前列腺增生伴逼尿肌无力患者电切术治疗后的临床分析

目的 探讨良性前列腺增生（BPH）膀胱出口梗阻（BOO）致膀胱逼尿肌收缩功能无力（DU）患者的临床诊断及治疗方式.方法 2006年1月至2010年12月经治的60例BPH老年患者,均行经尿道前列腺电切术（TURP）.根据逼尿肌收缩压力（Pdet）分为4组：A组逼尿肌正常组（Pdet＞ 40 cm H2O）,B组逼尿肌无力组（Pdet＜40 cm H2O）,再将B组细分为：B1组（轻度逼尿肌无力组）（20 cm H2O ＜Pdet＜40 cm H2O）及B2组（重度逼尿肌无力组）（Pdet＜20 cm H2O）,分别对其术后的排尿症状进行了2～6年的随访.结果 统计学比较术后A、B组间及B1、B2组间的生活质量评分（QOL）、排尿梗阻症状及刺激症状,差异无统计学意义（P＞0.05）.结论 BPH患者BOO解除后,逼尿肌功能状态可能并不影响下尿路症状（LUTs）的改善.因此对BPH合并DU的患者进行必要的沟通后行手术治疗解除梗阻,可改善患者生活质量.     

良性前列腺增生并急性尿潴留后的逼尿肌功能评估及其临床意义

目的评估良性前列腺增生(BPH)并急性尿潴留(AUR)后的逼尿肌功能及其临床意义。方法随机选择38例BPH并AUR患者行膀胱压力-容积和压力-流率测定,分析留置尿管时间、逼尿肌收缩力、逼尿肌无抑制性收缩(DI)、DI幅度、梗阻程度之间的相关性。结果38例患者中,发生DI者22例(57.9%),DI幅度3~176(100±41)cmH2O(1cmH2O=0.098kPa);有随意性逼尿肌收缩者32例(84.2%),明确诊断为膀胱出口梗阻者28例(73.7%);逼尿肌收缩力与留置尿管时间无相关性(r=-0.024,P>0.05),与DI、DI幅度、梗阻程度有相关性(r分别为0.377、0.604、0.473,P分别为<0.05、0.01、0.01);DI与梗阻程度无相关性(r=-0.222,P>0.05),DI幅度与梗阻程度呈显著性正相关(r=0.494,P<0.01)。结论BPH并AUR患者尿动力学检查前无需留置尿管2~3周以上;有DI者的逼尿肌收缩力强于无DI者;膀胱出口梗阻越严重,DI幅度越大,逼尿肌收缩力越强,手术效果越好。     

良性前列腺增生患者尿动力学及逼尿肌超微结构的相关性研究

目的 探讨良性前列腺增生(BPH)患者尿动力学检查与膀胱逼尿肌超微结构的关系.方法 BPH组患者43例,平均年龄(69.5±6.0)岁;无膀胱出口梗阻的其他疾病患者21例为对照组,平均年龄(65.4±7.2)岁.2组患者均行尿动力学检查,透射电镜观察膀胱逼尿肌超微结构.比较2组患者尿动力学检查及逼尿肌超微结构情况.结果 BPH组和对照组患者国际前列腺症状评分分别为(21.1±3.0)和(7.6土1.4)分,P<0.01;最大尿流率分别为(7.7±1.3)和(14.9±2.3)ml/s,P<0.01;最大尿流率时逼尿肌收缩压分别为(60.1±11.o)和(48.7±7.1)cm H2o(1 cm HzO=0.098 kPa),P<0.05;梗阻系数分别为44.8±9.9和19.0±5.9,P<0.01;膀胱逼尿肌细胞线粒体相对密度分别为0.81±0.24和1.03±0.11,P<0.05;膀胱逼尿肌细胞间隙分别为(19.4±4.8)和(14.1±2.0)nm,P<0.05.结论 BPH患者逼尿肌细胞线粒体水肿、相对密度减低,是导致逼尿肌收缩力减弱的原因之一;同时由于细胞间隙增宽,导致逼尿肌收缩速度减慢或不协调,引起膀胱协调收缩力下降.     

