McGuire E J, Woodside J R, Borden T A, Weiss R M
J Urol. 1981 Aug;126(2):205-9. doi: 10.1016/s0022-5347(17)54449-3.
We herein describe the clinical progress of 42 myelodysplastic patients studied urodynamically and followed for a mean of 7.1 years. Urodynamic evaluation included urethral pressure profilometry, simultaneous determination of urethral pressure, intravesical pressure and external anal or external urethral sphincter electromyography with fluoroscopic voiding cystourethrography. Assessment of urethral function showed 36 patients (86 per cent) with an open vesical outlet and nonfunctional proximal urethral. Cystometrography revealed that 7 of 42 patients (17 per cent) had reflex detrusor activity: 4 with coordinated micturition and 3 with detrusor-sphincter dyssynergia. Thirty-five patients (83 per cent) had areflexic detrusor dysfunction: 5 with atomic detrusor response and 30 with a progressive increase in pressure with increasing volume. The intravesical pressure at the time of urethral leakage was 40 cm. water or less in 20 patients and at pressures greater than this value in 22 patients. No patient in the low pressure group had vesicoureteral reflux and only 2 showed ureteral dilatation on excretory urography. In contrast, of the patients in the higher pressure group 15 (68 per cent) showed vesicoureteral reflux and 18 (81 per cent) showed ureteral dilatation on excretory urography. Thus, a striking relationship between the urethral closure pressure and intravesical pressure at the time of urethral leakage and the clinical course in this group of myelodysplastic patients is demonstrated. Every patient with a normally closed vesical outlet was continent on intermittent catheterization and an anticholinergic agent, while only 60 per cent of patients with open bladder outlets similarly treated achieved good urinary control and none was dry. An artificial sphincter device would seem to be a reasonable method to achieve urinary control in the latter patients but the detrusor response to filling also must be considered. Detrusor hypertonia should be controlled or controllable before a sphincter augmenting device can be used safely. Treatment options for patients with high urethral closure pressures include intermittent catheterization and anticholinergic medications or a sphincter ablative procedure to decrease the outlet resistance combined with anticholinergic therapy and implantation of an artificial sphincter. However, only longer followup will determine if these therapeutic regimens will prevent upper urinary tract deterioration.
我们在此描述了42例骨髓发育异常患者的临床进展，这些患者接受了尿动力学研究，并平均随访了7.1年。尿动力学评估包括尿道压力测定、尿道压力、膀胱内压力的同步测定以及外部肛门或外部尿道括约肌肌电图检查，并结合荧光透视排尿膀胱尿道造影。尿道功能评估显示，36例患者（86%）膀胱出口开放且近端尿道无功能。膀胱测压显示，42例患者中有7例（17%）存在逼尿肌反射活动：4例排尿协调，3例存在逼尿肌-括约肌协同失调。35例患者（83%）存在无反射性逼尿肌功能障碍：5例为无张力性逼尿肌反应，30例随着尿量增加压力逐渐升高。20例患者尿道漏尿时膀胱内压力为40厘米水柱或更低，22例患者压力高于此值。低压组患者中无1例发生膀胱输尿管反流，排泄性尿路造影仅2例显示输尿管扩张。相比之下，高压组患者中15例（68%）排泄性尿路造影显示膀胱输尿管反流，18例（81%）显示输尿管扩张。因此，在这组骨髓发育异常患者中，尿道漏尿时的尿道闭合压力与膀胱内压力之间以及临床病程之间存在显著关系。每个膀胱出口正常闭合的患者通过间歇性导尿和抗胆碱能药物可实现控尿，而膀胱出口开放的患者接受同样治疗时，只有60%能实现良好的尿控，且无1例完全无尿。人工括约肌装置似乎是使后一组患者实现尿控的合理方法，但也必须考虑逼尿肌对充盈的反应。在安全使用括约肌增强装置之前，应先控制或可控制逼尿肌张力亢进。尿道闭合压力高的患者的治疗选择包括间歇性导尿和抗胆碱能药物，或进行括约肌切除术以降低出口阻力，同时结合抗胆碱能治疗并植入人工括约肌。然而，只有更长时间的随访才能确定这些治疗方案是否能预防上尿路恶化。
