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Thread: BLADDER QUESTION

  1. #1
    Junior Member
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    Jul 2001
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    Minneapolis, Minnesota
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    BLADDER QUESTION

    Dr Young can you please explain how ditropan is instilled into the badder? How often it needs to be instilled. Is it instilled under a urologists care. I'm having a lot of pelvic floor spasms and would like to see if instlling ditropan into my bladder might help.

    Thanks

    Ron

  2. #2

    mnvikes

    Ron, I don't have any personal experience with the ditropan distillation but cannot imagine why it can't be done at home. One must of course use sterile solutions and catheterization to avoid the risk of infection. The procedure seems to be relatively simple and it is practiced in children at home [1]. My primary worry is that it is not long-acting enough but one recent paper suggest that it is possible to make a time-release version of the drug for bladder instillation [2] that lasts for as long as a week. A dose of 15 mg three times daily apparently is effective for people with bladder spasticity that is refractory to oral oxybutynin [3]. The standard intravesical dose is 0.3 mg/kg per day but doses up to 0.9 mg/kg per day was effective for even the most refractory cases although about 20% of the patients showed some systemic side-effects of the drug. [4] I do want to point out that several studies have shown that intravesical capsaicin or analogs provide long-term (3-6 month) relief from bladder spasticity and you may want to consider this instead [5-6].

    References cited
    1. Lapointe SP, Wang B, Kennedy WA and Shortliffe LM (2001). The effects of intravesical lidocaine on bladder dynamics of children with myelomeningocele. J Urol. 165 (6 Pt 2): 2380-2. Summary: PURPOSE: Other studies have suggested that intravesical lidocaine may temporarily improve bladder dynamics but details of these effects and their application to children have not been examined. We evaluated the effects of intravesical lidocaine on bladder urodynamics of children with myelomeningocele and tried to correlate these effects with subsequent clinical response to oral oxybutynin. MATERIALS AND METHODS: Charts of children with myelomeningocele who had undergone urodynamic examinations from 1992 to 1998 were reviewed retrospectively. In children with uninhibited contractions or poor compliance 150 to 300 mg. lidocaine were instilled for 8 minutes and cystometry was repeated. Changes in bladder capacity and compliance, number of uninhibited contractions and bladder volume at which pressure of 40 cm. H2O was reached were recorded before and after the lidocaine instillation. Clinical response to subsequent treatment with oral oxybutynin was assessed from chart review. RESULTS: A total of 48 urodynamic studies in 22 girls and 20 boys with a mean age plus or minus standard deviation of 8.3 +/- 5.7 years and myelomeningocele were evaluable. After instillation of lidocaine, urodynamics showed increased bladder capacity in 70.8% of studies (34 of 48), with an average increase in volume of 66% (p <0.05). No change or decreased bladder capacity occurred in 29.2% of studies. Bladder compliance improved in 61.7% of the studies (29 of 47, p <0.05) and worsened in 38.3%. Bladder volume at which the pressure of 40 cm. H2O was reached increased in 77.8% of studies (14 of 18, p <0.05). After lidocaine the number of uninhibited contractions decreased by 3.2 in 56.8% of studies (21 of 37, p <0.05). Correlation of lidocaine induced changes in bladder capacity, compliance and number of uninhibited contractions with improvement on oral oxybutynin was 70.6%, 64.3% and 66.7%, respectively. CONCLUSIONS: Intravesical lidocaine can improve bladder capacity and compliance and decrease the number of uninhibited contractions in many children with neurogenic bladder caused by myelomeningocele. These observations suggest that intravesical lidocaine has effects on the neurogenic bladder that improve bladder dynamics. Although intravesical lidocaine testing may not reliably predict clinical response to oral oxybutynin at the prescribed dosages, a possible therapeutic role for intravesical lidocaine or similar agents should be explored further. <http://www.ncbi.nlm.nih.gov/htbin-po...&uid=11371945> Department of Urology, Stanford University, Stanford, California, USA.

