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Rehabilitation in Multiple Sclerosis

1989; Elsevier BV; Volume: 64; Issue: 7 Linguagem: Inglês

10.1016/s0025-6196(12)61755-8

1942-5546

HOLLAND P. ERICKSON, MARGARET R. LIE, Mark A. Wineinger,

Peripheral Neuropathies and Disorders

Despite the lack of a definitive remedy for central nervous system demyelination in multiple sclerosis, certain manifestations of the disease are treatable. Recognition and identification of specific impairments, disabilities, and handicaps faced by the patient afford the physician the best opportunity to provide effective intervention. Impairments are ameliorated with difficulty; however, when comprehensive methods of rehabilitation are applied to the associated disabilities and handicaps, meaningful improvements can be achieved. The goal of rehabilitation in multiple sclerosis is to maximize the patient's physical, emotional, social, and vocational independence. Through the multidisciplinary efforts of numerous health-care workers in close cooperation with the patient and the family, this goal can be attained. Despite the lack of a definitive remedy for central nervous system demyelination in multiple sclerosis, certain manifestations of the disease are treatable. Recognition and identification of specific impairments, disabilities, and handicaps faced by the patient afford the physician the best opportunity to provide effective intervention. Impairments are ameliorated with difficulty; however, when comprehensive methods of rehabilitation are applied to the associated disabilities and handicaps, meaningful improvements can be achieved. The goal of rehabilitation in multiple sclerosis is to maximize the patient's physical, emotional, social, and vocational independence. Through the multidisciplinary efforts of numerous health-care workers in close cooperation with the patient and the family, this goal can be attained. Although the progressive demyelination of the central nervous system that occurs in multiple sclerosis (MS) is largely unresponsive to currently available therapy, other manifestations of the disease are treatable. To recommend an optimal plan of rehabilitation, the clinician must address the pertinent impairments, disabilities, and handicaps faced by the patient. As defined by the World Health Organization, impairment is “any loss or abnormality of psychological, physical, or anatomical structure or function.”1World Health Organization International Classification of Impairments, Disabilities, and Handicaps: A Manual of Classification Relating to Consequences of Disease. World Health Organization, Geneva1980Google Scholar For example, if demyelination occurs in the motor pathways, spasticity can result. Even though the demyelination (the disease) cannot be treated, the spasticity (the impairment) can be managed by means of stretching exercises, medication, intramuscular neurolysis, and prevention of nociceptive input. When an impairment precludes maintenance of personal independence in self-care and other activities of daily living, the result is a disability. According to the World Health Organization, a disability is “any restriction or lack (resulting from an impairment) of an ability to perform an activity in the manner or within the range considered normal.”1World Health Organization International Classification of Impairments, Disabilities, and Handicaps: A Manual of Classification Relating to Consequences of Disease. World Health Organization, Geneva1980Google Scholar In the aforementioned example, spasticity could produce a gait disturbance. If the spasticity (the impairment) cannot be minimized, the disability often can be minimized by use of gait aids, orthotics, and a wheelchair. The term “handicap” describes the situation in which a disability (or an impairment) precludes meeting responsibilities within one's social milieu. The World Health Organization states that “a handicap is a disadvantage for a given individual, resulting from an impairment or a disability, that limits or prevents the fulfillment of a role that is normal (depending on age, sex, and social and cultural factors) for that individual.”1World Health Organization International Classification of Impairments, Disabilities, and Handicaps: A Manual of Classification Relating to Consequences of Disease. World Health Organization, Geneva1980Google Scholar Thus, the gait disturbance can prevent stair-climbing. If the patient works on the second floor of an office building without an elevator, the inability to climb stairs may result in loss of employment (a handicap). Provision of an elevator or relocation of the office to the first floor would remove the handicap without changing the disability. Therefore, function must be addressed through attention to specific impairments, disabilities, and handicaps. From the perspective of rehabilitation, however, a troublesome aspect of MS is the lack of a single or static lesion. Because the functional status of the patient