Sacral coccygeal teratoma can produce significant neuro-urologic dysfunction and can be associated with upper tract deterioration due to high-grade reflux and abnormal bladder storage pressures. Öskan and colleagues identified 14 patients with sacral coccygeal teratoma, of whom detrusor overactivity was seen in 8, underactivity in 2. There was also abnormal urethral sphincteric activity in 54% of the patients, and 38% demonstrated sphincter dyssynergia. Eleven of 14 patients required clean intermittent catheter drainage for bladder emptying, and additionally, 5 required anticholinergics. Six patients had hydronephrosis, and seven had reflux (Ozkan et al, 2006).
Vale and colleagues (1993) summarized their experience with the occurrence of voiding dysfunction after external-beam irradiation. They describe an early radiation reaction most prominent at 4 to 6 weeks with an incidence as high as 70%. Symptoms are predominantly of the filling/storage type, and urodynamic studies have demonstrated reduced volume at first desire to void, reduced cystometric capacity, and reduced compliance. These parameters tend to return to pretreatment values by 6 months. Symptoms associated with later radiation effects are less common but may be progressive and intractable. Filling/storage symptoms predominate, and urodynamic studies, when positive, demonstrate reductions in first desire to void, maximum cystometric capacity, involuntary bladder contractions (in up to a third of patients), and an increase in maximum subtracted detrusor pressure during filling. Historical explanations have concentrated on urothelial injury and ulceration with fibrosis. These authors attempted to develop an experimental model in rats. They found a biphasic reduction in compliance, the first reduction developing at 4 to 6 weeks after irradiation, followed by recovery. A second reduction phase in compliance started at 10 to 12 weeks and persisted. Interestingly, only half the irradiated bladders demonstrated fibrotic infiltration of muscle bundles, and there was no association between the presence of fibrosis and the magnitude of reduction and compliance. Mast cells were more abundant in irradiated bladders than in controls. Electron microscopic studies showed, in the irradiated bladders, the presence of areas displaying focal degeneration of smooth muscle cells, these cells showing disaggregation of filaments and in some cases cytoplasmic organelles free in the intracellular space. In scattered foci, selective degeneration of unmyelinated axon profiles was noted, ranging from marked to lesser degrees of axonal injury. The authors were thus unable to confirm a fibrosis-based hypothesis of postirradiation bladder dysfunction in their experimental model but did show other changes that could contribute to such dysfunction: neural degeneration and changes in the detrusor muscle itself.
Choo and colleagues (2002) reported on video-urodynamic parameters in 15 of 17 patients completing studies at baseline and at 3 and 18 months after external-beam irradiation for prostate cancer. Between baseline and 18 months there were no statistically significant changes in detrusor pressure, peak flow rate, voided volume, postvoid residual, compliance, occurrence of detrusor overactivity, or outlet obstruction. There was a mean reduction in bladder capacity of 100 mL in the supine position and 54 mL in the upright position. There was no change in self-assessed qualitative urologic function (International Prostate Symptom Score, Quality of Life Assessment Index, and urinary frequency). There were, however, individual patients who developed decreased compliance (four patients) and detrusor overactivity (two patients), urgency (five patients), and urgency incontinence (three patients).
The timing of bladder defunctionalization and the age on the individual at time of defunctionalization may be predictive of bladder functionality. In fetal sheep urinary diversion results in loss of overall bladder weight with marked connective tissue infiltration and loss of smooth muscle organization. Also, a reduced response to carbachol stimulation and increased response to field stimulation was noted in tissue from animals undergoing early diversion (Matsumoto et al, 2003).
The previously normal defunctionalized bladder will often show decreased capacity and involuntary bladder contractions and/or decreased compliance. Previously abnormal bladders will generally demonstrate their prior pathology, many times with these additional abnormalities. Rehabilitation of a defunctionalized bladder is certainly possible and should definitely be attempted by cycling with progressively increasing volumes. Serrano and colleagues (1996) considered this subject while evaluating the outcome of transplantation into five long-term defunctionalized bladders. Successful bladder rehabilitation was accomplished, and the transplantation was successful without bladder augmentation, although one patient required CIC. Normal compliance was inferred by the fact that there was no evidence of hydronephrosis after long-term allograft function up to 10 years. The authors recommend that transplantation can be accomplished into a previously defunctionalized bladder when a capacity greater than 100 mL and a voiding pressure less than 100 cm/H2O are demonstrated during bladder rehabilitation.
Congenital adrenal hyperplasia (CAH) is associated with mixed urinary symptoms. Davies and colleagues (2005) studied 19 women with congenital adrenal hyperplasia (16 of whom had undergone childhood feminizing surgery). These were compared with age-matched controls. The CAH population had a higher incidence of urge incontinence (68%) and stress incontinence (47%) as compared with age-matched controls. The effects of congenital adrenal hyperplasia are uncertain and may be due to either the result of feminizing surgery (possible direct neuropraxia induced by surgery) or a primary affect of CAH (Davies et al, 2005).
