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Botox[R] for overactive bladders: a look at the current state of evidence.

Overactive bladder syndrome is used to identify a group of urinary symptoms (e.g., frequency, nocturia, urgency with or without urinary incontinence) related to detrusor activity without verification of urodynamic testing (Chen, 2010; Huether, 2012). Overactive bladder (OAB) symptoms occur during the storage and filling phases of urination during which the OAB experiences involuntary contractions of the detrusor muscle (Huether, 2012). Overactive bladder usually is diagnosed after other pathologies, such as a urinary tract infection, have been excluded (Nygaard, 2010). The cause of symptoms may be neurogenic or idiopathic. Patients with neurogenic OAB have an existing neurologic disorder, such as multiple sclerosis or a spinal cord injury. Patients whose symptoms have no apparent cause have idiopathic OAB (Ellsworth & Kirshenbaum, 2010).

Usual Pharmacologic Treatments to Control Detrusor Activity

The most common medications prescribed to control overactive detrusor activity include anticholinergics (rightfully called urinary antispasmodics). These are used along with behavioral treatments such as pelvic muscle rehabilitation and bladder training (Nabili, 2013). Anticholinergics most commonly prescribed for urinary incontinence are oxybutynin (Ditropan[R], Oxytrol[R]) and tolterodine (Detrol[R]). Newer anticholinergics approved for treatment of OAB include solifenacin (VESIcare[R]), darifenacin (Enablex[R]), and fesoteradine fumarate (Toviaz[R]) (Nabili, 2013). Urinary antispasmodics work by inhibiting acetylcholine from binding to the muscarinic receptors within the bladder smooth muscles (Ellsworth & Kirshenbaum, 2010). Some health care providers also prescribe tricyclic antidepressants (e.g., imipramine [Tofranil[R]] and doxepin [Sinequan[R], Adapin[R]]) for urge incontinence, but the mechanism of action of these medications for controlling detrusor activity is yet to be understood fully (Nabili, 2013). In postmenopausal women who experience urinary incontinence symptoms, estrogen usually is prescribed in conjunction with other medications (Nabili, 2013) or is similarly effective to usual anticholinergic treatments (Nelken, 0zel, Leegant, Felix, & Mishell, 2011). These medications will be discussed further in a future issue of MEDSURG Nursing.

Botulinum Toxins for Medical Use

A potent neurotoxin, botulinum toxin, is produced by the gram-positive anaerobic rod-shaped bacteria Clostridium botulinum (C. botulinum) (Chuang, Kuo, & Chancellor, 2010). The toxin was discovered by Dr. Justinus Kerner, a German poet and medical writer, while researching the deaths of people who ate smoked sausages. He concluded the victims died of food poisoning, now known as botulism, which was a result of the toxin's interference with motor and autonomous nervous system conduction. He suggested botulinum toxin's nerve conduction interference was similar to that of rest interfering with electric conduction. He then proposed possible medical uses of the toxin Cootulinum toxin A), most of which are not indicated for use today 0Nenzel, 2004).

C. botulinum produces seven distinct types of neurotoxins labeled from A to G (Yokoyama & Berkrot, 2011). Botulinum toxin produces neuromuscular transmission blockade by binding to receptor sites on motor nerve terminals, inhibiting the release of acetylcholine. The neurotoxin splits protein molecules necessary to "docking and releasing of acetylcholine from storage areas located within nerve endings" (Wilson, Shannon, & Shields, 2012, p. 187). All serotypes block nerve transmission at neuromuscular junctions to varying degrees. Botulinum toxin A has been studied extensively for therapeutic use due to its prolonged effects. Botulinum toxin A's neuromuscular transmission blockade lasts up to 4 months, whereas botulinum toxin B's and botulinum toxin E's blockade lasts 2 months and less than 4 weeks, respectively (Chuang et al., 2010).

Popularly known as a cosmetic agent for chemical face and neck rejuvenation, onabotulinum toxin A (Botox[R]) reduces wrinkles by targeting their major cause, the facial muscles (Felber, 2006). Aside from its cosmetic use, Botox has been approved for therapeutic use for strabismus (Kowal, Wong, & Yahalom, 2007), cervical dysphonia (Keam, Muir, & Deeks, 2011), blepharospasm (Coscarelli, 2010), severe axillary hyperhidrosis (Wheeler, 2012), and spasticity (Teasell, Foley, Pereira, Sequeira, & Miller, 2012). Medical researchers now are evaluating the possible therapeutic use of botulinum toxin in vocal dysphonias (Mendelsohn & Berke, 2012), migraine (Oterino, Rarino, & Pascual, 2011), allergic rhinitis, myofascial pain syndrome, and many other conditions (Felber, 2006). A systematic review of botulinum toxin's off-label uses by Cheng, Chen, and Patel (2006a, 2006b) showed it is effective for the following conditions: esophageal achalasia, essential tremor, other types of headache (e.g., tension and cervicogenic), and chronic anal fissure.