良性前列腺增生伴逼尿肌收缩无力的手术疗效分析及预判参数研究

目的探讨经尿道前列腺电切术(TURP)治疗良性前列腺增生(BPH)伴膀胱逼尿肌收缩无力的效果及预测其疗效的尿动力学参数。方法对57例术前尿动力学检查提示膀胱出口梗阻并伴有逼尿肌收缩无力的BPH患者予以TURP治疗,观察术后患者的症状及排尿情况,并将术前尿动力学参数与术后的排尿后剩余尿量及最大尿流率之间的相关性进行分析。结果本组患者术后国际前列腺症状评分(IPSS)、生活质量评分(QoL)、最大尿流率(Q_(max))、残余尿量(PVR)均有显著改善,术前与术后比较,差异有统计学意义(P0.05)。相对膀胱出口梗阻参数比膀胱出口梗阻指数、膀胱收缩指数与术后PVR及Qmax有更强的相关性。结论对合并逼尿肌收缩无力的BPH患者行TURP手术治疗,能取得良好的效果。相对膀胱出口梗阻参数比其它尿动力学参数对伴膀胱逼尿肌收缩无力的BPH患者的治疗抉择和疗效预测有更重要价值。     

逼尿肌储备功能与良性前列腺增生合并膀胱出口梗阻患者手术疗效的关系

良性前列腺增生(BPH)所致膀胱出口梗阻(BOO)多需手术处理.逼尿肌收缩障碍是术后疗效不良的主要原因.早期发现逼尿肌收缩功能受损患者对有效预测手术疗效具有重要意义.本研究初步探讨BPH所致B00患者逼尿肌收缩储备功能与手术疗效的关系.     

前列腺增生患者膀胱出口梗阻程度对尿动力学指标的影响

目的探讨前列腺增生患者膀胱出口梗阻程度对尿动力学指标的影响及临床意义。方法分析113例前列腺增生患者的尿动力学资料,根据膀胱出口有无梗阻分为梗阻组和非梗阻组,梗阻组又根据梗阻级别分Ⅲ、Ⅳ、Ⅴ、Ⅵ级四组。结果梗阻组的最大尿流率、膀胱顺应性值和逼尿肌收缩力减弱发生率明显低于非梗阻组,逼尿肌不稳定和急性尿潴留发生率明显高于非梗阻组。梗阻组内各梗阻级别之间在顺应性值、逼尿肌不稳定和急性尿潴留的发生率上无显著性差异,随梗阻级别增加尿流率和逼尿肌收缩功能受损发生率下降。结论一些反映排尿异常和逼尿肌功能的尿动力学指标受膀胱出口梗阻程度影响,在无法进行压力/流率分析时综合分析这些指标有助于判断出口梗阻及其程度。     

良性前列腺增生症不同术式术后疗效不良原因的研究

目的：探讨良性前列腺增生症（BPH）不同术式术后疗效不良的原因及特点,进一步提高手术成功率。方法：应用尿动力学检测其他检查手段对84例BPH术后症状改善不良的患者按手术方式的不同分组进行检查分析。结果：尿道前列腺电切术组术后改善不良的主要原因依次为膀胱出口再梗阻（84.9％）、逼尿肌收缩无力（30.4％）和逼尿肌不稳定（DI）（18.2％）。开放组主要原因依次为逼尿肌收缩无力（52.9％）、逼尿肌不稳定（35.2％）和膀胱出口再梗阻（33.3％）。2组数据经X^2检验差异有显著性意义（P=0.000）。结论：不同手术方式,其术后疗效不良原因差异有显著性。TURP组再梗阻率远高于开放组,在一定程度上反映目前TURP手术技术有待进一步提高。术前存在逼尿肌收缩无力和DI,是导致术后疗效不良的重要因素。     

