自制单孔与三孔后腹腔镜肾蒂淋巴管结扎术治疗乳糜尿的临床疗效比较

目的探讨自制单孔后腹腔镜肾蒂淋巴管结扎术治疗乳糜尿的安全性及临床疗效。方法回顾性分析2013年2月-2016年3月接受单孔后腹腔镜肾蒂淋巴管结扎术或三孔后腹腔镜肾蒂淋巴管结扎术治疗乳糜尿的34例患者临床资料,其中单孔组(16例)和三孔组(18例)。两组患者的年龄、体质指数(BMI)比较差异无统计学意义(P0.05)。比较两组的手术时间、术中出血量、术后引流管留置天数、术后住院天数、术后疼痛评分和外观满意度评分等指标。结果所有手术均获成功,无中转开放手术。单孔组平均手术时间长于三孔组[(132.4±21.6)vs(102.3±16.1)min,P0.05],两组在术中出血量、术后拔管时间和术后住院天数方面比较差异无统计学意义,但单孔组术后满意度评分、疼痛评分优于三孔组。结论自制单孔后腹腔镜肾蒂淋巴管结扎术治疗乳糜尿是一种安全有效、经济、微创的方法,术后疼痛较轻,美容效果更好。     

肾脂肪囊内两种途径行肾蒂淋巴管结扎术治疗乳糜尿的疗效分析

目的评价后腹腔镜下肾脂肪囊完全或次全性游离途径行肾蒂淋巴管结扎术的临床疗效。方法回顾性分析2006年1月至2012年4月经后腹腔镜下肾脂肪囊完全游离途径(A组40例)或次全游离途径(B组33例)行肾蒂淋巴管结扎术的73例乳糜尿患者的临床资料,比较2组基线水平、手术时间、术中出血量、术后镇痛率、术后胃肠功能恢复时间、放置引流管时间、术后住院时间及并发症等指标间的差异。结果 2组患者一般资料无统计学差异,具有可比性(P均>0.05);后腹腔镜下肾脂肪囊次全游离途径组在手术时间、术中出血量、术后镇痛率、术后胃肠功能恢复时间、放置引流管时间、术后住院时间及并发症方面均优于肾脂肪囊完全游离途径组,差异有统计学意义(P均<0.05)。结论后腹腔镜下肾脂肪囊次全游离肾蒂淋巴管结扎术治疗乳糜尿效果肯定,与传统肾脂肪囊完全游离手术途径比较,该方法创伤小、恢复快、并发症少,为一理想的改进手术。     

后腹腔镜与开放式肾蒂淋巴管结扎术治疗乳糜尿的临床效果比较*

摘要：目的 探讨后腹腔镜肾蒂淋巴管结扎术（RRPLD）与开放式肾蒂淋巴管结扎术（ORPLD）治疗乳糜尿的安全性、并发症及疗效,为临床提供参考。方法 回顾性分析2009年1月－2016年10月贵州省人民医院及德江县人民医院采用肾蒂淋巴管结扎术治疗的36例乳糜尿患者。根据手术方式分为ORPLD组和RRPLD组,分别为14和22例,比较两组的一般资料、手术时间、术中出血量、术后引流管留置时间、术后肠功能恢复时间、术后住院天数及术中并发症;术后随访1～18个月,比较两组的远期治疗效果。结果 两组患者治疗均获成功,术中均未见并发症。两组患者的一般资料比较,差异均无统计学意义（P >0.05）。RRPLD组术中出血量少于ORPLD组,差异有统计学意义（P <0.05）;RRPLD组切口疼痛发生率低于ORPLD组,差异有统计学意义（P <0.05）。两组手术时间、术后肠功能恢复时间、术后引流管留置时间和术后住院天数比较,差异均无统计学意义（P >0.05）。两组复发率比较,差异无统计学意义（P >0.05）。结论 ①RRPLD与ORPLD比较,后腹腔镜术式具有术中出血量少和术后切口疼痛发生率低的优点,是一种治疗乳糜尿更为安全的方法,但两种方法术后复发率没有差异;②RRPLD治疗乳糜尿的疗效肯定,是治疗乳糜尿理想的手术方式。     

