[Neurogenic bladder, neuromuscular bladder and intestinal bladder].
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The neurogenic bladder and bowel lead to many complications in individuals with spinal cord injury (SCI). Management of these neurological complications is a multidimensional challenge for persons with SCI and their caregivers, and can affect the person medically, economically, socially, and personally. This may result in social isolation, poor self-image, and overall decreased quality of life (QOL). When facing this challenge, nurses working with persons with SCI must expand their practice to include more than traditional preventive care. A newly available technique for promoting health with a neurogenic bladder and bowel is the VOCARE Bladder and Bowel Control System. Sixteen persons with SCI who received this system were interviewed by telephone and asked for their recollections of health and QOL pre-operatively in relation to bladder and bowel care and to rate changes in their QOL post-implant. Post-operatively, the recipients reported improved health, a decrease in costs of management of their neurogenic bladder and bowel, increased independence leading to less social isolation, increased sense of control, increased feelings of self-worth, and overall improvement in QOL. These outcomes illustrate the global impact that can be made on the lives of persons with SCI by health services that go beyond prevention of complications and into the realm of health promotion.
The uninhibited neurogenic bladder is a common entity. It is characterized by urge incontinence, frequency, enuresis, and recurrent urinary tract infections. The diagnosis can only be made by a thorough urologic investigation, including cystometrography. A sound treatment program involves the use of anticholinergic medication to abolish uninhibited contractions, frequent voiding to keep intravesical pressure low, and antibiotic treatment when indicated for concurrent infection.
Fifty patients with neurogenic bladder dysfunction were treated with methyldopa (Aldomet). The preliminary results that are presented suggest a beneficial action in patients with upper neuron lesions. The probable mechanism of the drug's action is discussed.
Three patients with spastic neurogenic bladder underwent sacral root stimulation and appropriate section of motor rootlets to the detrusor at the levels of the conus medullaris. Compared to the results obtained with rhizotomies at the sacral levels in a previous series of patients, urinary frequency and infection were inhibited for longer periods of time, but some uninhibited bladder activity recurred in all three patients. Analysis of anatomical and electrophysiological data serves to emphasize the complexity and asymmetry of efferent supply to detrusor muscle. The authors conclude that the role of selective rhizotomy for inhibition of the spastic bladder is inconclusive, and perhaps a combination of surgery and medications that inhibit smooth-muscle contraction may be required for long-term protection of urinary collection systems.
Seventy-three children with neurogenic bladder dysfunction were assessed for urinary continence over periods ranging from 6 months to 4 years. Acceptable continence was achieved in 35 (48%), the majority by means of intermittent clean catheterisation, usually with drug manipulation. Two children had tobe diverted purely for intractable incontinence. A plan of management for children with neurogenic bladder dysfunction is described.
The detrusor contraction induced by intramural nerve stimulation in human neurogenic bladders was investigated in comparison with control bladders. All the cases with the neurogenic bladder underwent ileocystoplasty in order to resolve intractable incontinence and/or vesicoureteral reflux due to low bladder compliance or severe detrusor uninhibited contraction. 1. The dose-response curve and ED50 value for KCl were not different between neurogenic and control bladders. 2. The response of neurogenic bladders induced by intramural stimulation was significantly stronger than that of control bladders. 3. After application of 10(-6) M atropine remaining contraction of neurogenic bladders was significantly greater than that of control bladders, i.e. 28.4% and 3.7% respectively. However, 10(-6) M tetrodotoxin almost completely inhibited the detrusor contraction in both groups. 4. The subthreshold KCl (5 mM or 10 mM) enhanced the detrusor contractility significantly in control bladders compared to neurogenic bladders. 5. After bathing medium was replaced into Ca-free Krebs' solution, the contractile response was decreased. The contraction of neurogenic bladders in Ca-free solution persisted longer than that of controls. In conclusion, though there was no intrinsic difference in detrusor contractility, contractile response to electrical field stimulation, atropine resistance, enhancement of response by potassium, and contractility in Ca-free solution were significantly different between neurogenic and control bladders.
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The experiences gained with the intravesical electrostimulation of Katona in 14 children with neurogenic bladders have shown that it is possible to rehabilitate children with neurogenic bladder damage. All these children had never experienced the urge to micturate and it was possible to produce in each of them the sensation of the urge of micturition. In four patients with total incontinence, continence lasting 1 to 1 1/2 hours could be achieved. In 6 patients with a retention overflow bladder micturition leaving no residual urine, a sterile urine and the ability to remain continent for up to 2 hours was achieved. In children with retention overflow bladders which are resistent to therapy, a combinatuon of electrostimulation and resection of the pudendal nerves in girls or external perineal sphincterotomy in boys has provided its value. Anal incontinence can also be cured by direct stimulation of the anal region as we have shown in four patients. These results as well as the results reported by Katona [18] encourage us to recommend electrostimulation in a large number of cases. Should this treatment fail, it is still possible to carry out urinary diversion.
Ureterovesical junction dysfunction in congenital or acquired neurogenic bladders represents a threat for the renal parenchyma. In order to evaluate the incidence, mechanisms of development and preventive and curative treatments proposed in diseases of the ureterovesical junction associated with neurogenic bladders, the files of 119 children were retrospectively evaluated. 68 patients suffered from congenital neurogenic bladder and 51 had an acquired neurogenic bladder. In the congenital neurogenic bladder group, vesico-ureteric reflux was observed in 22 cases (32%) and dilatation was observed in 18 cases (26.5%), while 21 patients had both dilatation and reflux. In the acquired neurogenic bladder group, reflux was observed in 8 cases (16%) and dilatation was observed in 3 cases (10%), one of whom had both reflux and dilatation. The predominant mechanism of decompensation of the ureterovesical junction in the two groups was a combination of low compliance and high peripheral resistance. In patients with abnormalities of the ureterovesical junction, the incidence of associated parenchymal lesions was similar (30%) whether neurogenic bladder was congenital or acquired. The disparities between these two comparable patient groups, the preventive and curative treatments proposed and their results are analysed in comparison with the data reported in the literature.
In nonneurogenic neurogenic bladder (NNNB), or Hinman syndrome, a functional bladder outlet obstruction is produced by voluntary contraction of the external sphincter during voiding. To determine whether any radiographic findings are diagnostic of this condition, the authors reviewed the genitourinary images of six boys in whom NNNB was diagnosed in the past 5 years. In contrast to true neurogenic bladder, findings of elongated, trabeculated, high-volume bladders with substantial postvoid residuals, obstructive uropathy, and vesicoureteral reflux were not associated with clinical, radiographic, or urodynamic evidence of an underlying neurologic abnormality. Furthermore, four boys had distention of the posterior urethra that the authors believe is suggestive of this condition. In these patients, the posterior urethra appeared entirely normal during early voiding, but distended after contraction of the external sphincter as voiding progressed. This posterior urethral distention may worsen the symptoms of enuresis, but may also reduce or retard the damage to the proximal urinary tract.
The evaluation and treatment of children with neurogenic bladders can be difficult because of the complexity of the neurologic deficit and the subjectivity of the history and physical exam. The primary emphasis of the physicians caring for these children should be to preserve renal function and facilitate continence when possible. As knowledge of both normal and abnormal lower urinary-tract dynamics increases, so does the ability to care for children with abnormal bladder dynamics caused by various neurologic conditions. With recent advancements in medical and surgical treatment of the neurogenic bladder, most children can maintain adequate renal function and attain urinary continence. This article reviews the pertinent innervation, anatomy, and physiology of the lower urinary tract, and discusses current evaluation and treatment of children with neurogenic bladders.
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