前列腺增生手术前后膀胱重量变化的研究

目的 探讨良性前列腺增生（BPH）经尿道前列腺切除术（TURP）手术前后膀胱重量的变化及临床意义。方法 BPH患者63例,其中术后随访资料完整者21例,以相同年龄段无下尿路症状30例男性作为对照组。经腹B超测量膀胱壁厚度并结合膀胱容量按照球形体积公式估算膀胱重量。以尿动力学检查评价膀胱出口梗阻（BOO）和膀胱功能。63例BPH患者术前膀胱重量（97±54）g,对照组为（41±14）g,膀胱重量与梗阻分级（LinPURR）呈正相关（R=0．47）,与最大尿流率（Qmax）呈负相关（R=-0．52）,与残余尿量呈正相关（R=0．48）,差异均有统计学意义（P〈0．01）,与逼尿肌收缩强度（WF）呈负相关（R=-0．40,P〈0．05）。21例患者术前B超估测膀胱重量（UEBW）（99±50）g。结果 21例患者术后UEBW为（56±21）g,与术前比较差异有统计学意义（P〈0．01）。术后UEBW平均下降43．68％,国际前列腺症状评分（IPSS）下降16．81分,Qmax平均增加8．38ml／8。结论 膀胱重量作为一项无创性检查方法,对前列腺增生症进展的监测、术前评估和术后疗效的评价具有临床应用价值。     

良性前列腺增生手术前后尿动力学检查及其临床价值

目的 探讨尿动力学检查在良性前列腺增生症(BPH)诊治中的价值.方法 回顾性分析72例良性前列腺增生症患者手术前后尿动力学检查结果 .结果 72例均有膀胱出口梗阻(BOO),其中40例伴有不稳定膀胱(DI),占55%.66例膀胱逼尿肌收缩正常或增强,6例膀胱逼尿肌收缩减弱.65例尿流率(UFR)低平,7例正常.手术后3个月,66例症状消失,2例出现并发症经再次处理治愈,不稳定膀胱15例,占21%,包括5例低顺应性膀胱.结论 通过对良性前列腺增生症患者术前术后详细的尿动力学检查,可明确患者有无下尿路梗阻、膀胱逼尿肌顺应性和收缩功能及尿道括约肌功能.这对于合理选择病人及术后疗效判定有重要的指导意义.     

良性前列腺增生症尿动力学检查的意义

目的:探讨尿动力学检查对良性前列腺增生症（BPH）治疗的意义。方法：通过对48例BPH患者的尿动力学检查,发现3例无膀胱出口梗阻（BOO）,6例可疑BOO,39例有不同程度的BOO,并发逼尿肌不稳定（DI）9例,逼尿肌收缩无力（逼尿肌收缩为W－以下）5例,高顺应性膀胱2例,低顺应性膀胱6例。结果：根据检查结果分别采用TURP或耻骨后前列腺开放切除术、耻骨上膀胱穿刺造瘘加药物治疗一段时间后再手术、药物治疗三种方法,取得较好的效果。结论：尿动力学检查是判定BPH患者是否需要手术治疗的客观量化指标,引流尿液及使用新斯的明和加兰他敏是治疗逼尿肌收缩无力的有效方法。     

Analysis of the pathophysiology of lower urinary tract symptoms in patients after prostatectomy

OBJECTIVES: To analyze the pathophysiology of persistent lower urinary tract symptoms (LUTS) in patients after transurethral prostatectomy (TURP). METHODS: A total of 185 patients who had persistent LUTS after TURP were enrolled into this study. All of these patients underwent multichannel videourodynamic studies and were classified into 6 groups according to the urodynamic results. Preoperative prostate volume, resected adenoma weight, and preoperative Q(max) were determined in each of the groups and the symptomatology and urodynamic findings were compared. RESULTS: A normal videourodynamic tracing was found in 17 patients (9.1%), pure detrusor instability in 18 (9.6%), low detrusor contractility in 35 (18.7%), detrusor instability and inadequate detrusor contractility (DHIC) in 27 (14.4%), poor relaxation of the urethral sphincter in 36 (19.3%), and bladder outlet obstruction (BOO) in 52 (27.8%). Incontinence was noted in 74 patients (40%), and 18 of them had BOO (24.3%). In urodynamic findings, Q(max) and residual urine showed no significant difference among patients with low contractility, poor relaxation of sphincter, DHIC and BOO. Concerning the preoperative prostatic volume, patients with low contractility, poor relaxation of urethral sphincter, and DHIC had a nonsignificantly smaller prostate volume and resected prostate weight than other groups. Preoperative Q(max) showed no significant difference among all groups. CONCLUSIONS: Symptoms alone are unreliable in predicting urodynamic findings with respect to obstruction and detrusor instability after TURP. Over half of the patients with persistent LUTS had a small prostate volume and small resected adenoma weight, indicating that some of these patients may not have had BOO. Videourodynamic study is helpful in making an accurate diagnosis for refractory LUTS after TURP.     

