Nerve Transfers for Treatment of Isolated Axillary Nerve Injuries

BACKGROUND:

The most common neurological defect in traumatic anterior glenohumeral dislocation is isolated axillary nerve palsy. Most recover spontaneously; however, some have persistent axillary neuropathy. An intact rotator cuff may compensate for an isolated axillary nerve injury; however, given the high rate of rotator cuff pathology with advancing age, patients with an axillary nerve injury are at risk for complete shoulder disability.

OBJECTIVE:

To review reconstruction of the axillary nerve to alleviate shoulder pain, augment shoulder stability, abduction and external rotation to alleviate sole reliance on the rotator cuff to move and stabilize the shoulder.

METHODS:

A retrospective review of 10 patients with an isolated axillary nerve injury and an intact rotator cuff who underwent a triceps nerve branch to axillary nerve transfer was performed. Patient demographics, surgical technique, deltoid strength, donor-site morbidity, complications and time to surgery were evaluated.

RESULTS:

Ten male patients, mean age 38.3 years (range 18 to 66 years), underwent a triceps to axillary nerve transfer for isolated axillary nerve injury 7.4 months (range five to 12 months) post-traumatic shoulder dislocation. Deltoid function was British Medical Research Council grade 0/5 in all patients preoperatively and ≥3/5 deltoid strength in eight patients at final follow-up (14.8 months [range 12 to 25 months]). There were no complications and no donor-site morbidity.

CONCLUSION:

A triceps to axillary nerve transfer for isolated axillary neuropathy following traumatic shoulder dislocation improved shoulder pain, stability and deltoid strength, and potentially preserves shoulder function with advancing age by alleviating sole reliance on the rotator cuff for shoulder abduction and external rotation.     

The utilization of smart trials in PCL retaining knees

Technical issues such as instability, mal-rotation, and mal-alignment continue to be issues leading to total knee replacement revision. Soft tissue balancing is critical to successful address these issues for successful total knee replacement outcomes. Intra-op sensors can now be used to dynamically balance knees in real time and mitigate negative outcomes.     

强化胰岛素治疗重型颅脑损伤的前瞻性研究

【摘要】〓目的〓比较强化胰岛素治疗与常规胰岛素治疗两种方法在治疗重型颅脑损伤患者上的预后差异。方法〓以2012年1月至2014年6月在我院进行治疗的重型颅脑外伤且合并应激性高血糖的116例患者为研究对象,按病情、年龄、性别等因素配对分成两组,将应用强化胰岛素治疗的58名患者为实验组,将常规胰岛素治疗的58例患者为对照组,并以死亡率、神经功能恢复情况、院内感染率、低血糖发生率为指标分析两组患者的预后差异。结果〓实验组和对照组两组死亡率差别无统计学意义,但实验组院内感染发生率低于对照组,实验组神经功能恢复情况优于对照组,实验组低血糖发生率高于对照组。结论〓强化胰岛素治疗能降低重型颅脑损伤患者院内感染发生率,并利于患者神经功能恢复,但需警惕其可能诱发患者低血糖的风险。     

124例急性重症胆管炎诊治体会

【摘要】 目的 介绍急性重症胆管炎治疗体会。方法〓回顾性分析我院2008~2013年收治124例急性重症胆管炎患者的临床资料。结果〓手术治疗组112例,109例痊愈,其中81例术后一个月拔除T管痊愈出院,4例因肝内胆管残留结石二期行肝切除术,肝内胆管及胆总管有残石14例,胆总管有残石6例二期手术行经T管胆道镜取石痊愈,PTCD(经皮经肝穿刺胆管引流术)2例,ENBD(经鼻胆管引流)2例。手术后死亡3例,其中1例PTCD后因多器官功能衰竭而死亡,2例胆囊造瘘术后因感染性休克而死亡。非手术组12例中有8例采取保守治疗成功后行二期手术痊愈,4例因多器官功能衰竭而死亡。结论〓急性重症胆管炎应早期诊断,手术治疗是首选方案,应选择快速、简单、有效的手术方法。     