Lower urinary tract symptoms and disorders are prevalent and bothersome in the elderly population. These problems are specifically and extensively considered in Chapter 76. When considering the effects of aging on the lower urinary tract, one cannot separate the effects of chronologic age itself from the various anatomic, neuromorphologic, neurophysiologic, neuropharmacologic, metabolic, and hormonal changes that coexist with aging, along with the effects of other coexisting disease processes. In addition to the material contained in Chapter 76, there is an excellent review of this area that was carried out by the Committee on Pathophysiology of the Urinary Bladder and Obstruction and Aging for the 4th International Consultation on BPH (Nordling et al, 2001).
Additionally, neurologic phenomena may masquerade as lower urinary tract symptoms associated with bladder outlet obstruction. These phenomena may include multiple cerebral infarctions, cervical spondylosis, and lumbar spondylosis. These findings were noted in the Olmsted County longitudinal study and are indicative of the need for urodynamics in older men with complex urinary symptoms (Woderich and Fowler, 2006).
The effect of disordered function of other organs within the pelvis is also potentially contributory to lower urinary tract dysfunction. Some of this disordered function may arise due to altered afferent neurologic activity induced by other organ disorders. The potential for visceral “cross talk” has been proposed as an etiology for patients with lower urinary tract dysfunction including syndromes such as interstitial cystitis and irritable bowel syndrome. In a rodent, the short- and long-term effects of acid-induced colitis on bladder function have been assessed. Bladder detrusor muscle contractility and histology were evaluated, both acutely and subacutely after induction of chemical colitis. During the active phase (3 days postinjury), bladder muscle structure appeared histologically normal and without inflammation. However, some abnormalities in detrusor muscle contractility in response to electrical field stimulation were noted. During the subacute period and after recovery of colitis (15 and 30 days), bladder muscle contractility returned to control levels with no discernible histologic change. These reversible changes were postulated to result from altered afferent input from the colon, resulting in “field” type changes affecting the bladder (Noronha et al, 2007).
No clear consensus yet exists as to the independent effects of child birth and hysterectomy on lower urinary tract function. A variety of explanations have been put forth regarding whether or not, in fact, lower urinary tract dysfunction is induced by these events and, if so, what the underlying pathophysiology may be.
In a multicenter Danish trial, patients undergoing hysterectomy (either total or subtotal) for benign uterine diseases were assessed. A total of 319 women were randomized to either total abdominal hysterectomy (158) or subtotal abdominal hysterectomy (161). At 1-year follow-up after intervention, urinary incontinence was less often noted in patients undergoing total abdominal hysterectomy. Both groups, however, did experience an increase in incomplete emptying requiring double voiding. Interestingly, both groups experienced an overall decrease in urinary incontinence frequency as compared with baseline (Gimbel et al, 2005).
No prospective trials, as yet, document the long-term follow-up relationship between urinary dysfunction and method of delivery, and no prospective clinical trials have been done to determine if caesarean section is protective against the development of incontinence. The debate regarding caesarean section as an alternative to spontaneous vaginal delivery and impact of each on the lower urinary tract also continues. The EPINCONT study assessed 15,307 women for the development of voiding dysfunction during longitudinal follow-up. The risk of urinary incontinence of all types was noted to be higher in women who had caesarean sections as compared with nulliparous women and those who had vaginal deliveries. However, the risk of moderate to severe incontinence was actually less in section patients than in patients who had had vaginal deliveries. Urgency incontinence was the only exception, being equal across all groups. The adjusted ratio for any incontinence in women after caesarean section was 1.5 versus 1.7 for women with vaginal deliveries. Stress incontinence appeared to be associated with mode of delivery (Rortveit, 2003a, 2003b).
McKinnie and colleagues (2005) studied 1004 women over an 18-month period to determine the relationship between urinary and fecal incontinence and type of delivery. In this study, pregnancy was identified as increasing the overall risk of urinary and fecal incontinence, and there was no apparent relationship to mode of delivery (McKinnie et al, 2005).
As of yet no agreement exists as to the putative causation of voiding dysfunction related to pregnancy and parturition. It would seem reasonable to believe that mass effect of the gravid uterus combined with peripheral nerve changes (neuropraxia related to stretch) may be contributory.
Any neurologic disease or injury can affect lower urinary tract function. Many have been mentioned in this chapter, but case reports and small series exist that document many others. The dysfunction produced by some is logically deducible on the basis of similarity to other neurologic lesions; for others the lower urinary tract dysfunctions are inconsistent and seemingly at odds with what would be predicted on the basis of neuroanatomic and neurophysiologic principles. For those who want to further pursue this subject, the following referenced list may be helpful:
In later chapters, the various therapies available for the treatment of lower urinary tract dysfunction are considered. Only a discrete number of such therapies are available, and these are easily categorized on a functional “menu” basis according to whether they are used primarily to assist urine filling/storage or voiding/emptying and according to whether their primary effect is on the bladder or on the outlet (see Tables 66–3 and 66–4).