前列腺增生致膀胱出口梗阻后逼尿肌功能改变对尿动力学参数的影响

目的探讨良性前列腺增生症（BPH）致膀胱出口梗阻（BOO）后逼尿肌功能改变对尿动力学参数的影响。方法109例具有完整尿动力学结果的BPH患者根据有无B00分为梗阻组和非梗阻组;梗阻组根据梗阻级别分Ⅲ、Ⅳ、Ⅴ、Ⅵ级4组;逼尿肌收缩力分为逼尿肌收缩力减弱（DCA）与收缩力正常组;逼尿肌不稳定（DI）分DI与非DI;膀胱顺应性（BC）分高、正常、低顺应性三组;28例患者行经尿道前列腺切除术（TURP）术前及术后尿动力参数对比。结果BOO组的前列腺体积（PV）、国际前列腺症状评分（IPSS）、DI、急性尿潴留（AUR）发生率明显高于非BOO组（P〈O．05）;BOO组的最大尿流率（Qmax）、BC值、DCA发生率明显低于非BOO组（P〈0．05）;逼尿肌收缩力正常组的残余尿（RV）与BC值明显低于减弱组（P〈0．05）,而BOO和DI的发生率明显高于减弱组（P〈0．01）;DI组的年龄、BC值及DCA的发生率明显低于非DI组（P〈0．05）,而B00级别和AUR的发生率明显高于非DI组（P〈0．01）;低BC组IPSS、BOO级别、AUR发生率明显高于正常及高BC组（P〈0．05）,而DCA发生率明显低于正常及高BC组（P〈0．01）;术后Qmax、BC值较术前明显升高（P〈0．05）,RV、IPSS、DI发生率较术前明显减小（P〈0．01）。结论①BOO常与低顺应性膀胱、DI、AUR合并存在;②IPSS评分不能提示是否存在DI,DI的存在不影响IPSS评分;③TURP是治疗前列腺增生的金标准;④尿动力检查能全面了解有无BOO及BOO所致逼尿肌功能改变情况,对BPH的临床鉴别诊断、预后估计及选择恰当治疗方案都具有重要意义。     

Is the short‐term outcome of transurethral resection of the prostate affected by preoperative degree of bladder outlet obstruction,status of detrusor contractility or detrusor overactivity?

AIM: The aim of this study was to investigate whether the preoperative degree of bladder outlet obstruction (BOO), detrusor underactivity (DUA) or detrusor overactivity (DO) affected the short-term outcome of transurethral resection of the prostate (TURP) for patients with lower urinary tract symptoms suggestive of benign prostatic hyperplasia (LUTS/BPH). METHODS: Ninety-two patients with LUTS/BPH aged 50 years or older who were considered to be appropriate candidates for TURP were included in this study. Pressure-flow study and filling cystometry were performed to determine BOO, DUA and DO before TURP. The efficacy of TURP was determined at 3 months after surgery using the efficacy criteria for treatment of BPH assessed by the International Prostate Symptom Score, QOL index, maximum flow rate and postvoid residual urine volume. RESULTS: On preoperative urodynamics, 60%, 40% and 48% of patients showed BOO, DUA and DO, respectively. After TURP, 76% showed 'excellent' or 'good' overall efficacy, whereas only 13% fell into the 'poor/worse' category. The efficacy was higher as the preoperative degree of BOO worsened. In contrast, neither DO nor DUA influenced the outcome of TURP. However, the surgery likely provided unfavorable efficacy for patients having DO but not BOO. Only 20% of the patients who had both DO and DUA but did not have BOO achieved efficacy. CONCLUSIONS: Transurethral resection of the prostate is an effective surgical procedure for treatment of LUTS/BPH, especially for patients with BOO. DUA may not be a contraindication for TURP. The surgical indication should be circumspect for patients who do not have BOO but have DO.     

