冰消散外敷辅助治疗复杂性胫骨平台骨折临床研究

目的：观察冰消散外敷辅助治疗复杂性胫骨平台骨折的临床疗效及对患者术后肿胀程度、凝血指标的影响。方法：选取85 例复杂性胫骨平台骨折患者,随机分为研究组43 例和对照组42 例。对照组给予常规术后治疗及康复指导,研究组在对照组的基础上加用冰消散外敷治疗。2 组均连续治疗7 d,治疗结束后比较2 组临床疗效,对2 组膝关节肿胀度、凝血功能、膝关节功能进行比较分析,并观察记录治疗期间并发症发生情况。结果：研究组临床总有效率为93.02%,对照组为83.33%,2 组比较,差异有统计学意义（P＜0.05）。治疗前,2 组膝关节肿胀度比较,差异无统计学意义（P＞0.05）;治疗后,2 组膝关节肿胀度均较治疗前减小（P＜0.05）,且研究组肿胀度小于对照组（P＜0.05）。治疗后,研究组凝血酶原时间（PT）、活化部分凝血活酶时间（APTT） 短于对照组,纤维蛋白原（Fib） 水平低于对照组,差异均有统计学意义（P＜0.05）。治疗后,研究组疼痛、僵硬、膝关节功能障碍评分及总分均低于对照组,差异有统计学意义（P＜0.05）。治疗过程中,2 组切口感染、关节僵硬、创伤性关节炎等并发症发生率比较,差异均无统计学意义（P＞0.05）。结论：冰消散外敷辅助治疗复杂性胫骨平台骨折疗效显著,可减轻患者膝关节肿胀程度,改善膝关节功能及凝血功能。     

脊髓损伤后的免疫抑制研究进展

脊髓损伤（SCI）致死率高、预后差,常导致患者终身瘫痪,可引起系统性神经源性免疫抑制综合征（SCI-IDS）^[1]。SCI后的免疫抑制会增加机体对病原体感染的易感性,导致患者并发症发生率及病死率增高。近年,国内外SCI的临床及动物模型研究证实,SCI可导致机体免疫细胞功能受损,免疫因子也发生一定程度的变化,从而引起免疫功能障碍^[2-3],但具体机制尚不明确。由于免疫系统可由中枢神经系统通过下丘脑-垂体-肾上腺轴（HPA）、交感神经系统（SNS）和副交感神经系统（PNS）进行调节,所以中枢神经系统的损伤可引起免疫相关的神经功能受损,进而引起免疫抑制,同时亦可造成内分泌功能障碍,间接引起免疫功能障碍^[4-5]。明确SCI导致机体防御系统受损的相关机制及脊髓平面、损伤程度等相关因素对发生SCI后免疫功能的影响,对治疗SCI、提高患者的生存质量至关重要。本文就HPA、SNS与SCI后的免疫抑制的可能关联、产生的适应性免疫抑制的相关机制及与其相关方向的治疗前景作如下综述。     

HCV感染与肾移植后糖尿病关系的荟萃分析

目的应用荟萃分析系统评价HCV感染是否为肾移植后糖尿病(PTDM)的相关危险因素。 方法系统检索中国期刊全文数据库、中国生物医学数据库、PubMed数据库、Embase数据库、Google scholar和Web of science database截至2019年12月公开发表的相关文献。应用Stata 15.1统计软件使用随机效应模型进行荟萃分析,计算相对危险度(RR)。 结果共纳入22篇文献,包含129 981例肾移植受者。荟萃分析结果显示,HCV感染的肾移植受者术后发生PTDM的风险为非HCV感染者的2.5倍(RR＝2.50, 95%CI: 1.95～3.20, P<0.001)。在亚洲、高加索和美洲人种中,HCV感染均为肾移植术后PTDM的危险因素。 结论HCV感染是促进肾移植术后发生PTDM的危险因素,感染者需尽早进行清除HCV的相关治疗。     