    2. Saito M, Tabuchi F, Otsubo K and Miyagawa I (2000). Treatment of overactive bladder with modified intravesical oxybutynin chloride. Neurourol Urodyn. 19 (6): 683-8. Summary: Intravesical oxybutynin chloride has been reported to be effective for overactive bladder, although sometimes the efficacy does not last long enough. To improve this deficiency, we report the effects of intravesical oxybutynin chloride with hydroxypropylcellulose (modified intravesical oxybutynin). Modified intravesical oxybutynin (5 mg/10 mL, twice a day) was administered to six overactive bladder patients for more than 1 year (two men and four women; average age, 56.5 years) who did not respond to oral anticholinergic agents and electric stimulation. Cystometography (CMG) was performed before, 2 hours, and 1 week after the start of modified intravesical oxybutynin. In addition, plasma levels of oxybutynin and its active metabolite, N-desethyl- oxybutynin (DEOB), were measured by high-performance liquid chromatography before, 1, 2, and 4 hours after the initial treatment of modified intravesical oxybutynin. CMG studies revealed that two of the six patients did not demonstrate uninhibited contractions 1 week after the treatment and that cystocapacity of before, 2 hours, and 1 week after the initial modified intravesical oxybutynin was 141.8+/-15.3, 210.0+/-35.5, and 305.0+/-21.3 mL, respectively. Plasma levels of oxybutynin and DEOB before, 1, 2, and 4 hours after the first instillation of modified intravesical oxybutynin were oxybutynin; not detected, 8.8+/-2.5, 6.8+/-1.1, 3.0+/- 1.0 ng/ml, and DEOB; not detected, 4.2+/-1.3, 6.4+/-1.7, 5.1+/- 1.4 ng/ml, respectively. No side effects were observed in any of the patients. Modified intravesical oxybutynin is an effective and safe therapy option for overactive bladder patients who do not respond to other treatments such as oral anticholinergic agents and electric stimulation. <http://www.ncbi.nlm.nih.gov/htbin-po...&uid=11071699> Department of Urology, Tottori University Faculty of Medicine, Yonago, Tottori, Japan. saitomo@grape.med.tottori-u.ac.jp

    3. Pannek J, Sommerfeld HJ, Botel U and Senge T (2000). Combined intravesical and oral oxybutynin chloride in adult patients with spinal cord injury. Urology. 55 (3): 358-62. Summary: OBJECTIVES: Detrusor hyperreflexia with elevated storage pressures presents a major risk factor for renal damage in patients with neurogenic lower urinary tract dysfunction. If standard anticholinergic treatment is unsuccessful, surgical treatment must be considered. We evaluated the effects of intravesical oxybutynin treatment on detrusor hyperreflexia in patients in whom standard oral treatment had failed. METHODS: Twenty-five patients (mean age 36. 7 years) with storage pressures greater than 40 cm H(2)O despite standard anticholinergic treatment received intravesical (15 mg three times daily) and oral oxybutynin chloride treatment. The follow-up evaluations included urodynamic testing, renal ultrasound, urine examination (urinalysis and urine culture), and evaluation of side effects. RESULTS: The mean follow-up was 6 months. Intravesical treatment led to an increase in bladder storage volume from 349 to 420 mL. The mean maximum storage pressure was significantly reduced from 54 to 26.5 cm H(2)O. Detrusor storage pressures returned to values less than 40 cm H(2)O in 21 of 25 patients. Dysreflexia was treated successfully in 3 of 5 patients. No patient developed renal damage. No severe side effects or drug-related discontinuation of treatment were observed. CONCLUSIONS: Intravesical oxybutynin therapy seems to be a safe and effective treatment option for detrusor hyperreflexia in adults and avoids surgical treatment in most patients. Long-term observations concerning side effects, acceptance, and efficacy are needed. <http://www.ncbi.nlm.nih.gov/htbin-po...&uid=10699610> Department of Urology, Ruhr-Universitat Bochum, Herne, Germany.