后腹腔镜肾蒂淋巴管结扎术治疗乳糜尿疗效观察

目的:探讨后腹腔镜肾蒂淋巴管结扎术治疗乳糜尿的手术方法和临床效果。方法:12例患者,男10例,女2例;年龄48~66岁。行后腹腔镜肾蒂淋巴管结扎术,观察手术时间、术中出血量、术后肠道功能恢复和术中术后并发症及手术效果。结果:手术平均时间107 min,术中平均出血量48 mL,术后肠道功能恢复时间24~48 h,术后当日乳糜尿消失,术后平均住院6.2 d,术中术后无明显并发症。随访2~24个月,无复发。结论:后腹腔镜肾蒂淋巴管结扎术治疗乳糜尿近期疗效较好,具有术中出血量少、微创、淋巴管结扎彻底、术后住院时间短、恢复快等优点,是目前治疗乳糜尿较理想的手术方式。     

后腹腔镜肾蒂淋巴管结扎术治疗乳糜尿

目的探讨后腹腔镜肾蒂淋巴管结扎术治疗乳糜尿的手术方法和临床效果。方法回顾性分析8例单侧乳糜尿患者行后腹腔镜肾蒂淋巴管结扎术治疗的临床资料。结果8例患者均手术成功,平均手术时间82 min,术中平均出血量70 mL,无意外损伤,术后平均住院7.2 d。患者出院时尿液均清亮,8例患者尿乙醚试验全部阴性。随访3～22个月,无复发。结论后腹腔镜肾蒂淋巴管结扎术治疗乳糜尿疗效较好,具有术中出血量少、创伤小、淋巴管结扎彻底、术后住院时间短、恢复快等优点,是目前治疗乳糜尿较理想的手术方式。     

后腹腔镜与开放手术行肾蒂淋巴管结扎治疗乳糜尿疗效比较

【目的】评价后腹腔镜技术行肾蒂淋巴管结扎术治疗乳糜尿的临床效果。【方法】乳糜尿患者21例,年龄43～72岁。经腹膜后腹腔镜手术（A组）12例,病变位于左侧7例,右侧3例,双侧2例;传统开放手术（B组）9例,病变位于左侧2例,右侧5例,双侧2例,行肾蒂淋巴管结扎术。比较两组的术中并发症、手术时间、术中出血量、术后肠道功能恢复时间、术后住院时间以及术后复发情况。[结果]21例患者术后近期乳糜尿消失。A、B两组手术时间分别为（78．4±32．3）min和（104．6±23．6）min（P〈0．01）;术中出血量分别为（56．3±34．8）mL和（131．5±75．3）mL（P〈0．01）;肠道功能恢复时间分别为（32．4±12．6）h和（47．9±18．3）h（P〈0．01）;引流管留置时间分别为（1．8±0．8）d和（2．7±1．8）d（P〈0．01）;术后住院时间分别为（5．7±2．5）d和（8．7±1．5）d（P〈0．01）。随访时间3～60个月,A、B组各有1例复发。B组中2例伤口延迟愈合。【结论】腹膜后腹腔镜技术行肾蒂淋巴管结扎术治疗乳糜尿具有创伤小、恢复快的优点,疗效与开放手术一致。     

后腹腔镜肾蒂淋巴管结扎术治疗乳糜尿

目的:探讨应用后腹腔镜肾蒂淋巴管结扎术治疗乳糜尿的手术方法、疗效和临床价值。方法:对5例乳糜尿患者行后腹腔镜肾蒂淋巴管结扎术,乳糜尿试验均为阳性,术前采用膀胱镜检查确定诊断。结果:5例患者手术均成功,手术时间60¹30 min,平均手术时间(69.0±11.9)min;术中出血量60130 min,平均手术时间(69.0±11.9)min;术中出血量60²00m L,平均术中出血(124.0±55.9)m L;术中和术后均无明显并发症,术后平均住院时间(5.8±1.3)d。5例患者出院时尿液均清亮,尿乙醚试验全部阴性。随访12200m L,平均术中出血(124.0±55.9)m L;术中和术后均无明显并发症,术后平均住院时间(5.8±1.3)d。5例患者出院时尿液均清亮,尿乙醚试验全部阴性。随访12³0个月无复发。结论:后腹腔肾蒂淋巴管结扎术具有微创、出血少、恢复快、术后无复发等优点,临床效果良好,达到开放手术临床效果,值得推广。     