前列腺动脉栓塞术与经尿道前列腺电切术治疗前列腺增生的Meta分析

目的比较前列腺动脉栓塞术(PAE)与经尿道前列腺电切术(TURP)治疗良性前列腺增生的疗效与安全性,为前列腺增生症适宜治疗方案的选择提供理论依据。方法通过检索PubMed、EMBASE、Cochrane Library、CNKI、CBM、维普和万方等数据库,筛选出符合要求的PAE和TURP对比研究,并对所有纳入文献进行质量评价和资料提取,最后应用统计学软件Rev Man 5.3进行Meta分析,比较PAE与TURP治疗良性前列腺增生的优劣势。结果本研究最终共纳入9篇文献,共计675例患者。Meta分析结果显示:①临床疗效方面,术后3个月,TURP组优于PAE组,疗效指标IPSS、QOL、Qmax、PVR、PV的改善差异有统计学意义;术后12个月,TURP组改善情况优于PAE组,虽然指标IPSS、PVR的改善差异无统计学意义,但其余指标QOL、Qmax、PV的改善差异具有统计学意义;术后24个月,PAE组与TURP组治疗效果相近,指标IPSS、QOL、Qmax、PVR、PV的改善差异无统计学意义;PAE组失败率(4.4%)大于TURP组(0.5%);②安全性方面,PAE组比TURP组术中出血量少[MD=-98.25,95%CI:-105.51^-91.00,P<0.00001]、留置导尿时间短[MD=-1.61,95%CI:-2.31^-0.90,P<0.0006]、住院时间短[MD=-3.07,95%CI:-4.40^-1.74,P<0.00001];两组手术时间差异无统计学意义[MD=17.28,95%CI:-15.92~50.48,P=0.31];PAE组并发症(21.6%)少于TURP组(33.7%)。结论PAE治疗良性前列腺增生短期疗效(3个月)不及TURP;但中长期疗效(24个月)与TURP相近。总体来说,PAE较TUPR安全性高,具有术中出血量少,留置导尿时间短、住院时间短、并发症少的优点,对于不能耐受麻醉及TURP者可选择PAE治疗良性前列腺增生。但PAE手术失败率相对较高,其疗效的稳健性相对较差,目前尚没有足够的证据认定PAE优于TURP。未来随着更大样本、更多中心以及设计精良的随机对照试验出现,PAE用于治疗前列腺增生的疗效可以得到进一步的论证。     

平行重叠吻合法在3D腹腔镜右半结肠癌根治术中的应用价值

目的探讨平行重叠吻合法在3D腹腔镜右半结肠癌根治术中的应用价值。方法采用回顾性横断面研究方法。收集2016年7月至2019年7月河南省人民医院收治的138例行3D腹腔镜右半结肠癌根治术患者的临床病理资料;男83例,女55例;中位年龄为64岁,年龄范围为30~76岁。138例患者术前右半结肠肿瘤均经肠镜及病理学检查确诊为恶性肿瘤;所有患者按日本大肠癌协会第9版《大肠癌规约》进行淋巴结清扫,严格遵循无瘤原则行右半结肠切除术。观察指标:(1)手术情况。(2)术后情况。(3)随访情况。采用门诊或电话方式进行随访,了解患者生存和肿瘤复发转移情况。随访时间截至2019年9月。正态分布的计量资料以±s表示。偏态分布的计量资料以M(范围)表示。计数资料以绝对数或百分比表示。结果(1)手术情况:138例患者均行3D腹腔镜右半结肠癌根治术,消化道重建采用平行重叠吻合法,无1例中转开腹。138例患者手术时间为(151.0±54.0)min,平行重叠吻合时间为(20.1±2.0)min,术中出血量为(60±21)mL。(2)术后情况:138例患者术后首次肛门排气时间为(2.5±0.4)d,术后进食半流质食物时间为(4.0±1.3)d,手术辅助切口长度为(3.0±0.2)cm,术后并发症发生率为3.62%(5/138)。5例术后发生并发症的患者中,1例肠梗阻经胃肠减压、营养支持等保守治疗后痊愈;1例吻合口漏,经胃肠减压、局部通畅引流、控制感染、营养支持等保守治疗后痊愈;1例腹腔积液伴感染行CT引导下置管引流后痊愈;1例切口感染给予控制感染,加强换药,局部冲洗引流后痊愈;1例肺部感染,经抗感染治疗后痊愈。138例患者术后清扫淋巴结数目为(19±8)枚,术后住院时间为(7.2±4.1)d,治疗费用为(4.8±1.4)万元。138例患者术后病理学检查结果示结肠腺癌,其中低分化腺癌27例,中分化腺癌92例,高分化腺癌10例,黏液腺癌9例。(3)随访情况:138例患者中,133例获得随访,随访时间为2~38个月,中位随访时间为18个月。随访期间,2例患者死亡(1例术后16个月发现多发肝转移,术后21个月死亡;1例术后20个月发现多发肝转移,术后24个月死亡),8例出现肿瘤远处转移,其中肝转移5例,肺转移1例,腹腔转移2例,死亡及转移患者的术后病理学分期均为Ⅲ期。其余123例患者一般情况良好。结论平行重叠吻合法应用于3D腹腔镜右半结肠癌根治术中安全、有效。     