    4. Haferkamp A, Staehler G, Gerner HJ and Dorsam J (2000). Dosage escalation of intravesical oxybutynin in the treatment of neurogenic bladder patients. Spinal Cord. 38 (4): 250-4. Summary: OBJECTIVE: We prospectively analyzed the dose dependent outcome and side effects of neurogenic bladder patients with intravesical application of oxybutynin at our centre. MATERIALS AND METHODS: We examined the data of 32 patients with neurogenic bladders and detrusor hyperreflexia. We registered clinical outcome, continence situation, side effects and urodynamic data of patients with (A) standard dosages of intravesical oxybutynin (0.3 mg/kg bodyweight per day) and (B) with increasing dosages in steps of 0.2 mg/kg bodyweight per day up to 0.9 mg/kg bodyweight per day. RESULTS: We examined 32 patients aged 1 to 34 years, mean age 12 years. 21/32 patients became totally continent with the dosage (A). They showed a significant (P<0.01) decrease in the median max detrusor pressure (MDP) and a significant (P<0.01) increase in the median compliance and the median age adjusted bladder capacity (AABC). Eleven out of 32 patients remained incontinent under this dosage (A). Their median MDP, their median compliance and their median AABC remained nearly unchanged. Seven out of 11 incontinent patients under dosage (A) were treated efficiently with the higher dosages (B). Their median necessary dosage escalation to achieve treatment success was 0.7 mg/kg bodyweight per day (range 0.5 to 0.9 mg/kg bodyweight per day). Their median MDP was significantly (P<0.05) decreased and their median compliance and median AABC were significantly (P<0.05) increased. Four out of 11 patients remained incontinent and showed only little improvement in urodynamic data. Two out of 11 patients with the dosage escalation (B) showed side effects at a dosage of 0. 9 mg/kg bodyweight per day. CONCLUSIONS: The intravesical application of oxybutynin was a well tolerated and efficacious therapy. The topical oxybutynin therapy dosage (A) was efficient in 66% of our selected patients, the escalating dosage titration (B) could increase the efficiency to 87%. <http://www.ncbi.nlm.nih.gov/htbin-po...&uid=10822396> Department of Urology, University of Heidelberg, Germany.

    5. Fowler CJ (2000). Intravesical treatment of overactive bladder. Urology. 55 (5A Suppl): 60-4; discussion 66. Summary: Intravesical agents for overactive bladder have mostly been used in patients with neurogenic bladder disorders. The patients have usually had severe detrusor hyperreflexia (DH) plus a disorder of bladder emptying, and because of residual urine have been performing intermittent self-catheterization. Intravesical medication has therefore been appropriate. Strategies for treating DH have been either to lessen the parasympathetic efferent activity or to de-afferent the bladder. Two types of treatment have been used: intravesical medications that block pelvic nerve-detrusor smooth muscle cholinergic transmission, or agents that block the afferent arm of the reflex that causes detrusor contraction. Intravesical oxybutynin is thought to have some local anesthetic effect, although its main mode of action is to block cholinergic transmission. It has been demonstrated to be effective in resistant DH. Intravesical atropine has been demonstrated to increase bladder capacity but its usefulness in the clinical management of DH has yet to be demonstrated. Local anesthetics can increase bladder capacity, but the effect is short-lived. Longer-acting agents may have a selective neurotoxic effect on capsaicin-sensitive bladder afferents. Many patients worldwide have now been treated with intravesical capsaicin. Resiniferatoxin (RTX) is an ultrapotent capsaicin analog that has the significant advantage of being a nonirritant. Intravesical agents appear to be attractive alternatives to oral medication and hold the exciting possibility of selectively targeting end organs implicated in pathophysiologic responses. <http://www.ncbi.nlm.nih.gov/htbin-po...&uid=10767456> Department of Uro-Neurology, National Hospital for Neurology and Neurosurgery, UCLH, Institute of Neurology, University College London, London, United Kingdom.

