糖尿病神经原性膀胱的治疗体会（附100例临床分析）

糖尿病神经原性膀胱的治疗体会（附１００例临床分析）白凤翔，杨耀华，杨君，何国芬糖尿病神经原性膀胱是由于神经病变累及支配膀胱和尿道括约肌的植物神经引起的排尿功能障碍。现就我院１９８６～１９９５年收治的１００例糖尿病（ＤＭ）神经原性膀胱（ＮＢ）回顾性分析...     

尿流动力学检查在小儿神经原性膀胱治疗中的应用

目的 根据尿流动力学检查结果，探讨神经原性膀胱的外科治疗方法。方法 110例神经原性膀胱患儿术前均行尿流动力学检查(测定逼尿肌反射情况、膀胱容量、漏点压、最大尿道压和最大尿道闭合压等)，根据检查结果，采用不同外科治疗方法(盆底肌加强、膀胱颈悬吊、膀胱扩大术和逼尿肌加强术)。结果 110例中获随访92例，平均随访2年，尿流动力学检查各项指标明显好转。结论 手术治疗神经原性膀胱，应根据患儿的不同情况制定相应的治疗方案，才能取得满意效果。     

尿道内括约肌切断术治疗神经原性膀胱

４例神经原性膀胱伴较多残余尿患者，采用经膀胱镜的尿道内括约肌切断术治疗，取得了满意效果。我们采用Ｆ２４Ｗｏｌｆ电切镜在膀胱颈部１２点处作纵行切开，手术是安全和简便的。本文还讨论了手术适应症、技术及结果。     

胰激肽原酶治疗糖尿病神经原性膀胱132例临床观察

目的　探讨胰激肽原酶 (怡开 )治疗糖尿病神经原性膀胱的临床疗效。方法　 1 32例糖尿病神经原性膀胱随机分为两组 :治疗组 66例接受怡开 40 IU qd im 8w;对照组给予 Vit B1 2 50 0μg qd im 8w。分别观察治疗不同时期膀胱壁厚度、残余尿量的变化和症状的改变。结果　两组患者经过治疗 ,怡开组病人膀胱壁厚度在治疗 3w后已由治疗前的 1 2 .2 0± 2 .1 4 mm减少到 1 0 .0 0± 1 .91 mm,而且随治疗时间延长厚度减少愈明显 ;而对照组在治疗后第 7周才由治疗前的 1 3.1 0± 1 .69mm减少到 1 1 .0 2± 2 .0 8mm。残余尿量的变化同膀胱厚度改变相似 ,怡开组病人膀胱残余尿量在治疗 3w后已由治疗前的 2 93± 32 .5cm3减少到 1 1 6± 51 .3cm3,而且随治疗时间延长残余尿量减少愈明显。而对照组在治疗后第 7周才由治疗前的 30 4± 47.8cm3减少到 2 54± 2 1 .3 cm3,两者差异显著 (P<0 .0 5)。结论　怡开在改善糖尿病神经原性膀胱功能障碍 ,减轻膀胱壁厚度和减少膀胱残余尿量方面明显优于对照组     

西沙比利治疗老年糖尿病神经原性膀胱功能障碍40例分析

糖尿病神经原性膀胱功能障碍是由于糖尿病人中枢神经系统或周围神经系统中调节膀胱功能的部位受到损害而发生的排尿障碍,是糖尿病常见的并发症之一。我们从收治1例典型患者应用西沙比利治疗取得明显疗效开始,有目的     

糖尿病神经原膀胱的治疗现状

糖尿病神经原膀胱(DNB)是糖尿病在泌尿系统最主要的并发症,其发病机制复杂,目前尚无特效的治疗方法.营养神经、调节神经递质、抗氧化应激、电刺激、导尿术等单一化学药物或物理治疗常难以达到临床治疗要求,理化联合治疗可协同增加疗效.近年来,干细胞和基因研究的兴起为DNB的治疗提供了新思路,但仍处于实验探索阶段     

胰激肽原酶对糖尿病神经原性膀胱的疗效观察

目的探讨胰激肽原酶（PK）对糖尿病神经原性膀胱的疗效。方法40例糖尿病神经原性膀胱女性患者随机分为PK治疗组（PK组）、对照组（Con组）各20例。PK组日1次肌注PK40U；Con组日1次肌注维生素B12 500μg。治疗前及治疗后的1个月、2个月检测尿流率、残余尿、最大尿流率、平均尿流率及排尿期逼尿肌压。结果治疗后PK组残余尿量显著降低，最大尿流率、平均尿流率及排尿期逼尿肌压均显著增加（P〈0.05）。Con组治疗后1个月各项结果较治疗前无统计学差异（P〉0.05）。治疗后2个月残余尿量轻度降低，最大尿流率及排尿期逼尿肌压升高，较治疗前差异有统计学意义（P〈0．05）。PK组与Con组比较，残余尿量更低，最大尿流率、平均尿流率及排尿期逼尿肌压更高，差异有统计学意义（P〈0.05）。结论胰激肽原酶可以作为治疗糖尿病神经原性膀胱的用药之一。     