腹腔镜下膀胱腰大肌悬吊法处理输尿管中长段损伤的初步研究

目的评价腹腔镜下膀胱腰大肌悬吊输尿管膀胱再植术治疗输尿管远端缺损的有效性及安全性。方法回顾性分析本院2014年4月至2018年3月期间行腹腔镜下膀胱腰大肌悬吊法处理的输尿管下段较长缺损患者15例。其中男性患者6例,女性患者9例,年龄23~68岁,平均42岁。病变位于左侧10例,右侧5例。彩超提示肾盂分离平均2.7(1.4~5.2)cm,患者平均体重指数(BMI)为23.8(19.8~28.5)kg/m^2。术前评估缺损段长度平均4.8(3.0~8.0)cm。结果所有患者手术均经腹腔镜顺利完成,无中转开放。患者平均手术时间为125(90~210)min,平均手术失血量是75(30~150)mL。术后平均尿管拔除时间为7.2(5.0~11.0)d,术后平均住院8.7(5.0~14.0)d,术后输尿管支架管平均拔除时间为46(28~90)d,平均随访时间19.2(4.0~34.0)个月。围手术期无重大并发症,所有患者均出现症状缓解,排尿良好。结论腹腔镜下膀胱腰大肌悬吊输尿管膀胱再植术治疗输尿管下段较长缺损安全、有效,具有学习曲线短,手术创伤小,出血少,术后恢复快,并且可以完全保证输尿管无张力及连续性等优点,短期随访效果满意。     

腹腔镜袖状胃切除术中夹闭切缘血管减少胃切缘出血的回顾性研究

目的探讨腹腔镜袖状胃切除术(LSG)胃切缘出血的相关因素与处理措施。 方法回顾性分析2017年1月至2018年12月82例行LSG术患者资料,采用SSPS20.0软件统计分析,统计术中胃切缘出血与切缘血管处理及术中血压的关系,采用χ²检验,P<0.05差异具有统计学意义。 结果患者BMI≥40、高血压、有阻塞性睡眠呼吸暂停(OSA)与胃切缘出血率的关系密切(P<0.01);切割胃壁后胃切缘出血60例(73.2%),胃切缘无出血22例(26.8%)。术中胃壁切割闭合前,进行切缘血管预夹闭28例,切割后发生出血10例;未进行切缘血管预夹闭54例,切割后发生出血50例(χ²＝30.39,P＝0.000)。切割胃壁过程中26例患者血压大于130 mmHg,其中14例切缘出血需要处理;56例患者血压小于等于130 mmHg,其中15例切缘出血需要处理(χ²＝5.69,P＝0.017)。 结论LSG中预夹闭切缘血管可有效减少胃切缘出血,控制术中血压130 mmHg以下可减少胃切缘出血,且胃切缘出血后通过夹闭切缘血管和降低血压至130 mmHg以下可以有效控制出血。     

Application of pediatric donors in split liver transplantation: Is there an age limit?

The experience of using pediatric donors in split liver transplant is exceedingly rare. We aim to investigate the outcomes of recipients receiving split pediatric grafts. Sixteen pediatric recipients receiving split liver grafts from 8 pediatric donors < 7 years were enrolled. The donor and recipient characteristics, perioperative course, postoperative complications, and graft and recipient survival rates were evaluated. The mean follow‐up time was 8.0 ± 2.3 months. The graft and recipient survival rates were 100%. The liver function remained in the normal range at the end of the follow‐up time in all recipients. No life‐threatening complications were seen in these recipients, and the only surgery‐related complication was portal vein stenosis in 1 recipient. Cytomegalovirus infection was the most common complication (62.5%). The transaminase level was significant higher in extended right lobe recipients in the early postoperative days, but the difference vanished at the end of first week; postoperative complications and graft and recipient survival rates did not differ between left and right graft recipients. Notably, the youngest split donor graft (2.7 years old) was associated with ideal recipient outcomes. Split liver transplant using well‐selected pediatric donors is a promising strategy to expand pediatric donor source in well‐matched recipients.     