MicroRNA-687 Induced by Hypoxia-Inducible Factor-1 Targets Phosphatase and Tensin Homolog in Renal Ischemia-Reperfusion Injury

Ischemia-reperfusion injury contributes to tissue damage and organ failure in clinical settings, but the underlying mechanism remains elusive and effective therapies are still lacking. Here, we identified microRNA 687 (miR-687) as a key regulator and therapeutic target in renal ischemia-reperfusion injury. We show that miR-687 is markedly upregulated in the kidney during renal ischemia-reperfusion in mice and in cultured kidney cells during hypoxia. MiR-687 induction under these conditions was mediated by hypoxia-inducible factor-1 (HIF-1). Upon induction in vitro, miR-687 repressed the expression of phosphatase and tensin homolog (PTEN) and facilitated cell cycle progression and apoptosis. Blockade of miR-687 preserved PTEN expression and attenuated cell cycle activation and renal apoptosis, resulting in protection against kidney injury in mice. Collectively, these results unveil a novel HIF-1/miR-687/PTEN signaling pathway in ischemia-reperfusion injury that may be targeted for therapy.     

IL-25 Elicits Innate Lymphoid Cells and Multipotent Progenitor Type 2 Cells That Reduce Renal Ischemic/Reperfusion Injury

IL-25 is an important immune regulator that can promote Th2 immune response-dependent immunity, inflammation, and tissue repair in asthma, intestinal infection, and autoimmune diseases. In this study, we examined the effects of IL-25 in renal ischemic/reperfusion injury (IRI). Treating IRI mice with IL-25 significantly improved renal function and reduced renal injury. Furthermore, IL-25 treatment increased the levels of IL-4, IL-5, and IL-13 in serum and kidney and promoted induction of alternatively activated (M2) macrophages in kidney. Notably, IL-25 treatment also increased the frequency of type 2 innate lymphoid cells (ILC2s) and multipotent progenitor type 2 (MPP^type2) cells in kidney. IL-25–responsive ILC2 and MPP^type2 cells produced greater amounts of Th2 cytokines that associated with the induction of M2 macrophages and suppression of classically activated (M1) macrophages in vitro. Finally, adoptive transfer of ILC2s or MPP^type2 cells not only reduced renal functional and histologic injury in IRI mice but also induced M2 macrophages in kidney. In conclusion, our data identify a mechanism whereby IL-25-elicited ILC2 and MPP^type2 cells regulate macrophage phenotype in kidney and prevent renal IRI.     

Evaluation of the Patient-Specific Functional Scale in hand fractures and dislocations

Background

Generic upper extremity disability questionnaires utilize standardized items. The Patient-Specific Functional Scale (PSFS) allows the patient to identify specific self-reported items. This study evaluated the validity of the PSFS to assess outcome in patients with hand fractures or dislocations.

Methods

Adults with hand fractures or dislocations, who completed hand therapy between January 2012 and January 2013, were eligible for inclusion. At the initial and final assessment, each patient was asked to complete the PSFS. Each patient identified three items that were difficult or they were unable to perform, and the degree of difficulty was ranked from 0 to 10 (able to perform at pre-injury level). We excluded patients with an incomplete PSFS. Statistical analyses evaluated the relationships between the PSFS and the independent variables.

Results

There were 63 patients (37 men, 26 women); 21 of the 63 patients underwent surgery for fracture fixation. The mean duration of hand therapy treatment was 2.2 ± 1.4 months. The mean PSFS scores were as follows: initial 3.2 ± 2.2; final 8.1 ± 2.2. There was a significant improvement in PSFS scores from initial to final assessment (p < 0.001) and a moderate correlation (r = 0.3, p = 0.02). There was no statistical difference in PSFS scores between men and women or surgery and no surgery.

Conclusions

In these patients with hand fractures or dislocations, the PSFS indicated significant improvement in function. Using items identified by the patient, the PSFS provides a valuable perspective of outcome and may be used in conjunction with generic disease-specific questionnaire for assessment of the upper extremity.     

