奋（Ｅ）、抑制（Ｉ）及无反应（ＮＲ）３种形式的反应，表明大鼠Ｌ２节段脊髓存在躯体、内脏和躯体内脏反应性神经元，并有会聚和阻塞现象。在脊髓缺血再灌流时，神经元对ＰＮＶ、ＶＬＮＶ、ＳＶ也产生Ｅ、Ｉ、ＮＲ３种形式的反应，提示脊髓缺血再灌流时神经元对躯体和内脏传入刺激的反应形式不受影响；但缺血时ＳＣＵＤｓ对ＰＮＶ、ＶＬＮＶ产生反应的单位数减少，这表明脊髓缺血损伤时神经元对躯体和内脏传入刺激的反应性减弱，随着缺血损伤加重，脊髓神经元对躯体内脏信号的整合功能下降     

Flexor digitorum profundus tendongrafting (extrasynovial donor tendons)

Although the prevalence of flexor tendon grafting has decreased since the early part of this century, the technique isstill an important part of a hand surgeons armamentarium. Primary and staged flexor tendon grafting are appropriate techniques used to restore digital function after failed or neglected repairs. Appropriate patient selection, meticulous reconstructive techniques, and respect for basic biological principles of healing and repair are essential elements for successful tendon grafting.