Use of concentrate growth factors gel or membrane in chronic wound healing: Description of 18 cases

Treating chronic skin wounds in patients with diabetes, bed sores, or stasis dermatitis is typically a time‐consuming and costly process, and the outcome is not always promising. Concentrated growth factor (CGF) obtained from the autologous venous blood of patients via fractional centrifugation is employed for producing a CGF gel or membrane that can be applied to expedite self‐regeneration of skin wounds. In this case report, we presented the results from 18 patients with chronic skin wounds treated with a CGF gel or membrane produced from autologous venous blood. Noticeable granulation tissue and regenerated epidermal coverage were observed in 16 patients who received CGF treatment over various time courses, thereby demonstrating the significant therapeutic effects of CGF treatment in overall wound healing. The other two patients with stasis ulcers in their calves failed to respond to the treatment because of the comorbidity of iliac vein thrombosis. In addition, by culturing HaCaT keratinocytes using CGF membrane as the foundation, we observed that HaCaT cells attached to the CGF membrane migrated and proliferated to form an epithelium‐like structure. Comprehensively, the clinical results infer that CGF gel can expedite the regeneration of the soft tissue at the wound, whereas CGF membrane may facilitate its marginal re‐epithelialisation. The combination of the two can promote autologous regeneration of both deep and superficial wounds effectively and safely.     

Innate immune molecule surfactant protein D attenuates sepsis‐induced acute kidney injury through modulating apoptosis and NFκB‐mediated inflammation

The objective of this study is to investigate the mechanism whereby innate immune molecule surfactant protein D (SP‐D) attenuates sepsis‐induced acute kidney injury (AKI) through modulating apoptosis and nuclear factor kappa‐B (NFκB)‐mediated inflammation. In the present study, a mouse sepsis model was established by cecal ligation and puncture in SP‐D knockout (KO) mice and wild‐type (WT) mice. A sham‐operated group was included as the control. The experimental materials were extracted 6 and 24 hours postoperatively. The plasma levels of tumour necrosis factor alpha (TNF‐α) and MCP‐1 were determined by enzyme‐linked immunosorbent assay (ELISA). Apoptosis was measured by double staining with Annexin V/propidium iodide and flow cytometry. The levels of NFκB in renal tissues were measured by ELISA and Western blotting assay. Apoptosis was detected by TUNEL assays. There were no significant differences in plasma TNF‐α levels between the WT sham group and the KO sham group at 6 and 24 hours postoperatively (P < .05), but the levels of TNF‐α in the WT sepsis and KO sepsis groups were significantly higher than those in controls (P < .05). The levels of TNF‐α in the KO sepsis group were significantly higher than those of the WT sepsis group (P < .05). TNF‐α levels in the WT sepsis group and the KO sepsis group at 24 hours postoperatively were significantly higher than those at 6 hours postoperatively (P < .05). The levels of MCP‐1 in the WT sepsis group and the KO sepsis group at 6 and 24 hours postoperatively were significantly higher than those in the control group (P < .05), and MCP‐1 levels in the KO sepsis group were significantly higher than those in the WT sepsis group (P < .05). MCP‐1 levels in the WT sepsis group and the KO sepsis group at 24 hours postoperatively were significantly higher than those at 6 hours postoperatively (P < .05). The expression of SP‐D in WT kidneys was significantly lower at 6 and 24 hours postoperatively (P < .05). The number of TUNEL‐positive cells in the kidneys from septic SP‐D KO mice was significantly higher (P < .05). The levels of NFκB in septic mice were significantly increased at 6 and 24 hours after induction of sepsis compared with the sham‐operated group compared with those of septic SP‐D KO mice and WT mice (P < .05). Innate immune molecule SP‐D significantly decreased plasma levels of inflammatory cytokines in mice and attenuated sepsis‐induced AKI by inhibiting NFκB activity and apoptosis.