시원항병원
051) 331-7275논문발표
| 번호 | 제목 | 등록일 | 조회수 |
|---|---|---|---|
| 24 | Is There an Association Between Fecal Incontinence and Lower Urinary Dysfunction? [2001년 6월 DCR] | 2011-11-17 | 3360 |
|
Jane Manning, M.B.B.S., M.R.A.C.O.G., Anthony A. Eyers, M.B.B.S.(Hons.), F.R.A.C.S.,Andrew Korda, M.A., M.B.B.S., F.R.A.C.O.G., F.R.C.O.G., C.U.,Chris Benness, M.B.B.S., F.R.A.C.O.G., M.D.,Michael J. Solomon, M.B., B.Ch.(Hons.), M.Sc.(C1. Epid.), F.R.A.C.S.
From the Urogynaecology Unit and Department of Colorectal Surgery, Royal Prince Alfred Hospital, and
Department of Surgery, University of Sydney, Sydney, Australia BACKGROUND: Urinary and fecal incontinence in females are both common and distressing conditions. Because common pathophysiologic mechanisms have been described, an association between the two would be expected. The aim of this study was to determine whether patients with
lower urinary tract dysfunction have concomitant fecal incontinence when compared with age and gender matched community controls and, second, to determine whether they have predisposing factors that have led to lower urinary tract symptoms and concomitant fecal incontinence. METHODS: A case-control study was performed by means of detailed questionnaire and review of investigation results. One thousand consecutive females presenting for urodynamic investigation of lower urinary tract dysfunction, were compared with 148 age and gender matched colrmaunity controls. RESULTS: Frequent fecal incontinence was significantly more prevalent among all cases than among community conta'ols (5 vs. 0.72 percent, P = 0.023). Occasional fecal incontinence was also more prevalent (24.6 vs. 8.4 percent, P < 0.001). Fecal incontinence was not significantly more prevalent among females with genuine stress incontinence (5.1 percent) when compared with females with detmsor instability (3.8 percent) or any other urodynamic diagnosis. Symptoms of fecal urgency and fecal urge incontinence were significantly more prevalent among those with a urodynamic diagnosis of detrusor instability or sensory urgency than among females with other urodynamic diagnoses or commmlity controls. Multivariate analysis comparing cases with fecal incontinence with other cases and also with community controls did not indicate that individual obstetric factors contributed significantly to the occurrence of fecal incontinence in these patients. CONCLUSIONS: There is an association between genuine stress incontinence, lower urinary tract dysfunction, and symptoms of fecal incontinence, but the exact mechanism of injury related to childbirth trauma is questioned. Urinary and fecal incontinence are both common, distressing conditions that affect females. Because common pathophysiologic mechanisms have been described, an association between the two would be expected and has been demonstrated by several investigators. The most common mechanism
considered is obstetric injury, in particular, pelvic floor denervation occurring during childbirth, because this has been demonstrated to be important in the cause of genuine stress incontinence (GSI) as well as fecal incontinence. It is argued that this may not be the predominant mechanism for fecal or urinavy" incontinence after childbirth, because pelvic floor denervation is temporary in the majority of cases. Urodynamics refers to the investigation of lower urinary tract dysfunction. It encompasses a wide variety
of investigations, the most important of which are the assessment of the bladder pressure during filling and voiding (cystometry) and the assessment or urine flow parameters (uroflowmetry). Urodynamic studies are often required to make an accurate diagnosis, because a clinical diagnosis made on history and examination alone is often incorrect. The most common urodynamic diagnoses in females with lower urinary tract symptoms are GSI, detrusor instability and voiding dysfunction. GSI is essentially an anatomic problem manifested by urine loss at times of raised intra-abdominal pressure, whereas DI is a functional problem where the detmsor muscle contracts inappropriately giving rise to symptoms and possibly incontinence. These conditions may coexist, and both can only be accurately diagnosed after urodynamic assessment. The pelvic floor also sustains direct muscular and connective tissue injury during childbirth, particularly
when instrumental delivery is required, and this may contribute to both conditions. However, because fecal incontinence is also prevalent in men, obstetric injury cannot be the only major causative factor for this condition. After obstetric injuries, the irritable bowel syndrome has been identified as a potentially important risk factor for fecal incontinence. This syndrome has recently been demonstrated to be associated with
the occurrence of urinary incontinence due to detrusot instability (DI), suggesting that a generalized disorder of smooth muscle function might be a common causative mechanism for the two conditions. An association between chronic straining and both urinary or fecal incontinence has also been demonstrated, with pudendal nerve injury suggested as the possible mechanism. Connective tissue factors have recently been demonstrated to be important in the cause of urinary
incontinence, and connective tissue disease has been associated with fecal incontinence. Benign joint hypermobility syndrome (BJHS) is a common condition affecting predominantly females. BJHS is thought to be caused by genetic disorders of collagen formation, may be associated with connective tissue disorders, and has been associated with uterovaginal prolapse and rectal prolapse. Although sought, a clear association with GSI or fecal incontinence has not been previously demonstrated, yet such connective tissue abnormalities could be a further possible common causative factor. Swash has remarked that fecal and urinary incontinence commonly occur in isolation and also that
neuropathy is not always demonstrated when these conditions do occur together. This emphasizes an impression that, although pudendal neuropathy is considered the most important common causative factor, other factors may be important and may act selectively. The objectives of this case-control study were 1) to investigate the prevalence of fecal incontinence
