压力-血流研究作为神经源性尿道松弛失败的评价方法

Ryuji Sakakibara , Clare J Fowler , Takamichi Hattori , Iqbal F Hussain , Michael J Swinn , Tomoyuki Uchiyama , Tomonori Yamanishi
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引用次数: 26

摘要

排尿困难是神经系统疾病的共同特征,可归因于尿道括约肌和逼尿肌功能障碍。肌电图(EMG) -膀胱术可以显示逼尿肌-外括约肌协同功能障碍(DESD)的存在,但内括约肌对排尿的功能不容易评估。压力-血流研究被广泛用于诊断前列腺肥大引起的良性出口阻塞。为了评价神经源性尿道松弛衰竭,我们应用压力-血流研究方法。我们招募了71名患有神经系统疾病的患者。所有患者均为60岁以下的男性,平均年龄44岁,年龄从18岁到59岁不等。前列腺数字检查和超声检查均无异常。标准膀胱术显示33例患者逼尿肌反射增高,36例患者尿残留。43例患者中有7例出现DESD。通过尿动力学计算得到最大流速(Qmax)点的压流关系曲线和逼尿肌压力(Pdet)(即PdetQmax)。abrams - griffiths (AG)数(PdetQmax ~ 2Qmax)显示出口阻塞,特别是在40以上。患者的PdetQmax点可分为三种类型,19.7%为梗阻,52.1%为模糊,28.2%为通畅。DESD患者AG数大于40的比例(57.1%)高于非DESD患者(8.4%)(p < 0.05)。DESD患者的平均AG数为46.4,大于非DESD患者的平均AG数17.1 (p < 0.01)。逼尿肌高反射症患者AG数大于40的比例(42.4%)高于膀胱测量曲线正常(0%)(p < 0.01)。逼尿肌高反射症患者的平均AG数为30.6,高于膀胱测量曲线正常患者的平均AG数13.6 (p < 0.01)。结果显示:19.7%的神经系统疾病患者有梗阻型(高压排尿),表现为尿道松弛衰竭,尿逼肌收缩相对保留。DESD是导致患者尿道松弛失败的一个因素。结果还显示逼尿肌反射亢进与梗阻模式之间的关系,可能反映了逼尿肌反射亢进与DESD或逼尿肌-内括约肌协同障碍的共同发生。
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Pressure–flow study as an evaluating method of neurogenic urethral relaxation failure

Voiding difficulty is a common feature in neurological diseases, which can be attributed to dysfunction of the urethral sphincter and the detrusor. Electromyography (EMG)–cystometry can reveal the presence of detrusor–external sphincter dyssynergia (DESD), however, internal sphincter function on voiding is not easily evaluated. Pressure–flow study is widely used to diagnose benign outlet obstruction due to prostatic hypertrophy. We applied pressure–flow study in neurological patients in order to evaluate neurogenic urethral relaxation failure. We recruited 71 patients with neurological diseases. All were men under 60 years, with mean age of 44 years, ranging from 18 to 59 years. None had abnormal finding of digital examination or ultrasound echography of the prostate. Standard cystometry showed detrusor hyperreflexia in 33 patients and residual urine was noted in 36. DESD was noted in seven of 43 patients. Pressure–flow relation curve and a detrusor pressure (Pdet) at the point of maximum flow rate (Qmax) (i.e., PdetQmax) were obtained by urodynamic computers. The Abram–Griffiths (AG) number (PdetQmax−2Qmax), showing outlet obstruction particularly over 40, was also obtained. The points of PdetQmax of the patients fell into three categories of the AG nomogram, showing obstruction in 19.7%, equivocal in 52.1% and unobstructed in 28.2%. Patients with DESD had AG number over 40 more commonly (57.1%) than those without DESD (8.4%) (p<0.05). The mean AG number was 46.4 in patients with DESD, which was larger than 17.1 in patients without DESD (p<0.01). Patients with detrusor hyperreflexia had AG number over 40 more commonly (42.4%) than those with normal cystometric curve (0%) (p<0.01). The mean AG number was 30.6 in patients with detrusor hyperreflexia, which was larger than 13.6 in patients with normal cystometric curve (p<0.01). The results showed that 19.7% of patients with neurological diseases had obstructive pattern (high pressure voiding), evidence of urethral relaxation failure with relatively preserved detrusor contraction. DESD is a factor contributing to the urethral relaxation failure of the patients. The results also indicated a relationship between detrusor hyperreflexia and obstructed pattern, probably reflecting co-occurrence of detrusor hyperreflexia with DESD or detrusor–internal sphincter dyssynergia.

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