解剖性后腹腔镜肾蒂淋巴管结扎治疗乳糜尿(附15例报告)

目的 总结解剖性后腹腔镜肾蒂淋巴管结扎术治疗乳糜尿的临床经验.方法 15例乳糜尿患者行解剖性后腹腔镜肾蒂淋巴管结扎术,该手术对经典后腹腔镜下肾蒂淋巴管结扎术做了以下改进:精细解剖肾脏动、静脉,如为左侧手术则解剖出精索或卵巢内静脉及肾上腺中央静脉,离断其周围组织,保留以上血管;于肾门处显露肾上腺下极,自此平面以上肾脏脂肪纤维结缔组织不游离.结果 15例手术顺利,无中转开放手术者,手术时间45～80 min,平均(50±10.2)min,术中出血量20～100 mL,平均(30±23.5)mL,无1例肾血管损伤,均术后次日即下床活动,出院时正常饮食下尿液清凉,尿乳糜实验均阴性.随访3 ～ 40个月,未见乳糜尿复发、肾下垂及肾萎缩.结论 后腹腔镜解剖性肾蒂淋巴管结扎术治疗乳糜尿安全有效,具有血管显露清晰、无需完全游离肾脏、淋巴管结扎彻底、手术时间短、出血少、并发症少及术后患者恢复快等优点,值得推广.     

后腹腔镜肾蒂淋巴管剥脱术治疗重症乳糜尿的护理

目的总结后腹腔镜肾蒂淋巴管剥脱术治疗重症乳糜尿的治疗及护理经验,更好地服务临床工作。方法采用经后腹腔镜肾蒂淋巴管剥离术治疗21例重症乳糜尿患者,做好围手术期护理工作,特别是术前心理护理,术后病情监护,并发症防治等。结果本组21例乳糜尿患者术后病情平稳,无高碳酸血症和腹腔出血等并发症的发生。术后3日复查尿乳糜试验阴性。随访6～20个月无复发,营养状况明显改善。结论后腹腔镜下肾蒂淋巴管剥离术治疗乳糜尿是一种安全、有效的治疗方法。加强围手术期护理,予术前护理准备充分,术中严密监护,术后细致观察,是确保手术顺利进行,患者顺利康复,减少并发症,防止复发的重要护理措施。     

后腹腔镜肾蒂淋巴管剥脱术治疗重症乳糜尿的护理

目的 总结后腹腔镜肾蒂淋巴管剥脱术治疗重症乳糜尿的治疗及护理经验,更好地服务临床工作.方法 采用经后腹腔镜肾蒂淋巴管剥离术治疗21例重症乳糜尿患者,做好围手术期护理工作,特别是术前心理护理,术后病情监护,并发症防治等.结果 本组21例乳糜尿患者术后病情平稳,无高碳酸血症和腹腔出血等并发症的发生.术后3日复查尿乳糜试验阴性.随访6～20个月无复发,营养状况明显改善.结论 后腹腔镜下肾蒂淋巴管剥离术治疗乳糜尿是一种安全、有效的治疗方法.加强围手术期护理,予术前护理准备充分,术中严密监护,术后细致观察,是确保手术顺利进行,患者顺利康复,减少并发症,防止复发的重要护理措施.     

