Summary There are several important reasons why clinicians need to focus on neurogenic bladder dysfunction in multiple sclerosis (MS): Impaired bladder function is common in MS, affecting up to 90% of people with MS at some time during the course of their illness; Urinary symptoms are disruptive, interfering with critical life areas such as social, vocational and sexual activities; Complications from urinary dysfunction can cause morbidity and mortality; Bladder symptoms can be successfully managed and urinary complications prevented.
Reports of urinary that more than 70% or patients treated symptoms in multiple (MS) are high, with up to 90% of people with MS affected at some time during the course of their disease (McGuire & Savastano, 1984). Bladder symptoms may occur at the onset of MS or at any time thereafter, and do not correlate well with underlying pathology. One study documented That more than 70% of patients treated on the basis of history and physical examination alone received inappropriate therapy (Blaivas, Bhimani & Labib, 1979). It is critical therefore, to identify the underlying pathology before attempting to relieve symptomatic manifestations. In addition to the frequent occurrence of bladder symptoms, there are compelling reasons for the clinician's attention. Morbidity and mortality can be high. A 1964 review of autopsies of MS patients, attributed 55% of deaths to hydronephrosis or pyelonephritis (Samellas & Rubin, 1965), while a more recent study cites only 5% related to urinary tract involvement (Betts, D'Mellow & Fowler, 1993). This dramatic decrease in mortality related to urologic factors is attributed to improved diagnostic methods and intermittent catheterization (Chancellor & Blaivas, I993). These advances must be communicated and implemented if the reduction in serious consequences is to be realized. Bladder symptoms also interfere with vital life activities. Urgency, frequency and incontinence can destroy a person's ability to socialize, be employed outside of the home and engage in satisfying sexual activities. Most importantly, with application of current knowledge in this area, the distressing and disruptive symptoms can be managed; the associated morbidity and mortality can be avoided.
Types of Dysfunction
There are a variety of classification schemata for neurogenic bladder dysfunction, with some based upon neuroanatomy, such as upper or lower motor neuron types of disturbance. The most practical and easily comprehended model is functional, i.e. related to the bladder's ability to fulfill it's function of storing urine between voidings. The types of dysfunction in this taxonomy are: failure to store (storage dysfunction), failure to empty (emptying dysfunction) and combined dysfunction (Blaivas and Kaplan, 1988, ).
In order for normal urination to occur, the detrusor or bladder muscle must contract simultaneously with the relaxation of the internal and external sphincters. The detrusor provides an expulsive force, while the relaxed sphincters allow for an unobstructed outlet (Blaivas, 1979). Urinary collection occurs slowly with expansion of the bladder until a critical amount of approximately 200 ml has accumulated, signaling a reflex contraction and the desire to urinate.
Storage dysfunction reflects an inability of the detrusor to inhibit emptying contractions until a reasonable amount of urine has accumulated. A strong urge to void is experienced when only a small amount of urine is in the bladder. The patient may report symptoms of urgency, frequency, nocturia and incontinence. These symptoms may be present in varying degrees, depending upon other factors such as diminished bladder sensation. Storage dysfunction may also occur following removal of a long-present Foley catheter. In this situation the bladder neck or internal sphincter may have been permanently damaged by the indwelling catheter. There is no known compensatory mechanism for this damage, and continuous urinary drainage is the intervention of choice. Emptying dysfunction often represents a weakened force of contraction results in retention. Detrusor- external sphincter dyssynergia (DESD) is another factor, with simultaneous detrusor and e external sphincter contraction resulting in urinary retention. This phenomenon is usually associated with combined dysfunction, but may be the predominant pathology in emptying dysfunction. One study reports hypocontractile rather than DESD (Mayo & Chetner, 1992). This is most likely a classification issue, since DESD has traditionally been associated with combined dysfunction more than emptying dysfunction. Since bladder sensation may be concurrently altered, symptoms may mimic those of storage dysfunction. Hesitancy or sensation of incomplete bladder emptying may also be present.