组织学绒毛膜羊膜炎与早产儿脑损伤相关性分析

目的探讨组织学绒毛膜羊膜炎(HC)及合并胎儿血管炎(FV)时与早产儿脑损伤的相关性。方法回顾性分析347例住院的出生胎龄28~32周早产儿的临床资料。根据病理检查结果将早产儿分为HC组和对照组,HC组再根据是否合并胎儿血管炎分FV组及无FV组。早产儿定期行头颅B超检查,比较早产儿脑室周围白质软化(PVL)、脑室周围-脑室内出血(PVH-IVH)和脑室周围白质软化并脑室周围-脑室内出血的发生情况。结果 HC组、对照组PVL发生率分别为17.9%、10.4%,PVL合并PVH-IVH发生率分别为5.5%、1.5%,差异均有统计学意义(P0.05);而PVH-IVH的发生率分别为29.0%、26.2%,差异无统计学意义(P0.05)。在HC组中,FV组、无FV组的PVL发生率则分别28.1%、9.9%,差异有统计学意义(P0.05);PVH-IVH的发生率为34.3%、24.7%,PVL合并PVH-IVH发生率分别为7.8%、3.7%,差异均无统计学意义(P0.05)。结论 HC可使早产儿PVL、PVL合并PVH-IVH的发生率增加,而对PVH-IVH的影响不大,合并FV会增加早产儿脑损伤发生率。     

吸入一氧化氮对急性肺损伤大鼠内源性一氧化氮及纤溶酶原激活物抑制剂-1表达的影响及其相关研究

目的 探讨早期吸入一氧化氮(NO)对急性肺损伤大鼠纤溶酶原激活物抑制剂-1(PAI-1)mRNA和蛋白表达的影响及其意义;观察吸入NO后急性肺损伤大鼠诱生性NO合酶(iNOS)和内源性NO的变化及其与PAI-1表达的关系.方法 采用内毒素(LPS)二次打击方法建立4～5周SD大鼠急性肺损伤模型.对照组和LPS组分别随机给予吸入空气(A)、20×10-6 NO,干预24 h.应用荧光实时定量PCR方法测定大鼠肺组织PAI-1 mRNA水平,免疫组织化学测定2组大鼠肺组织PAI-1蛋白的表达水平,并测定肺组织iNOS活性和NO水平;同时行肺组织病理评分和纤维素染色.结果 造模后气体干预24 h时肺组织PAI-1 mRNA和蛋白表达在NO干预的LPS-NO组较LPS-A组显著降低(4.94 ±0.52比5.56±0.27;1.31 ±0.40比1.69 ±0.16,P均＜0.05).同时NO干预后LPS-NO组iNOS活性和肺组织NO水平均显著低于LPS-A组[(0.84±0.36)U/mg prot比(2.30±0.25) U/mg prot;(1.90±0.84) μmol/g prot比(3.38±0.73) μmol/g prot,P均＜0.05).iNOS活性与PAI-1 mRNA和蛋白表达呈正相关(r=0.481,P=0.005;r =0.667,P=0.000);肺组织NO水平与PAI-1 mRNA和蛋白表达呈正相关(r=0.532,P=0.002;r =0.784,P=0.000).肺病理评分在干预24 h时,LPS-NO组较LPS-A组下降,差异有统计学意义(4.28±0.94比6.12±1.51,P＜0.05).光镜下LPS-NO组大鼠肺纤维素沉积较吸入空气的大鼠有所减少.结论 早期吸入20×10-6 NO可抑制急性肺损伤大鼠PAI-1的高表达,缓解纤溶失衡,减少纤维蛋白沉积,减轻肺损伤;吸入NO可减少急性肺损伤时肺组织iNOS活性和NO产量,此作用与PAI-1表达下调密切相关,因此可将研究内源性NO系统调节PAI-1表达的信号通路作为下一步的研究方向,为设计新疗法提供思路.