糖尿病神经原膀胱的诊断与治疗

糖尿病(DM)病人可以出现各种类型的膀胱尿道功能异常即糖尿病神经原性膀胱尿道功能障碍(DNBUD，diabetic neurogenic bladder and urethrae dysfunction)，后者终因顽固的尿道“梗阻——感染——梗阻”恶性循环出现肾功能衰竭而致命。近年来，国外在DNBUD的发病情况、原因和机理、临床表现、诊断和治疗等方面进行了大量的研究，现综述如下。     

中西医结合治疗糖尿病神经原性膀胱功能障碍32例

我们从1989年9月～1995年9月采用中药内服配合西药冲洗治疗糖尿病神经原性膀味功能障碍32例，疗效显著．现报告如下。1资料与方法1．l一般资料：全部病例均为糖尿病（DM）住院患者．诊断符合1985年WHO标准，接受胰岛素或口服降糖药物治疗．有多种合并症（尤以植物神经病变中的糖尿病神经原性膀眈与顽固性下尿路感染并见为主）出现．经用胰岛素、抗生素及拟胆碱药物治疗2个月以上，疗效不显著．且以高度尿满留、小便失控为主要临床表现．经双肾、膀眈（男性患者加做前列腺）彩色超声检查，提示双肾（前列腺）无异常改变．膀航容积扩大（＞l…     

骶神经根切断吻合治疗脊髓损伤后痉挛性膀胱

对40例脊髓损伤(SCI)后痉挛性膀胱患者行选择性骶神经根切断、吻合术,重建跟腱-膀胱反射弧.术后随访22个月,患者膀胱充盈后可引起自控性排尿,尿流动力学显示排尿完全由膀胱逼尿肌的收缩引发,优良率达85%.认为骶神经根切断后重新吻合建立新的跟腱-膀胱反射弧能恢复SCI后痉挛性膀胱患者的排尿功能.     

Acupuncture for diabetic neurogenic bladder: A protocol for systematic review and meta-analysis

Background:Diabetic neurogenic bladder (DNB) is one of the common complications of diabetes mellitus, which has a high prevalence rate. Some research suggested that acupuncture can improve the clinical symptoms of diabetic neurogenic bladder patients, but there is no systematic review or meta-analysis to assess this therapy. Therefore, this study aims to explore the effectiveness and safety of acupuncture for patients with DNB.Methods:In this study, we will search for electronic databases including the Cochrane Library, Web of Science, PubMed, MEDLINE, EMBASE,China National Knowledge Infrastructure (CNKI), Wan-Fang, and Baidu Scholar Database from inception to December 2020. We will select randomized controlled trials that have been published in English or Chinese related to acupuncture for DNB. Selection of study, extraction of data, and assessment of study quality will be performed independently by 2 researchers, and we will use Revman 5.3 software which is provided by Cochrane assistance network, to perform the data analysis.Results:This study will provide evidence of the effectiveness and safety of acupuncture for DNB.Conclusion:This study will clarify whether acupuncture is an effective treatment for DNB, and will also provide a reference for clinical practice and guidelines development.     

Assessing Patient-Reported Outcomes for Patients with Neurogenic Bladder

Neurogenic bladder is a term applied to a malfunctioning urinary bladder due to a neurologic dysfunction or disease of the central, peripheral, or autonomic nervous system. In a patient with a neurologic disease whose quality of life (QOL) may already be severely affected, urinary incontinence (UI) can result in further reduction of QOL. While no cures are currently available for the most common neurologic diseases, there is much that can be done to improve the QOL of people with neurologic diseases, including those with neurogenic bladder. However, in order to positively impact QOL, it must first be measured. One type of measure for assessing QOL is patient-reported outcomes (PROs). Here we review the current PROs in patients with neurogenic bladder. Assessing PROs in patients with neurogenic bladders is a difficult undertaking since the groups of patients are diversified in their neurogenic conditions and symptoms.     