Combined dysfunction exhibits features of both storage and emptying disorders. DESD is the classic pathophysiology and requires a multi-pronged approach. As stated previously, symptoms are not useful in determining the type of problem, and any combination of reported complaints may be present (see Figure 2, Betts, D'Melow & Fowler, 1993). The physiological phenomenon, which involves incoordination of the emptying mechanism - the detrusor is contracting at the same time that the external sphincter contracts, presents a significant health threat. The intravesical pressure rises due to outlet obstruction coincident with detrusor contraction. The risk is that urine will be forced up the ureters causing upper urinary tract damage. Should urinary tract infection (UTI) be present, pyelonephritis may occur as well as hydronephrosis.
The initial screening for any type of urinary complaint is to rule out UTI by routine and microscopic, and culture and sensitivity testing of the urine. In some instances treatment of a urinary infection will be sufficient to relieve symptoms. In the absence of UTI, further exploration must occur.
There are several ways to identify the underlying pathology. The simplest and least expensive is to measure the post-void residual volume. To do this, the patient is instructed to drink two litres of fluid the day preceding testing and two glasses of liquid on the day of testing prior to the assessment. The patient is instructed to communicate the desire to void (either at home or in the outpatient setting) to the nurse. The patient is then instructed to urinate and the voided amount is measured. Next, the patient is I catheterized and the residual amount measured. The combination of these two figures calculates bladder capacity. Is the capacity 200ml or above, indicating a sufficient volume to trigger emptying? There are a number of ways to determine the post-voiding residual (PVR) volume and the bladder capacity besides the catheterization procedure.
Also useful are the intravenous urogram, radioisotope scan and sonogram. Ultrasound is perhaps the fastest growing (and minimally expensive) diagnostic imaging technique to facilitate identification of the underlying pathophysiology (Wagner, 1992). However, the accuracy of ultrasound measured residual urine is known to vary widely, and is an important consideration (Smith, Aison & Scheinberg, 1986). The algorithm in figure 3 illustrates the decision making process that is most successful in addressing MS neurogenic bladder dysfunction (Blaivas, Holland, Giesser, LaRocca, Madonna & Scheinberg, 1984).
Effective management is available for most people experiencing MS related bladder dysfunction. Interventions are categorized according to the type of dysfunction and are easily followed by a health professional or team concerned with the outcomes of MS related bladder interventions.
Anticholinergic type of medication is the most effective in managing storage dysfunction. Propantheline bromide and oxybutynin are administered q4-6h, while the tricyclic imipramine can be taken as a single bedtime dose for its retentive side effects. A more recent intervention, which particularly addresses nocturia, is DDAVP (1-desamino, 8-[D] arginine vasopressin).
A pilot study of eight patients evaluated the outcome of intranasal DDAVP taken HS for intractable nocturia. Five patients reported complete relief and two considerable benefit, with six to eight hours of antidiuresis reported (Valiquette, Abrams & Herbert, 1992).
Capsaicin, the pungent ingredient in red pepper, has been instilled intravesically for relief of detrusor hyperreflexia, with or without DESD, in patients with unsatisfactory response to anticholinergic agents. Considerable sustained improvement was reported in four out of five MS patients empirically tried on this agent (Fowler, Jewkes & McDonald, 1992), and varied length or improvement in nine out of twelve people with detrusor instability secondary to spinal cord injury or of unknown etiology (Nitti, 1994). Intravesical instillation of oxybutynin chloride has also been used as a treatment for uninhibited bladder contractions, with 55% experiencing improved bladder function in a limited exploratory trial (Weese, Roskamp, Leach & Zemmern, 1993).
Intermittent catheterization is the intervention of choice for emptying dysfunction, with non-sterile technique and multiple use of non-sterile catheters. A study of 30 spina bifida patients revealed no difference in positive urine cultures between sterile and clean self-catheterization techniques for patients per- forming the procedure in the home or other out-patient setting (Moore, Kelm, Sinclair & Cadrain, 1993). The conclusion was that clean technique is acceptable and reuse of catheters a reasonable cost- effective measure. Self- catheterization may be performed by the people with impaired dexterity, reduced sensation in the hands or genitalia, and/or diminished vision. Even with greatly reduced physical capacity, many individuals are capable ~ of self-catheterization. This has enormous implications I for self-care and avoidance of potentially critical complications.
Presence of combined dysfunction usually requires both anticholinergic medication and intermittent catheterization. A careful balance of medication and catheterization must be worked out on an individual basis, with ongoing consultation between the bladder specialist and the MS patient. For intractable cases, consideration should be given to DDAVP or possible intravesical instillation of capsaicin or oxybutynin, as described in the section on management of storage dysfunction.