symptoms among females presenting for investigation of lower urinary, tract (LUT) dysfunction and to compare this with the prevalence of symptoms in age and gender matched community controls; 2) to establish whether an association between urinary and fecal incontinence is selectively associated with GSI, because this would provide indirect evidence for the view that a single cause may be responsible for any association between the two conditions; 3) to test previous findings of an association between detrusor instability and symptoms of the irritable bowel syndrome; and 4) to determine whether there are any variables that may be important in the cause of both LUT dysfunction and fecal incontinence, with particular interest in obstetric factors and symptoms of BJHS. DISCUSSION
An association between fecal incontinence and symptoms of LUT dysfunction and specifically GSI has been demonstrated. Although obstetric injury is a factor, the findings of this study do not support the
belief that this association is caused predominantly by any one individual obstetric variable. Fecal soiling was in fact least common among females with GSI. Females with LUT dysfunction and fecal incontinence are not more likely than other females with LUT dysfunction to have vaginal delivery or perineal suturing, suggesting that this is not the major reason for the association. The overall comparison of females with both conditions of incontinence when compared with community controls, demonstrates an association between these two conditions and bowel motility disorders, frequent loose stools, symptoms of obstructive defecation, vaginal delivery, a history of minor perianal, and rectal surgery and vaginal prolapse surgery. The association between symptoms of fecal urgency and fecal urge incontinence, irritable bowel
symptoms or frequent loose stools, and a diagnosis of urinary urgency or detrusor instability suggests that a common either central or peripheral disorder of smooth muscle function might also be a factor in the cause of both conditions. This association and the association between fecal incontinence and bowel motility disorders has been previously reported. Another reason for an association between fecal incontinence and LUT dysfunction may relate to
symptoms of obstructive defecation and chronic straining at stool that are experienced more commonly by both groups of females. It has been suggested that chronic straining may contribute to fecal incontinence by stretching and injuring the pudendal nerve. Additionally, if chronic straining and constipation result in hemorrhoids and anal fissures, the resulting anal surgery might additionally impair anal sphincter function. This might explain an increased prevalence of minor perianal surgery among females with LUT dysfunction when compared with community controls. The association between symptoms of BJHS and fecal incontinence in females with LUF dysfunction
suggests that this common connective tissue disorder may also impair mechanisms of both fecal and urinary continence, either directly or indirectly. Females with symptoms of BJHS strained more at stool. They were more likely to describe disordered bowel motility, and BJHS was associated with childhood and also current constipation and with symptoms of obstructed defection (Manning J, Korda A, Benness C. Unpublished data, 1999). Thus, BJHS may contribute to both fecal incontinence and LUT dysfunction by a direct effect on the connective tissue that supports sphincter mechanisms or indirectly by encouraging lifelong straining. Uterovaginal and rectal prolapse are associated with BJHS. Rectoceles and rectal prolapse might aggravate straining, resulting in a vicious circle. Although speculative, another possible mechanism for fecal incontinence in females with BJHS is increased perineal descent. Females with BJHS might be expected to have increased mobility of the pelvic floor on straining and this has been associated with pudendal neuropathy and fecal incontinence. Weight (body mass index) in this study may be a common factor in the cause of fecal incontinence and LUT dysfunction and has been associated with GSI in other studies. Vaginal prolapse surgery was more prevalent in females with fecal incontinence and LUT dysfunction.
Vaginal prolapse surgery may not itself be the common causative factor but may instead reflect the effects of trauma, denervation and inadequate connective tissue on the pelvic floor in these females. It is also possible that females presenting for evaluation of LUT symptoms may also be more likely to present for help with other gynecologic problems; however, this would not explain the increased prevalence of uterovaginal prolapse among females with fecal incontinence and LUT dysfunction when compared with other females with symptoms of LUT dysfunction. Females with fecal incontinence presenting for evaluation of LUT dysfunction are a highly selected
group, and differences noted between these females and community controls might be considered to relate more to their LUT symptoms than their fecal incontinence. However, among females with LUT dysfunction, minor perianal surgery, symptoms of obstructive defecation, uterovaginal prolapse and pelvic surgery as well as symptoms of BJHS remain significantly more prevalent among those with fecal incontinence, suggesting that these factors are important predictors of fecal incontinence. This study may have been limited by the use of a self-completed questionnaire to collect the majority of
the data; clinical details were not subsequently verified by direct intet-eiew. Although this technique may have resulted in some inaccuracies, it would be likely to bias both cases and controls equally. There is limited evidence to suggest that it may have resulted in a more accurate estimate of bowel symptomatology, although symptom prevalence is generally considered to be underestimated when self-report questionnaires are used. Community- controls were not examined, and although they denied troublesome incontinence, it is quite possible that a proportion of them did have lower urinary tract dysfunction. |
|||