with MS changes with exacerbations and remissions, function must be reassessed after each fluctuation in disease activity, and intervention must be altered to adapt to the changes. Comprehensive rehabilitative assessment and management are best provided through the multidisciplinary efforts of a neurologist, a physiatrist, a urologist, an orthopedist, a nurse, a physical therapist, an occupational therapist, a speech therapist, a recreational therapist, a neuropsychologist, and a social worker. Optimal care is achieved when each of these health-care professionals contributes unique knowledge and skills to the team. Both optimal planning of rehabilitation and optimal outcome necessitate the active and knowledgeable involvement of the patient and the family. The first step must be education. In a positive, yet honest, manner the physician should educate both the patient and the family about the basic pathophysiologic changes and the multifocal, intermittent, and potentially progressive nature of the disease. The physician then introduces the concept of the rehabilitation team and explains the roles of individual team members. The patient and family learn that, although the disease itself is not curable, the patient can develop behaviors that may help to avoid some exacerbations and that the rehabilitation team will assist in obtaining the training, equipment, and support necessary to minimize the manifestations of MS, if and when they occur. Even in the absence of appreciable weakness, the spasticity associated with MS can reduce energy, inhibit motor control, and interfere with self-care, sexuality, vocational responsibilities, and avocational pursuits. It can be mildly bothersome, or it can totally prohibit useful motor activity, but at times it is of some benefit. A weak patient may rely on spasticity to stabilize the limbs during transfers and ambulation. Because demyelination occurs throughout the central nervous system, spasticity may be the result of spinal or supraspinal lesions. A single treatment regimen is often inadequate, and the physician should identify the origin of the spasticity before initiation of intervention. The management of spasticity can conveniently be viewed as a hierarchy (Fig. 1), in which the clinician initiates management with easily administered and noninvasive modalities and subsequently uses interventions with greater potential risk as they become necessary. Nociceptive input into the central nervous system augments spasticity. Consequently, management begins with general medical care to prevent or to treat urinary tract calculi and infection, decubitus ulcers, constipation, deep venous thrombosis, contracture, and other irritative conditions. The mainstay of management of spasticity is exercise. The patient and family are taught techniques, used twice daily, to stretch spastic muscles and to extend joints crossed by spastic muscles through a full range of motion. In addition to the prevention of muscle shortening and joint contracture, stretching presumably modulates spasticity by decreasing primary spindle afferent activity.2Merritt JL Management of spasticity in spinal cord injury.Mayo Clin Proc. 1981; 56: 614-622PubMed Google Scholar Cold, electrical stimulation, and inhibitive positioning are adjunct physical measures in the management of spasticity. Use of pharmacologic intervention is based on the origin of the spasticity and the presence of concomitant impairments. Baclofen, a derivative of γ-aminobutyric acid, provides both presynaptic and postsynaptic inhibition of monosynaptic and polysynaptic spinal reflexes.3Davidoff RA Pharmacology of spasticity.Neurology. 1978; 28: 46-51Crossref PubMed Google Scholar, 4Davidoff RA Antispasticity drugs: mechanisms of action.Ann Neurol. 1985; 17: 107-116Crossref PubMed Scopus (276) Google Scholar According to the manufacturer, however, it may be ineffective for spasticity of supraspinal origin. Baclofen is less likely than dantrolene to augment weakness and fatigue, and it has been found useful for treatment of spasticity of spinal origin,5Basmajian JV Lioresal® (baclofen) treatment of spasticity in multiple sclerosis: further experience with double-blind cross-over.Am J Phys Med. 1975; 54: 175-177PubMed Google Scholar, 6Feldman RG Kelly-Hayes M Conomy JP Foley JM Baclofen for spasticity in multiple sclerosis: double-blind crossover and three-year study.Neurology. 1978; 28: 1094-1098Crossref PubMed Google Scholar, 7Sawa GM Paty DW The use of baclofen in treatment of spasticity in multiple sclerosis.Can J Neurol Sci. 1979; 6: 351-354PubMed Google Scholar particularly in patients who already have difficulty with weakness or fatigue. The initial dosage of baclofen, which is administered orally, is 5 mg three times a day; this regimen is increased by 5 mg per dose every 3 days to a recommended maximum of 20 mg four times a day. Using the lowest dosage that yields an optimal response is suggested. Diazepam modulates spasticity primarily through spinal mechanisms.4Davidoff RA Antispasticity drugs: mechanisms of action.Ann Neurol. 