    6. Dmochowski RR and Appell RA (2000). Advancements in pharmacologic management of the overactive bladder. Urology. 56 (6 Suppl 1): 41-9. Summary: Continued developments in the understanding of lower urinary tract function have led to improvements in the pharmacologic manipulation of bladder dysfunction. Drug delivery changes have produced drugs that provide better efficacy and tolerability, thus improving patient compliance. Improvements in drug delivery systems have altered drug bioavailability and pharmacokinetics. Active current investigation in new agents and delivery systems for intravesical delivery has yielded intriguing early results that may substantially add to the armamentarium for the management of the overactive bladder (urgency, frequency, urge incontinence). New developments in the understanding of the neuropharmacology of the bladder, peripheral pelvic nerves, and sacral cord may provide agents with entirely new drug effects, either as primary agents or agents to be used in combination with currently available drugs. We herein review newer agents and drug delivery systems. <http://www.ncbi.nlm.nih.gov/htbin-po...&uid=11114562> North Texas Center for Urinary Control, (RRD), Fort Worth, Texas, USA.

  3. #3
    Ron,
    I'm a T4 para 18 years post injury and managing my neurogenic bladder -- staying continent -- has probably been the worst feature of my injury (and that's saying something).

    For the first 10 years or so I relied on wearing an external catheter and leg bag. Along the way, at the urging of my (then) urologist, I tried assorted anticholinergic medications but found the side effects -- dry mouth, blurred vision -- too burdensome. There came a point, however, when my bladder pressures, as measured during my annual urodynamic studies, began increasing to a point where I had no choice but to take anticholinergics. Fortunately, the side effects of these meds abated over time, but I was never able to attain a reliable state of continence even at very high doeses (e.g., 40mg of DitropanXL).

    About 6 weeks ago I began a regimen of intravesical Ditropan and as I've reported in other threads here, it has transformed my life. SpinalNurse described the regimen that's used at the facility where she works and I've adapted it to my own needs and style.

    I've departed from the regimen she described in several areas. For starters, I'm not using brand name Ditropan, the generic, oxybutinin chloride, is considerably cheaper and I haven't found any shortfall in performance. And I'm also not using a sterile technique. (I use LoFric catheters which I need to be wet to activate its lubricity. I use my bathroom sink tap water so there goes any attempt at sterile technique. I must be doing something right, however, I rarely get UTIs.)

    Here's what I do: I take a 5mg tablet and drop it in to an empty 60cc syringe. Next, while covering the opening of the syringe, I pour approx. 30cc of water (filtered water from my kitchen tap) and put the plunger in. The tablet dissolves in less than 2 minutes. After emptying my bladder, I leave the catheter in place and connect the syringe to the funnel opening of the catheter and infuse. I do 3 infusions per day.

    As I reported earlier, I had a urodynamic study performed and the results confirmed my experience: my bladder pressures dropped dramatically and conversely, my bladder capacity was way up. Prior to starting this new regimen I was almost certainly headed for an augmentation cystoplasty -- MAJOR SURGERY. If my success with the intravesical ditropan continues, I will have dodged that enormous bullet.

    [This message was edited by stephen212 on July 30, 2001 at 09:34 PM.]

    [This message was edited by stephen212 on July 30, 2001 at 09:35 PM.]

    [This message was edited by stephen212 on July 30, 2001 at 09:36 PM.]

  4. #4

    bladder question

    Stephen212 - Thanks for sharing a very clear explanation, that includes the oxybutynin infusion, about your bladder management program. It seems that you have arrived at a process that is practical and works for you. I think that learning how to efficiently and comfortably live with the challenges of SCI is such an important and valuable contributions that those of you, who have lived with SCI for many years, can share with those newer to SCI. Many thanks, CRF.

  5. #5

    Clarification

    Ditropan will only help with bladder (detrusor muscle) spasm or tone, not with pelvic floor (external sphincter) spasm or tone. This is a completely different muscle.

    The bladder is smooth muscle and contraction is caused by parasympathetic (autonomic) nerve stimulation, which is partially blocked by Ditropan or other anticholergics.

    The pelvic floor is made up primarily of the pubococcygeal muscle, which is a striated (somatic) muscle. It sometimes can be relaxed with the use of antispasticity drugs such as Baclofen, Dantrium or Zanaflex, but would not be relaxed with the use of Ditropan or Detrol. (KLD)

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