开颅手术应用条带状备皮的效果

[目的]探讨神经外科手术术前应用小区域条带状备皮的可行性,以减轻女性病人的心理压力。[方法]选择神经外科手术女性病人12 0例,随机分为观察组60例和对照组60例,对照组采用常规开颅手术的备皮方法,实验组采用条带状备皮方法。比较两组备皮时病人的疼痛不适感、头皮损伤、手术野皮肤的无菌准备和术后切口感染的发生率。[结果]观察组备皮时病人的疼痛不适感和头皮损伤均显著低于对照组(P <0 .0 1) ,两种备皮法对手术野皮肤的无菌准备质量和术后切口愈合并无显著影响(P >0 .0 5 )。[结论]小区域条带状备皮在开颅手术中的应用是安全的,具有一定的优越性。     

Genetics of lymphatic anomalies

Lymphatic anomalies include a variety of developmental and/or functional defects affecting the lymphatic vessels: sporadic and familial forms of primary lymphedema, secondary lymphedema, chylothorax and chylous ascites, lymphatic malformations, and overgrowth syndromes with a lymphatic component. Germline mutations have been identified in at least 20 genes that encode proteins acting around VEGFR-3 signaling but also downstream of other tyrosine kinase receptors. These mutations exert their effects via the RAS/MAPK and the PI3K/AKT pathways and explain more than a quarter of the incidence of primary lymphedema, mostly of inherited forms. More common forms may also result from multigenic effects or post-zygotic mutations. Most of the corresponding murine knockouts are homozygous lethal, while heterozygotes are healthy, which suggests differences in human and murine physiology and the influence of other factors.     

The lymphatic vasculature revisited

Lymphatic vessels constitute a ubiquitous countercurrent system to the blood vasculature that returns interstitial fluid, salts, small molecules, resorbed fat, and cells to the bloodstream. They serve as conduits to lymph nodes and are essential for multiple physiologic activities. However, they are also hijacked by cancer cells to establish initial lymph node metastases, as well as by infectious agents and parasites. Despite these obvious important functions in human pathologies, a more detailed understanding of the molecular mechanisms involved in the regulation of the lymphatic vasculature has trailed that of the blood vasculature for many years, mainly because critical specific characteristics of lymphatic endothelial cells were discovered only recently. In this Review series, several major aspects of the active and passive involvement of the lymphatic vasculature in human disease and physiology are presented, with a focus on translational findings.Many scientific fields develop in waves that vary in frequency and amplitude, with rapid progress initiated by serendipitous findings in seemingly unrelated fields. Research on the structure and function of the lymphatic vasculature exemplifies this model. As presented in this Review series, novel insights into the involvement of lymphatic vessels in human disease and physiology have not only provided additional information on pathogenesis, but have changed the prevailing paradigms of disease mechanisms as a prelude to improved targeted therapies.Historically, the identification of lymphatic vessels relied on their content, known as “white blood” (1). Their macroscopic visualization was made possible by intradermal injection of colloid tracers in fresh cadavers, and striking examples of the results are provided by the anatomical wax models produced in Florence around 1770 and on display in the Josephinum in Vienna ( www.josephinum.ac.at). A model of the cervical lymphatic network is depicted on the cover of this series. These techniques primarily detect large branches of the lymphatic system, i.e., the collecting vessels that serve as peristaltic pumps to move the lymphatic fluid toward the thoracic duct by a precisely coordinated contraction of the smooth muscles in their media, while strategically positioned valves prevent reflux. Recent advances in our understanding of smooth muscle contraction (2) and formation and stability of the valves (3) have clarified these processes. In this series, Eva Sevick-Muraca and colleagues (4) summarize the current state of in vivo visualization that reveals the lymphatic vasculature in much better resolution. Though our understanding of the collecting vessels has improved, we are progressively gaining detailed knowledge concerning the initial microvascular segment, which is arguably the most functionally relevant part of the vascular lymphatic tree and hence the topic of most Reviews in this series. Under the microscope the initial lymphatic capillaries are composed of sacs of endothelial cells and are devoid of pericytes. These capillaries merge into a precollector vessel segment with few pericytes that opens into the collectors (Figure ​(Figure11). Open in a separate windowFigure 1Basic design of the initial segment of the lymphatic microvasculature of the dermis.The initial capillaries start as blind sacs. Their LECs form overlapping junctions, express large amounts of the membrane mucoprotein podoplanin (green), and release the chemokine CCL21. This attracts CCR7⁺ immune cells, such as dendritic cells and Tregs. The precollectors contain LECs with low amounts of podoplanin, and the LECs produce CCL27, which attracts inflammatory CCR10⁺ T lymphocytes. This precollector segment opens into the collecting vessels that are endowed with podoplanin-low endothelial cells and that form valves. Pericytes/mural cells partially cover the precollectors and completely ensheath collecting vessels. At the center of the current increase in lymphatic research are new insights into the biology of the lymphatic endothelial cells (LECs). This phase was heralded by detailed ultrastructural investigations of initial lymphatic vessels (5). The critical breakthrough to a functional understanding was achieved with the discovery of the main lymphangiogenic growth factor, VEGFC, and its receptor, VEGFR3 (6). This was followed by the identification of proteins that discriminate between endothelial cells of the lymphatic and blood vessel lineages (7) that can serve as selective markers for the localization and isolation of LECs (8, 9), a development reviewed by Kari Alitalo and colleagues in this series (10). Since the lymphatic system is as branched and widely distributed as the blood vasculature, it is not surprising that it is involved in most disease processes, ranging from inflammation to metastatic spreading of cancers. It is becoming increasingly clear that the lymphatics do not just serve as passive conduits for interstitial fluid and cells, but are actively involved in disease, as reviewed in detail in this series. Below, I highlight a few selected aspects of current research that could become clinically relevant in the coming years.     