良性前列腺增生患者膀胱出口梗阻及逼尿肌收缩强度对剩余尿的影响

目的　探讨良性前列腺增生 (BPH)患者膀胱出口梗阻 (BOO)及逼尿肌收缩强度与剩余尿的关系。　方法　应用尿动力学方法检测 181例BPH患者BOO情况和逼尿肌收缩强度 ,以导管法结合膀胱灌注量与排出量之差确定剩余尿 ,对相互关系进行统计学分析。　结果　 181例患者剩余尿量 0～ 2 0 0ml。逼尿肌收缩强度减弱 ,剩余尿量增多 (F =12 .14 3,P =0 .0 0 1) ;BOO加重 ,剩余尿量无明显改变 (F =2 .386 ,P =0 .0 71)。 2 5例 (13.8% )患者逼尿肌收缩强度减弱或正常时仍有较多剩余尿(>10 0ml)。　结论　剩余尿增多主要由逼尿肌收缩强度减弱所致 ,而随着BOO加重 ,剩余尿量无明显变化     

良性前列腺增生患者膀胱出口梗阻和逼尿肌功能的分析

目的：探讨尿动力学检查对BPH患者膀胱出口梗阻（BOO）和逼尿肌功能的诊断意义.方法：对95例BPH患者进行压力-容积和压力-流率测定.结果：95例BPH患者中BOO 57例,无BOO23例,其余15例为可疑或分析困难.BOO组前列腺体积大于无BOO组（62.4±16.1）cm^3 vs（41.0±7.1）cm^3（P＜0.05）,最大尿流率（Qmax）小于无BOO组（5.4±1.9）ml/s vs（12.4±5.0）ml/s（P＜0.05）,两组IPSS评分无差别（23.7±4.4）分vs（25.2±4.9）分（P＞0.05）.BOO组有逼尿肌不稳定收缩（DD34例,无BOO组D119例.结论：尿动力学检查有助于判断有无BOO存在,了解BPH患者的逼尿肌功能.IPSS不能判断患者的下尿路症状（LUTS）是否因BOO导致.BPH患者前列腺体积不足很大,但LUTS明显时,应行尿动力学检查.自由尿流率测定对BOO诊断有一定帮助.DI是无BOO患者发生LUTS的重要因素.     

逼尿肌活动低下在下尿路症状中的临床特征及诊疗策略分析

目的:探讨逼尿肌活动低下(DU)在下尿路症状(LUTS)患者中的流行病学现状、临床特征及诊疗策略。方法:回顾性分析了我院1 019例排除神经源性膀胱及解剖结构异常的LUTS患者的尿流动力学检查结果及随访资料,探讨DU在LUTS中的流行病学及临床诊治特点,并对106例DU患者治疗前后行尿流动力学检查,结合文献进行临床分析。结果:在就诊患者中,储尿期症状最为多见,在男性患者中,排尿期症状稍多于储尿期症状,而女性患者储尿期症状明显多于排尿期症状。男性患者中膀胱出口梗阻(BOO)的患者为57.9%,而女性患者中压力性尿失禁(SUI)患者达到了43.3%。27.4%男性及23.2%女性诊断为DU,男性及女性患病率差异无统计学意义。DU患者与非DU患者的临床表现无明显差异,均以LUTS为主要表现。DU可能合并有逼尿肌过度活动或BOO。DU随着年龄的增加,患病率逐渐增加。106例DU患者经治疗后行尿动力学检查发现逼尿肌收缩力有一定提高,治疗前后逼尿肌肌力差异有统计学意义。结论:DU是LUTS患者的常见病因,并有可能同时合并有逼尿肌过度活动或BOO。目前针对DU患者的治疗有一定效果。     