1985; 17: 107-116Crossref PubMed Scopus (276) Google Scholar When used alone at a dose sufficient to decrease spasticity, however, it often worsens preexisting fatigue, cognitive impairment, and depression. It seems to be particularly useful when used in low dosages (1 to 5 mg three times daily) in conjunction with baclofen. Dantrolene is potentially useful as an antispasticity agent in MS; however, because it inhibits skeletal muscle contraction directly by blocking the release of calcium from the sarcoplasmic reticulum,8Pinder RM Brogden RN Speight TM Avery GS Dantrolene sodium: a review of its pharmacological properties and therapeutic efficacy in spasticity.Drugs. 1977; 13: 3-23Crossref PubMed Scopus (112) Google Scholar decreased spasticity often is accompanied by a proportionate increase in muscle weakness. Serious hepatic toxicity can occur, particularly in female patients and in all persons older than 35 years of age;9Joynt RL Dantrolene sodium: long-term effects in patients with muscle spasticity.Arch Phys Med Rehabil. 1976; 57: 212-217PubMed Google Scholar therefore, use of dantrolene should be limited to special situations. It may be considered for younger male patients with spasticity not accompanied by severe weakness or for patients with severe weakness and no useful motor function when spasticity interferes with personal hygiene and positioning. Other pharmacologic agents have been reported to decrease spasticity—for example, phenytoin, carbamazepine, and the phenothiazines—through both spinal and supraspinal mechanisms. Generally, however, their effects are minor when they are administered in the small doses that produce no side effects.4Davidoff RA Antispasticity drugs: mechanisms of action.Ann Neurol. 1985; 17: 107-116Crossref PubMed Scopus (276) Google Scholar Recently, several new antispasticity agents have been described. Progabide, a γ-aminobutyric acid agonist, has been reported to decrease spasticity without associated weakness;4Davidoff RA Antispasticity drugs: mechanisms of action.Ann Neurol. 1985; 17: 107-116Crossref PubMed Scopus (276) Google Scholar, 10Rudick RA Breton D Krall RL The GABA-agonist progabide for spasticity in multiple sclerosis.Arch Neurol. 1987; 44: 1033-1036Crossref PubMed Scopus (21) Google Scholar unfortunately, hepatic dysfunction has been common in study participants.10Rudick RA Breton D Krall RL The GABA-agonist progabide for spasticity in multiple sclerosis.Arch Neurol. 1987; 44: 1033-1036Crossref PubMed Scopus (21) Google Scholar In two double-blind placebo-controlled trials, tizanidine, a new antispasticity agent with central effects, effectively decreased spasticity, hyperactive stretch reflexes, and clonus.11Rinne UK Tizanidine treatment of spasticity in multiple sclerosis and chronic myelopathy.Curr Ther Res. 1980; 28: 827-836Google Scholar, 12Lapierre Y Bouchard S Tansey C Gendron D Barkas WJ Francis GS Treatment of spasticity with tizanidine in multiple sclerosis.Can J Neurol Sci. 1987; 14: 513-517PubMed Google Scholar It reportedly has less of a tendency than baclofen or diazepam to produce weakness, and it causes less drowsiness than diazepam. The Food and Drug Administration, however, has not yet released this drug for clinical use in the United States. When a selective decrease in spasticity is desired, intramuscular neurolysis (”motor point blocks”)13Halpern D Meelhuysen FE Phenol motor point block in the management of muscular hypertonia.Arch Phys Med Rehabil. 1966; 47: 659-664PubMed Google Scholar can be considered. During this relatively safe but tedious procedure, small amounts of a 5 or 7% phenol solution are injected percutaneously near small intramuscular motor nerves identified by an electrical stimulator. Although the effects last only until reinnervation occurs (a maximum of 6 months), sufficient respite is gained for stretching, splinting, and positioning so that lasting benefit may result. The procedure can be repeated without substantial risk. If spasticity remains a problem despite these measures and if contracture occurs, invasive and destructive procedures may be necessary. Percutaneous peripheral nerve, nerve root, or intrathecal phenol blocks, surgical neurectomy or rhizotomy, tenotomy, tendon lengthening, and myotomy all have been used to decrease spasticity and its sequelae. A report by Merritt2Merritt JL Management of spasticity in spinal cord injury.Mayo Clin Proc. 1981; 56: 614-622PubMed Google Scholar presents further useful information about the management of spasticity. Paresis may occur in patients with MS as a consequence of several factors—motor pathway demyelination that results in upper motor neuron dysfunction, the added effort of moving against spasticity and ataxia, and disuse. Once spasticity has been minimized, as described in the preceding section, the physical therapist uses upper motor neuron reeducation techniques to facilitate voluntary motor activity while inhibiting unwanted motor patterns. Debate continues about the safety and benefit of muscle strengthening. Excessive muscle fatigue can result in increased paresis, increased body temperature, and ataxia.14Cailliet R Rehabilitation in multiple sclerosis.in: Licht S Rehabilitation and Medicine. Waverly Press, Baltimore1968: 446-459Google Scholar The increased body temperature usually associated with prolonged exertion leads to impairment of nerve fiber conduction in proportion to the degree of demyelination.15Schauf CL Davis FA Impulse conduction in multiple sclerosis: a theoretical basis for modification by temperature and pharmacological agents.J Neurol Neurosurg Psychiatry. 