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Significance of urethral vascular pulsations in genuine stress urinary incontinence

  • David B. Hebert
    Correspondence
    Reprint requests: David B. Hebert, M.D., Department of Obstetrics and Gynecology, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, Texas 78284
    Affiliations
    Department of Obstetrics and Gynecology, University of California, Irvine, California USA

    California College of Medicine Orange, California USA

    Women's Hospital, Memorial Hospital Medical Center of Long Beach Long Beach, California USA
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  • Larry N. Francis
    Affiliations
    Department of Obstetrics and Gynecology, University of California, Irvine, California USA

    California College of Medicine Orange, California USA

    Women's Hospital, Memorial Hospital Medical Center of Long Beach Long Beach, California USA
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  • donald R. Ostergard
    Affiliations
    Department of Obstetrics and Gynecology, University of California, Irvine, California USA

    California College of Medicine Orange, California USA

    Women's Hospital, Memorial Hospital Medical Center of Long Beach Long Beach, California USA
    Search for articles by this author
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      Abstract

      Urodynamic tracings of 100 women with genuine stress incontinence revealed urethral vascular pulsations in 15 patients, while 85 lacked vascular pulsations. The presence of vascular pulsations correlated with the maximal urethral closure pressure and identified a subgroup of genuine stress incontinence with normal sphincter strength and reflex activity. The only identifiable cause of stress incontinence for each patient in this group was a deficiency in the anatomic supports of the urethrovesical junction responsible for poor transmission of intra-abdominal pressure to the urethra during stress. Those patients lacking vascular pulsations demonstrated resting sphincter weakness as well as decompensation of the sphincteric mechanism with changes in bladder volume and posture. In most women with genuine stress incontinence, the etiology is a combination of urethral sphincter dysfunction and poor anatomic support of the urethrovesical junction.
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