Mechanisms of lymphatic metastasis

Malignant tumors release growth factors such as VEGF-C to induce lymphatic vessel expansion (lymphangiogenesis) in primary tumors and in draining sentinel LNs, thereby promoting LN metastasis. Surprising recent evidence suggests that lymphatic vessels do not merely represent passive channels for tumor spread, but that they may actively promote tumor cell recruitment to LNs, cancer stem cell survival, and immune modulation. New imaging approaches allow the sensitive visualization of the earliest LN metastases and the quantitative, noninvasive measurement of the function of tumor-draining lymphatic vessels, with potential applications in the development of biomarkers for prognosis and measurement of therapeutic response.Cancer metastasis, the dissemination of cancer cells from the primary tumor to organs, where they initiate malignant growth, is the primary cause of cancer-related deaths. There has been a plethora of studies addressing the mechanisms of tumor metastasis via the bloodstream to distant organs; however, the majority of epithelial cancers first develop metastatic growth by spreading via lymphatic vessels to their draining LNs. Indeed, the detection of metastases within the sentinel LNs (SLNs; the first LNs into which a tumor drains) has major prognostic implications for patient survival and often also determines the choice of adjuvant therapies (1). Despite the obvious clinical importance of LN metastasis, the mechanisms leading to tumor spread via lymphatic vessels have remained unknown for decades. In fact, the prevailing view suggested that lymphatic vessels only play a passive role in tumor metastasis, serving merely as channels for tissue-invading tumor cells. The limited knowledge in this field was due to the relatively low scientific interest in lymphatic vessels as compared to the blood vasculature, the lack of reliable molecular markers to distinguish between lymphatic and blood vessels, the absence of identified growth factors for the lymphatic system, and the paucity of suitable experimental models to study and quantify LN metastasis. During the last 15 years, however, there has been substantial progress in the field of lymphatic vessel biology, which has rapidly lead to the recognition of the lymphatic vascular system as a major player involved in a multitude of human diseases (2). In this article, we will discuss the major discoveries made by our laboratory and many other researchers that have led to the recognition of a major role for the lymphatic vasculature in promoting cancer metastasis and to the new concepts of tumor-associated and LN lymphangiogenesis with a specific focus on the development of new strategies to image and therapeutically target the lymphatic system in cancer.