1974; 37: 152-161Crossref PubMed Scopus (153) Google Scholar Yet, both selective strengthening of muscles innervated by the less involved or uninvolved upper motor neurons and improved cardiopulmonary function yield enhanced physical function with less effort and a greater sense of well-being. Selective and judicious muscle strengthening that does not lead to appreciable fatigue or increased core temperature seems warranted. One of the most common symptoms in the patient with MS is fatigue, yet it may be incomprehensible to the family. It is a complex combination of upper motor neuron weakness, spasticity, malfunction of demyelinated nerve fibers with exertion and increased core temperature, and, at times, depression. It spans the range from bothersome tiredness after effort to apparently spontaneous and overwhelming exhaustion that can prevent the completion of basic activities of daily living; Fatigue often becomes a self-fulfilling prophecy. The patient spends the first part of the day rushing to complete personal and family responsibilities before the dreaded exhaustion supervenes, and because of this overexertion, it does materialize. Management hinges on education of both the patient and the family, and it begins with “economy of effort” training with the occupational therapist, a type of energy conservation in which paced effort and energy-saving techniques are interspersed with intervals of rest. Warm ambient temperature should be avoided, cool baths and ice packs should be used when the patient is overheated, and air-conditioning is considered a medical necessity in all but the coolest climates. In a recent double-blind crossover study, amantadine administered orally at 100 mg twice daily was found to lessen fatigue substantially in some patients with MS.16Canadian MS Research Group A randomized controlled trial of amantadine in fatigue associated with multiple sclerosis.Can J Neurol Sci. 1987; 14: 273-278PubMed Google Scholar Ataxia, both midline and appendicular, is a common impairment, and attempts to ameliorate it directly are unlikely to be successful. Although traditional treatment has included attempts at reestablishment of efficient motor patterns by means of repetitive coordination exercises, improvement seldom is realized in the presence of progression of MS. Fatigue exaggerates ataxia and should be avoided. For appendicular ataxia, intervention is often directed at dampening the tremor by the use of small weights applied to the distal aspect of the extremity or use of weighted utensils. Weakness can augment the impairment and, in selected cases, proximal extremity bracing may lessen ataxia in distal segments during activities. Some patients with cerebellar postural and action tremor will respond to isoniazid at high dosages (300 to 400 mg three times a day).17Hallett M Lindsey JW Adelstein BD Riley PO Controlled trial of isoniazid therapy for severe postural cerebellar tremor in multiple sclerosis.Neurology. 1985; 35: 1374-1377Crossref PubMed Google Scholar, 18Duquette P Pleines J du Souich P Isoniazid for tremor in multiple sclerosis: a controlled trial.Neurology. 1985; 35: 1772-1775Crossref PubMed Google Scholar, 19Bozek CB Kastrukoff LF Wright JM Perry TL Larsen TA A controlled trial of isoniazid therapy for action tremor in multiple sclerosis.J Neurol. 1987; 234: 36-39Crossref PubMed Scopus (38) Google Scholar The potential risk of hepatitis and the need for pyridoxine to prevent peripheral neuropathy must be considered. No available intervention will decrease sensory impairment directly. Management includes augmentation of intact senses to replace lost sense of touch, temperature, and pain and prevention of complications such as pressure ulceration and thermal injury. The patient and the family are taught to inspect insensate skin twice daily for evidence of poorly fitting shoes, braces, or other equipment, to use a thermometer to monitor bathwater temperature, and to seek medical care immediately when dermatologic problems are noted. If buttock skin is insensate in a patient who uses a wheelchair, a pressure-distributing seat cushion should be provided, and the patient should be instructed to perform pressure-relieving weight shifts every 15 minutes. Sheepskin and water or foam mattresses may be used for protection of the skin. Pain is an inconsistent