良性前列腺增生患者膀胱内前列腺突人程度的超声测定

目的 探讨良性前列腺增生(BPH)患者膀胱内前列腺突入程度(IPP)测定对膀胱出口梗阻及膀胱功能的预测与评价. 方法 BPH患者206例,年龄55～84岁,均为首次就诊,有不同程度的尿频、尿急等下尿路症状.行经腹B超测定IPP并根据程度分2组:研究组78例(IPP>10mm)和对照组128例(IPP≤10 mm),分析2组患者临床资料及尿动力学检查结果 间的关系. 结果 研究组和对照组前列腺体积[(73.7±35.9)、(62.8±36.5)ml]、前列腺特异性抗原[(1.81±0.67)、(1.64±0.36)ng/ml]、残余尿量[(290.2±217.2)、(228.2±167.9)ml]、急性尿潴留发生率(33.3%、18.0%)及膀胱小梁化发生率(23.1%、11.7%)比较差异均有统计学意义(P<0.05).IPP与前列腺体积、残余尿量呈正相关(r分别为0.401,0.342).2组患者排尿期最大尿流率[(7.6±4.1)、(9.1±3.6)ml/s]、膀胱过度活动症发生率(82.1%,17.2%)、膀胱顺应性降低率(35.9%,12.5%)、最大逼尿肌压力[(109.8±84.9)、(84.9±44.1)cm H2O,1 cm H2O=0.098 kPa]及膀胱出口梗阻指数(75.2±27.1、65.9±34.6)比较差异均有统计学意义(P<0.05); IPP与最大尿流率呈负相关(r=-0.284),与最大逼尿肌压力及膀胱出口梗阻指数呈正相关(r分别为0.252,0.456).经保守治疗后,2组患者急性尿潴留复发率分别为64.3%(9/14)和23.5%(4/17)(P<0.05). 结论 IPP可以作为初步预测及评价膀胱出口梗阻程度和膀胱功能的指标之一;前列腺突入膀胱的BPH患者膀胱出口梗阻及膀胱功能受损程度明显高于无突入患者,对于前列腺突入膀胱的BPH患者.尤其是合并急性尿潴留患者应及早采取外科手术治疗.     

Bladder overactivity in mice after 1 week of outlet obstruction. Mainly afferent dysfunction?

PURPOSE: Partial bladder outlet obstruction (BOO) is an established way to create bladder overactivity in animals. However, the micturition pattern achieved can vary considerably. We investigated the correlation between different micturition patterns, post-void residual urine, bladder capacity, bladder weight and in vitro contractility in a conscious mouse model of BOO. MATERIALS AND METHODS: Female MNRI mice with moderate (urethral) outlet obstruction were used. After 7 days of BOO cystometry without anesthesia was performed with the animal in a metabolic cage. Results were compared with those in unoperated controls and sham operated animals. In vitro contractility studies were performed. RESULTS: The majority of obstructed animals had an overactive voiding pattern with increased nonvoiding detrusor activity and without increased bladder weight. The remaining obstructed animals had significantly increased bladder weight and normal micturition volume but increased threshold pressure, bladder capacity and post-void residual urine. Subtle in vitro differences were found among the groups. CONCLUSIONS: The urodynamic characteristics of BOO mice correlate with bladder weight. However, detrusor overactivity in obstructed mice may develop without an increase in bladder weight and with only subtle changes in smooth muscle function, as investigated in vitro. This observation suggests that major disturbances caused by BOO may lie in the afferent arm of the signaling pathway.     

The detrusor muscle: an innocent victim of bladder outlet obstruction

OBJECTIVES: Benign prostatic hyperplasia (BPH) is considered a frequent cause of bladder outlet obstruction (BOO) and lower urinary tract symptoms (LUTS), although the physiopathologic mechanism through which BPH causes LUTS is not clear. Several morphologic and functional modifications of the bladder detrusor have been described in patients with BPH and could play a direct role in determining symptoms. The opinion is spreading that the enlarged prostates in patients with LUTS is nothing more than a mere bystander. Evidence has accumulated, however, supporting the role of BPH-related BOO as the direct cause determining bladder dysfunction and indirectly causing urinary symptoms. The present review addresses the bladder response to BOO, particularly focusing on the physiopathologic cascade that links obstructive BPH to bladder dysfunction. METHODS: A literature review of peer-reviewed articles has been performed, including both in vivo and in vitro studies on human tissue and animal model experiments. RESULTS: Epithelial and smooth muscle cells in the bladder wall are mechanosensitive, and in response to mechanical stretch stress caused by BOO, undergo modifications of gene expression and protein synthesis. This process involves several transduction mechanisms and finally alter the ultrastructure and physiology of cell membranes, cytoskeleton, contractile proteins, mitochondria, extracellular matrix, and neuronal networks. CONCLUSIONS: BOO is the initiator of a physiopathologic cascade leading to deep changing of bladder structure and function. Before being a direct cause of storing-phase urinary symptoms, the bladder is the first innocent victim of prostatic obstruction.