Twelve Months Follow‐up of Injection of OnabotulinumtoxinA into Vesical Submucosa for Refractory Non‐neurogenic Overactive Bladder

Objective: The aim of the present study was to assess the effects of onabotulinumtoxinA injection for refractory non‐neurogenic overactive bladder (OAB) for 12 months. Methods: For patients with persistent urgency urinary incontinence (UUI) more than once a week despite taking anti‐cholinergic agents or incapability to continue the agents because of adverse effects, 100 units of onabotulinumtoxinA was injected at 30 sites in the sub‐epithelial bladder wall. Efficacy was assessed every month up to 12 months after injection, using a three‐day frequency‐volume chart (FVC) and postvoid residual urine (PVR), three questionnaires, and a simple score of Global Response Assessment (GRA). Failure was defined as when GRA was negative and additional treatment was administered. Results: Nine men and eight women aged 67 ± 12 years were included. On FVC, frequencies of urgency, UUI and daytime urination significantly decreased up to the 11th month. PVR significantly increased at the first and second months but no patient required catheterization. The total scores of Overactive Bladder Symptom Score and International Consultation on Incontinence Questionnaire Short Form were significantly decreased for 10 and eight months, respectively. The score of GRA was significantly improved for eight months. The median time to failure was 11.0 months. Conclusion: This study suggests that onabotulinumtoxinA submucosal injection is promising for refractory non‐neurogenic OAB. It is anticipated that the treatment is effective for eight to nine months and approximately 40% of the patients do not require anticholinergics at the 12th month postoperatively.     

糖尿病神经源性膀胱患者血清铁蛋白水平的改变及其临床意义

目的 探讨糖尿病神经源性膀胱（DNB）患者血清铁蛋白（SF）水平变化及两者的相关性.方法 选取单纯T2DM患者（T2DM组）,DNB患者（DNB组）和正常对照（NC组）者,各30例,采用化学发光法测定SF水平. 结果 DNB组和T2DM组SF水平均高于NC组,且DNB组高于T2DM组[（689.75±67.31）vs（498.98±49.76）vs（278.15±38.65） ng/ml,P＜0.01].SF水平与TC、TG、HbA1 c水平均呈正相关（r=0.48、0.42、0.57,P均＜0.01）.非条件Logistic回归分析显示,DNB与病程、年龄、SBP、HbA1 c、FIns、TC及SF呈正相关（P＜0.05或P＜0.01）. 结论 SF的升高与DNB的发生发展密切相关,可作为DNB的检测指标之一,为临床干预治疗提供理论依据.     

Pathophysiological and Therapeutic Considerations for Non‐Neurogenic Lower Urinary Tract Dysfunction in Children

Non‐neurogenic lower urinary tract dysfunction (LUTD) in children is very common in clinical practice and is important as an underlying cause of lower urinary tract symptoms, urinary tract infection and vesicoureteral reflux in affected children. LUTD in children is caused by multiple factors and might be related with a delay in functional maturation of the lower urinary tract. Behavioral and psychological problems often co‐exist in children with LUTD and bowel dysfunction. Recent findings in functional brain imaging suggest that bladder bowel dysfunction and behavioral and psychiatric disorders in children might share common pathophysiological factors in the brain. Children with suspected LUTD should be evaluated properly by detailed history taking, validated questionnaire on voiding and defecation, voiding and bowel diary, urinalysis, screening ultrasound, uroflowmetry and post‐void residual measurement. Invasive urodynamic study such as videourodynamics should be reserved for children in whom standard treatment fails. Initial treatment of non‐neurogenic LUTD is standard urotherapy comprising education of the child and family, regular optimal voiding regimens and bowel programs. Pelvic floor muscle awareness, biofeedback and neuromodulation can be used as a supplementary purpose. Antimuscarinics and α‐blockers are safely used for overactive bladder and dysfunctional voiding, respectively. For refractory cases, botulinum toxin A injection is a viable treatment option. Prudent use of urotherapy and pharmacotherapy for non‐neurogenic LUTD should have a better chance to cure various problems and improve self‐esteem and quality of life in affected children.     

The Management of the Pediatric Neurogenic Bladder

Neurogenic bladder is a heterogeneous entity that may result from a variety of conditions affecting the central or peripheral nervous systems. Regardless of etiology, the overall goals of management are primarily twofold. As a neurogenic bladder may affect the ability to store urine safely and to empty the bladder efficiently, early management is focused on optimization of bladder storage function to prevent irreversible injury to either the upper or lower urinary tracts. In older children, this goal is added to the challenge of maximizing quality of life through achievement of urinary continence and independence in bladder management that continues into the transition to adulthood.In this review, we seek to bring the reader up-to-date regarding management of the pediatric neurogenic bladder with a focus on literature published in the past year. We discuss key contributions related to fetal intervention for myelomeningocele, monitoring and medical management of the neurogenic bladder and prediction of postoperative outcomes. Put together, these studies highlight the continued need for further research to improve evidence-based medical and surgical decision-making strategies for children affected by neurogenic bladder.     