impairment in patients with MS. Its varied manifestations have been described as lancinating pain, painful dysesthesias, or aching. Attempts at relief include use of transcutaneous electrical stimulation, carbamazepine, and amitriptyline. The clinician should remember that the patient with MS can have a painful musculoskeletal and neurologic condition that is unrelated to the MS and potentially is correctable. Impairment of vision is common in patients with MS. Diminution of vision may be partially ameliorated with corrective lenses, and all patients with MS who have complaints about visual acuity should have optimal ophthalmologic care. Those blinded by their disease should be referred promptly to Services for the Blind. Braille reading material, Braille typewriters, and Braille computer keyboards are available; however, in many patients with MS, their use is preempted by concomitant digital sensory loss. For diplopia, an eye patch is used to avoid the problem of double images; the patch should be alternated from one eye to the other every few days. Nystagmus is difficult to resolve. Cognitive and perceptual impairments (discussed elsewhere in this series) necessitate assessment through psychometric and functional testing for characterization of the deficits. After such an assessment, the intervention may include cognitive and perceptual training, task simplification, environmental manipulation, and vocational rehabilitation. In MS, communication disability most often results from impairment of speech production and, to a lesser extent, from language and cognitive deficits. Nevertheless, only 10% of the patients with MS have disability severe enough to interfere with activities of daily living.20Kraft GH Freal JE Coryell JK Disability, disease duration, and rehabilitation service needs in multiple sclerosis: patient perspectives.Arch Phys Med Rehabil. 1986; 67: 164-168Abstract Full Text PDF PubMed Scopus (100) Google Scholar Dysarthria, which may be ataxic, spastic, or mixed, should be evaluated by a speech pathologist to identify potentially remedial measures. Other approaches to management include decreasing the spasticity, minimizing the use of medications that cause dry mouth, and maximizing the patient's breathing capacity by achieving optimal pulmonary function through medical means, by diaphragmatic exercises, and by the use of an abdominal binder. When other methods fail to produce intelligible speech, use of electronic speech aids should be considered. Demyelination within brain-stem pathways can result in dysphagia for liquids and solids and consequent malnutrition. Dietary counseling to identify foods and liquids of manageable consistency and adequate nutritional value is a necessity. Videofluoroscopy of the swallowing process may disclose deficits that are responsive to training. When oral intake is inadequate to maintain nutrition despite all efforts, a feeding gastrostomy or gastroenterostomy may be considered. In patients who do not have dysfunction of swallowing, obesity due to the combination of inactivity and excessive intake of calories can further hinder mobility that is already compromised by motor impairments. Adequate hygienic skills are necessary for the disabled patient to maintain self-image and health. The patient with MS without such skills has a considerable risk for irritative dermatitis, skin and urinary tract infections, and limited social interaction. Related factors include mobility skills, sitting and standing balance, fatigue, impairment of vision, and upper-extremity motor skills. Physical and occupational therapists often can train the patient in new skills, but adaptive aids and equipment are frequently necessary to substitute for lost abilities. A bath bench, shower chair, bidet, long-handled brushes, skin inspection mirrors, and electric razor may be helpful. The proper scheduling of a cool bath or shower also may help to minimize fatigue later in the day. Dressing in street clothes is necessary to enable the patient with MS to enter the community, yet incoordination, spasticity, tremors, or weakness may make this task difficult or impossible. Clothes should be kept readily accessible. Lowering of closet rods, changing of handles on drawers, and even lubricating of drawer slides could be considered. Aids that may simplify the task of dressing include alternative clothing fasteners (Velcro closures, large buttons), elastic shoelaces, and long-handled shoehorns. When dressing takes a prolonged time despite these measures and thus causes overfatigue, assistance from family members or an attendant should be considered. Bathrooms must be accessible to the patient with MS both at the doorway and at the toilet. With a wall-hung toilet, more room is available for a wheelchair. For the ataxic or weak patient, a raised toilet seat and grab bars are often needed. Bidet units can assist in hygiene when deficient hand motor skills preclude effective cleansing. If the bathroom is inaccessible, a bedside commode is