The initial choice of a mode of management for a given problem is multifactorial. Although many of us who lecture and write about the management of neurogenic lower urinary tract dysfunction are associated primarily with one approach or another, all would doubtless agree on certain goals of management for voiding dysfunction (Table 65–2). The fact that these goals have remained relatively unchanged over the past few editions of this text attest to their general validity. As a corollary, absolute or relative indications for changing or augmenting a particular regimen exist, and, likewise, there is general agreement on these, although the relative importance of the indication for change might be disputed (Table 65–3). It should be remembered that the term inadequate, when applied to storage and emptying, applies not only to volumes (capacity, voided volume, residual) but also to unacceptably high detrusor pressures during either or both of the two phases of the micturition cycle. In the planning of goals of therapy and reasons for change, the concept of a “hostility score” such as that of Galloway (1989) is attractive. His hostility score includes five urodynamic characteristics—bladder compliance, overactivity, dyssynergia, outlet resistance, and VUR. Each is allocated a score of 0, 1, or 2. The best possible score is 0 and implies normal compliance, no inappropriate detrusor activity, a synergic sphincter, a low leak pressure, and no reflux.
Table 65–2 Voiding Dysfunction: Goals of Management
Table 65–3 Reasons to Change or Augment a Given Regimen
The results of treatment of voiding dysfunction are rarely perfect, and they do not have to be. The goals are satisfaction and avoidance of adverse outcomes. A flexible approach must be adopted in choosing therapy that takes into account the individual wishes of each patient and family and the practicality of each proposed solution for that particular patient (Table 65–4). The therapeutic decisions are thus made with the patient and with the family. In every case, within the limits of practicality, the following should be discussed: reversibility, side effects that occur with some regularity, ultimate best and worst possible scenario, frequency and extent of follow-up, and alternate methods of management. Treatment should always begin with the simplest most reversible form(s) of therapy, proceeding gradually up the ladder of complexity, but with the knowledge that it is only the patient (and/or family) who is (are) empowered to say when “enough is enough.” Again, avoidance of adverse outcomes and satisfaction are the primary goals. A combination of therapeutic maneuvers can sometimes be used to achieve a particular end, especially if these modalities act through different mechanisms and their side effects are not synergistic or additive. There are circumstances and locales in which health care resources and hospital bed use must also be considered.
Table 65–4 Patient Factors to Consider in Choosing Therapy
New therapies continue to be proposed for those patients with neurogenic lower urinary tract dysfunction refractory to medical therapies. The use of dorsal penile or clitoral nerve stimulation for controlled neurogenic detrusor overactivity has been recently described. Hansen and colleagues (2005) studied a group of 16 patients (2 women and 14 men) with neurogenic detrusor overactivity and diminished bladder capacity associated with complete or incomplete SCI. After stimulation of the dorsal nerve, 13 of 16 were noted to have increased bladder capacity and improved storage pressures during stimulation. The average bladder capacity increase was 53% in the study group. Detrusor pressures were also modulated below those associated with ureterovesical reflux (Hansen et al, 2005).
Pudendal nerve stimulation has been used for improving neurogenic voiding dysfunction. Spinelli and colleagues treated 15 patients with neurogenic voiding dysfunction (varied causes). After pudendal stimulation, there was a significant decrease in incontinence episodes, with 8 of 15 patients becoming continent during stimulation, and two with improvement approximating 90%. Twelve of 15 ultimately progressed to permanent implantation. In the chronically implanted patients, maximal cystometric capacity was noted to significantly increase and maximum detrusor pressure was also noted to decrease substantially. Neurophysiologic guidance was considered critical for adequate implantation (Spinelli et al, 2005).
Another form of neuromodulatory therapy for which more experience is being reported in SCI is anterior root stimulation. One of the largest experiences with sacral deafferentation and anterior root stimulator implantation was reported by Kutzenberger and colleagues (2005). Four-hundred and sixty-four paraplegic patients received this intervention, with most patients receiving the intradural approach. Four-hundred and forty of these patients were available for long-term follow-up with a mean of 6.6 years. Complete deafferentation was successful in 94% of the patients. Four-hundred and twenty patients used the sacral anterior root stimulator for voiding, and 401 used it for defecation. Overall, 364 (83%) of patients were continent. Urinary tract infections decreased from a mean of six to a mean of one, postoperatively, and kidney function remained stable in this population. Complications included cerebral spinal fluid leaks in six and infected implants in five. Additionally, later complications included device failure or cable failure in 35 patients. Interestingly, autonomic dysreflexia also disappeared or was resolved in most of these cases (Kutzenberger et al, 2005).
As a treatment of last resort, urinary diversion may provide significant functional improvement in addition to improved quality of life in selected patients with neurologic dysfunction. For patients with significant lower urinary tract dysfunction who are unable to catheterize, an alternative may also be urinary diversion. Stein and colleagues (2005) reported 24 patients undergoing Mainz pouch diversion. Urinary diversion was associated with stability of the upper tracts and daytime continence but with some nocturnal incontinence per stoma. Comparing this group with a separate group of patients undergoing bladder augmentation with suburethral fascial sling, all patients in the augmentation group had stability of the upper tracts and 8 of 10 were continent. Both alternatives were considered adequate for neurogenic voiding dysfunction (Stein et al, 2005).
The authors want to express their utmost appreciation to Rosemarie Larmer and Edna Johnson for their forbearance and expertise in assisting in the production of this chapter.
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