The need for surgical intervention is rare, but options should be mentioned for completeness of management overview: bladder augmentation for hypertonic contracted bladder artificial sphincter continent vesicostomy (abdominal placement of urethral opening for intermittent catheterization) (Benchekroun, 1982) The secondary manifestations of adduction spasm (caused by MS lesion(s) and impacting urination, but not directly impairing bladder function) also responds to aggressive interventions: Phend injections as nerve blocks or motor point blocks Baclofen orally or via baclofen pump Botox injections
Management decisions are complex and based upon a delicate balance of history and neurophysiologic examination, with ongoing monitoring and modification. New possibilities are always present and require careful investigation before inclusion in recommended protocols. The key factors are recognition of the significance of the problem, knowledge of appropriate diagnostic and therapeutic modalities and involvement of the person with MS and significant other (s) in assessment, diagnostic, educational, intervention and evaluative phases of management of urinary dysfunction.
Benchekroun, 'Continent Caecal Bladder', Br J Urology 54:505,1982 Betts CD, D'Mellow MT, Fowler CJ, 'Urinary Symptoms and the Neurological Features of Bladder Dysfunction in Multiple Sclerosis', J Neurol Neurosurg Psychiatry 1993; 56:254-250 Blaivas JG, Bhimani G and Labib KB, 'Vesico-Urethral Dysfunction in Multiple Sclerosis', J Urol 122:342, 1979 Blaivas JG, "Management of Bladder Dysfunction in Multiple Sclerosis" Neurology 30(2), July 1980. Blaivas JG, Kaplan SA "Urologic Dysfunction in Patients with Multiple Sclerosis" Seminars in Neurology, Vol 8 No 2, Summer 1988 Blaivas JG, Holland NJ, Geisser B, LaRocca N, Madonna M, Scheinberg L, 'Multiple Sclerosis Bladder: Studies and Care' in Multiple Sclerosis: Experimental and Clinical Aspects, Eds, Scheinberg & Raine, Annals of the New York Academy of Sciences Vol 436,1984 Chancellor MB, Blaivas JG, 'Multiple Sclerosis' in Problems in Urology Vol 7 No 1, March 1993, JB Lippincott Co Fowler CJ, Jewkes D, McDonald WI, 'Intravesical Capsaicin for Neurogenic Bladder Dysfunction', The Lancet Vol 339, May 16,1992 Leibowitz U, Kahana E, Jacobson SG, Ater M, 'The Cause of Death in Multiple Sclerosis' in Leibowitz U ed. Progress in Multiple Sclerosis: Research and Treatment, New York: Academic Press; 196-209,1972 McGuire EJ, Savastano JA, 'Urodynamic Findings and Long-term Outcome Management of Patients with Multiple Sclerosis-induced Lower Urinary Tract Dysfunction' J Urol 132:102,1984 May ME, Chetner MP, 'Lower Urinary Tract Dysfunction in Multiple Sclerosis' Urology, Vol XXXIX No 1, 67-70, Jan 1992 Moore KN, Kelm M, Sinclair 0, Cadrain G, 'Bacteruria in Intermittent Catheterization Users: The Effect of Sterile Versus Clean Reused Catheters' Rehabilitation Nursing Vol 18 No 5, Sept/Oct 1993 Nitti V, 'Intravesical Capsaicin for Treatment of Neurogenic Bladder' The Lancet Vol 343, June 11,1994 Samellas W, Rubin B, 'Management of Upper Urinary Tract Complications in Multiple Sclerosis by Means of Urinary Diversion to an Ileal Conduit' J Urol 93:548,1965 Smith CR, Aison MC, Scheinberg L, 'Symptomatic Management of Multiple Sclerosis' in McDonald WI, Silberberg DH, Eds, Multiple Sclerosis 1986:166-83 London, Butterworths Valiquette G, Abrams G, Herbert J, 'DDAVP in the Management of Nocturia in Multiple Sclerosis' Annals of Neurology Vol 31 No 5 Wagner Mary, 'Ultrasound Evolution', Modern Healthcare April 6,1992 Weese D, Roskamp D, Leach G., Zimmern P, 'Intravesical Oxybutynin Chloride: Experience with 42 Patients' Urology Vol 41, June 1992