preferable to a bedpan. Stool incontinence and constipation are frequently experienced by the patient with MS. Dysfunction may be due to a spinal cord lesion, decreased activity, dehydration, medications, or nutritional factors; most often, it results from the additive effects of several of these factors. Intake of fluids should be adequate (see subsequent section on neurogenic bladder) but not excessive, or it will interfere with bladder management. A high-fiber diet, bulk formers, and stool softeners are useful for maintaining stool consistency, but the use of laxatives and enemas should be minimized. Bowel care should be performed every other day at approximately 45 minutes after the largest meal of the day, to take advantage of the gastrocolic reflex. Rectal evacuation may be augmented by use of glycerin or Dulcolax suppositories or digital stimulation. Prevention of problems is preferable to relying on only responding to them. Several weeks may be needed for the program to become effective. When severe problems are already present, use of laxatives and enemas may be necessary before institution of the bowel care program. Bladder dysfunction occurs in many patients with MS. Initially, the dysfunction may be subtle, but careful questioning often reveals hesitancy, urgency, frequency, loss of sensation, incontinence, and retention. Questioning should be directed to a possible history of urinary tract infections and urolithiasis. In early stages of MS, urodynamic studies may disclose almost any combination of increased or decreased detrusor, bladder neck, and external sphincter tone, but the end-stage bladder generally is hyperreflexic in association with sphincter dyssynergia (sphincter contraction during detrusor contraction). The initial evaluation should include laboratory assessment of kidney function and a search for and identification of infection. Bladder-emptying function should be assessed with one or more catheterizations to measure the postvoiding residual urine volume. If emptying is sufficiently defective, excretory urography should be performed to evaluate the kidneys and upper urinary tract and to detect stones. Cystoscopy is used to search for outlet obstruction and bladder stones and to evaluate the anatomy of the bladder. Finally, urodynamic studies—including a cystometrogram for the measurement of detrusor contraction and intravesical pressure in conjunction with concomitant surface electromyographic monitoring of the muscles of the perineal floor (CMG-EMG), urethral pressure profile to monitor outlet resistance, and urinary flow studies—will identify the type of bladder dysfunction. During the CMG-EMG, the effect of abdominal tapping, Credé's maneuver, straining, and other therapeutic maneuvers on detrusor and sphincter activity can be determined. Management of the neurogenic bladder in patients with MS is summarized in Table 1. With minor dysfunction (postvoiding urine volume less than 100 ml), only regulation of intake of fluids and a schedule for voiding may be necessary to avoid overstretching of the bladder and to minimize urgency and frequency. If, however, the retained urine volume is high or detrusor-sphincter dyssynergia has been identified, intermittent catheterization is recommended. Unless contraindicated by weakness, ataxia, disturbance of vision, or cognitive dysfunction, the patient may be instructed in intermittent self-catheterizaton techniques. Bladder retraining, with use of tapping, Credé's maneuver, or straining, may be considered for selected patients.21Opitz JL Bladder retraining: an organized program.Mayo Clin Proc. 1976; 51: 367-372PubMed Google ScholarTable 1Management of Neurogenic Bladder in Patients With Multiple Sclerosis1.Regulated schedule of intake of fluids (1,800 ml/24 h): 400 ml with each meal 200 ml in midmorning (10 a.m.), midafternoon (2 p.m.), and late afternoon (4 p.m.)2.Regulated schedule of voiding: Voiding attempted every 3 hours during waking hours3.Intermittent catheterization after attempts at voiding: Catheterization every 6 hours, unless catheterized volumes exceed 500 ml, in which case catheterization every 4 hours until patient complies with the schedule for intake of fluids4.Suppression of urinary bacterial growth: Trimethoprim-sulfamethoxazole (1 double-strength tablet orally at bedtime) Methenamine hippurate (1 g orally twice a day)5.Instructions for intermittent self-catheterization, if necessary6.Bladder retraining in selected patients7.Indwelling catheter drainage, if necessary: Intake of fluids should exceed 2,000 ml/24 h No asymptomatic bacterial suppression therapy is used Catheter is changed every 2 to 4 weeks Open table in a new tab If the aforementioned measures are not possible, indwelling catheter drainage should be considered. Other indications for use of an indwelling catheter include a need for hygiene to alleviate pressure sores, lack of an attendant to perform catheterizations, travel situations in which catheterization is difficult, and severe inco