Nitti V W, Adler H, Combs A J
Department of Urology, New York University School of Medicine, New York, USA.
J Urol. 1996 Jan;155(1):263-6.
The etiology of voiding dysfunction was determined in men after a cerebrovascular accident who were at risk for obstructive uropathy to evaluate whether the cause of voiding dysfunction could be predicted by the type (obstructive or irritative) or onset of symptoms.
We evaluated 38 men with complaints of voiding dysfunction following a cerebrovascular accident. All patients were of the age when bladder outlet obstruction secondary to benign prostatic hyperplasia would otherwise be prevalent. After a comprehensive history and physical examination, all patients underwent multichannel urodynamic studies at a medium fill rate (20 to 50 ml. per minute). Findings were classified by the Abrams-Griffiths nomogram as obstruction, no obstruction or equivocal.
Mean patient age was 70 years (range 54 to 87). Patients were grouped according to the presenting voiding complaints (purely irritative in 42%, purely obstructive in 34% or mixed in 24%). In 34 patients (89%) the onset of symptoms paralleled the occurrence of the cerebrovascular accident. Detrusor hyperreflexia was noted in 82% of the patients. There was no statistically significant difference in the occurrence of detrusor hyperreflexia among the 3 symptom groups (Fisher's exact test). Pressure-flow analysis clearly showed obstruction in 24 patients (63%), no obstruction in 9 (24%) and equivocal results in 5 (13%) according to the nomogram. There was no statistically significant difference in the incidence of obstruction among the 3 symptom groups (Fisher's exact test).
Presenting symptoms did not predict the urodynamic findings of bladder outlet obstruction or detrusor hyperreflexia. The significant incidence of onset of symptoms after stroke suggests that the cerebrovascular accident induced voiding dysfunction in the face of preexisting bladder outlet obstruction may exacerbate the symptoms of the latter condition or vice versa.
确定脑血管意外后有梗阻性尿路病风险的男性排尿功能障碍的病因,以评估排尿功能障碍的原因是否可通过症状类型(梗阻性或刺激性)或症状发作来预测。
我们评估了38例脑血管意外后有排尿功能障碍主诉的男性。所有患者均处于良性前列腺增生继发膀胱出口梗阻通常高发的年龄。在进行全面的病史采集和体格检查后,所有患者均以中等充盈速率(每分钟20至50毫升)接受多通道尿动力学检查。根据艾布拉姆斯-格里菲思列线图将结果分类为梗阻、无梗阻或不明确。
患者平均年龄为70岁(范围54至87岁)。患者根据出现的排尿主诉进行分组(单纯刺激性症状占42%,单纯梗阻性症状占34%,混合性症状占24%)。34例患者(89%)症状发作与脑血管意外同时发生。82%的患者出现逼尿肌反射亢进。3个症状组中逼尿肌反射亢进的发生率无统计学显著差异(费舍尔精确检验)。根据列线图,压力-流率分析明确显示24例患者(63%)有梗阻,9例(24%)无梗阻,5例(13%)结果不明确。3个症状组中梗阻发生率无统计学显著差异(费舍尔精确检验)。
出现的症状不能预测膀胱出口梗阻或逼尿肌反射亢进的尿动力学检查结果。中风后症状发作的显著发生率表明脑血管意外在已有膀胱出口梗阻的情况下诱发排尿功能障碍可能会加重后者的症状,反之亦然。