Management of Low Compliant Bladder in Spinal Cord Injured Patients

Low bladder compliance means an abnormal volume and pressure relationship, and an incremental rise in bladder pressure during the bladder filling. It is well known that at the time bladder capacity decreases, intravesical pressure increases, and the risk of upper deterioration increases. Hypocompliance is usually thought to be the range from 1.0 to 20.0 mL/cmH₂O. Though the exact cause of hypocompliance is not known, it may be caused by changes in the elastic and viscoelastic properties of the bladder, changes in detrusor muscle tone, or combinations of the two. Management aims at increasing bladder capacity with low intravesical pressure. The main is a medical therapy with antimuscarinics combined with clean intermittent catheterization. The results are sometimes unsatisfactory. Various drugs or agents through the mouth or the bladder, including oxybutynin, new antimuscarinics, capsaicin and resiniferatoxin were tried. Among them botulinum toxin‐A is promising. Some patients eventually required surgical intervention in spite of the aggressive medical therapy. Finally most patients undergo the surgical treatment including autoaugmentation, diversion, and augmentation cystoplasty. Among them augmentation cystoplasty still seems the only clearly verified treatment method.     

Pathophysiology of refractory overactive bladder

Overactive bladder (OAB) is a common condition. The International Continence Society defines OAB as a symptom complex characterized by urgency with or without urge incontinence, usually with frequency and nocturia. The first‐line treatment for OAB includes behavioral therapy, such as caffeine reduction, fluid intake modification, weight reduction, bladder training, and pelvic floor muscle training, as well as treatment with antimuscarinic or β₃‐adrenoceptor agonist medications. However, less than half of all cases achieve satisfactory outcomes following first‐line treatment. Second‐line therapy considered if satisfactory responses are not achieved after 8 to 12 weeks treatment with first‐line therapy include intradetrusor botulinum toxin injection, neuromodulation, and surgical treatment. Patients with refractory OAB may have more severe symptoms or underlying pathophysiologies that were not resolved by the initial medication. The pathophysiologies of refractory OAB include occult neurogenic bladder, undetected bladder outlet obstruction, urethral‐related OAB, urothelial dysfunction with aging, chronic bladder ischemia, chronic bladder inflammation, central sensitization, and autonomic dysfunction. This article discusses the possible pathophysiologies of refractory OAB.     

Comparison of the Effects by Obybutynin and Tolterodine on Spina Bifida Patients: A Pilot Crossover Study

Objectives: To compare the effects of obybutynin and tolterodine in neurogenic bladder patients with spina bifida in a crossover study. Methods: Seven myelomeningocele and one spinal lipoma cases, maintained with obybutynin and clean intermittent catheterization for more than 60 months, were enrolled. Age ranged from 8 to 23 years (mean 12.0, male/ female = 2/6). After 2 weeks of washout period, obybutynin (0.3 mg/kg, maximum 12 mg) or tolterodine (0.12 mg/kg, maximum 4 mg) was administered for 4 weeks, and then switched to the other drug for 4 weeks. At the end of the three periods, the patients and/or parents documented urinary storage status and adverse effects, and urodynamic study was performed. Results: In seven cases undergoing sequential urodynamic study, the baseline compliance of the patients (6.81 ± 1.83) increased to 9.98 ± 4.97 by obybutynin and 10.16 ± 2.53 by tolterodine (P < 0.05 for each). Better compliance was noted in two cases with tolterodine and in two cases with obybutynin. Stronger adverse effects were reported in three out of eight patients (37.5%) by obybutynin and three out of eight patients (37.5%) by tolterodine. Although storage effect and side effects were equivalent for total patients, markedly diverse response was noted for each patient, with five choosing tolterodine and three choosing obybutynin. Conclusions: Individualized evaluation is required for optimal choice of anticholinergics.     

Detrusor Underactivity: The Current Concept of the Pathophysiology

Based on evidence from available literature, we review the pathophysiology of detrusor underactivity (DU). DU is likely to be multifactorial. Aging reduces detrusor activity, but other concomitant causes may aggravate this condition, resulting in decrease of detrusor contractility. Impaired detrusor contractility has been regarded as a major etiologic factor of DU. However, a more complex pathology has been proposed. As contributing factors to DU, we discuss disturbances of the sensory afferent side of the micturition reflex, the central nervous system (CNS) and the efferent side of the reflex, including nerves and the detrusor muscle. Particularly, dysfunction of afferent nerves in the bladder and urethra may play a crucial role in the pathogenesis of DU. In addition, recent studies suggest that chronic bladder ischemia and resultant oxidative stress cause detrusor overactivity progressing to DU and inability to empty the bladder.