Medical Use for Overactive Bladder

The U.S. Food and Drug Administration (FDA) approved the use of botulinum toxin A for overactive bladder due to neurological conditions, such as multiple sclerosis, spinal cord injury, stroke, and Parkinson's disease (Allergan, 2012; Yukhananov & Berkrot, 2011). The exact mechanism of action on how botulinum toxin A works in reducing symptoms of OAB is not understood fully. There are separate mechanisms that may be attributed to its success as a urologic therapy. The following theories have been postulated by medical researchers regarding its mechanism of action in the urinary system. First, botulinum toxin is thought to suppress the release of acetylcholine, adenosine triphosphate, and substance P in the urothelium, all of which contribute to the symptomatic reflexes in OAB. Second, botulinum toxin is known to act on the parasympathetic nervous system by inhibiting release of acetylcholine on nerve endings, including the detrusor muscle in the bladder. Lastly, it is believed the neurotoxin acts on C-fiber afferents, which is thought to cause lessened sensation of urgency (Duthie, Vincent, Herbison, Wilson, & Wilson, 2011).

The most common method of injecting botulinum toxin A is through suburothelial delivery when the patient is under anesthesia in the hospital (Chuang et al., 2010). This way the toxin is delivered through the suburothelial nerve pathways instead of directly paralyzing the detrusor muscle. However, due to the thinness of the bladder wall, the detrusor muscle and the suburothelium may be difficult to differentiate. Injection into the bladder trigone and bladder base is also possible as the trigone is rich in sensory nerve fibers (Chuang et al., 2010). Research indicates injection sites are irrelevant to the effectiveness of botulinum toxin A on the bladder (Kuo, 2007). Another method of delivery of botulinum toxin A for OAB is through transurethral delivery under local anesthesia. "A rigid or flexible injection cystoscope is inserted into the bladder and injections delivered thereafter" (Chuang et al., 2010, p. 1050). The health care provider is careful not to puncture any blood vessels. Through this route, initial improvements in OAB symptoms appear after 4-7 days, and significant improvements in 4 weeks (Kalsi et al., 2008).

State of Evidence

Early studies of botulinum toxin injections aimed at improvement of symptoms, urodynamic variables, and quality of life (QOL) in patients either with neurogenic or idiopathic overactive bladder refractive to oral anticholinergics. More recent studies focused on determining the appropriate dosage of botulinum toxin, the long-term effectiveness of the treatment, and the effectiveness and safety of subsequent injections.

A wide variation exists across studies in regard to design and outcomes measures. Although not all studies addressed QOL, the International Continence Society recommends including QOL measures when assessing OAB therapies (M Taweel, Mokhtar, & Rabah, 2011). To address QOL, the Urinary Distress Inventory-6, King's Health Questionnaire (KHQ), Incontinence Impact Questionnaire, Qualiveen Questionnaire, and Incontinence Quality of Life Questionnaire (IQOL) were used in a variety of studies. Cruz and co-authors (2011) and Herschorn and associates (2011) reported improved QOL in patients treated with 200 or 300 U of onabotulinumtoxin A based on the IQOL. Ehren and colleagues (2007) reported a higher QOL in patients treated with 500 U BTX-A through 26 weeks based on the Qualiveen Questionnaire. The improvements included decreased bother from urinary leakage during the day and night, decreased usage of continence pads, and decreased need to have a set timetable for passing urine during activities. No improvement was seen in time spent passing urine, personal hygiene problems away from home, or restricted socialization (Ehren et al., 2007). This study only involved patients with neurogenic OAB, so their QOL problems could be due to other health limitations not relevant to patients with idiopathic OAB. Sahai, Dowson, Khan, and Dasgupta (2009) reported improved QOL for patients with idiopathic OAB treated with 200 U BTX-A based on the KHQ.

Symptom scores addressed improvements in frequency, urgency, and incontinence episodes. A meta-analysis of urinary frequency performed by Duthie and colleagues (2011) favored treatment with botulinum toxin to placebo for up to 12 weeks. The mean reduction of frequency seen at 12 weeks (-3.37 episodes per day) was less than the reduction seen at 4 and 6 weeks (-6.5 episodes per day). The meta-analysis also favored treatment over placebo with regard to incontinence episodes. The reduction was greater at 12 weeks (-2.74) than at 4 and 6 weeks (-1.58). Herschorn and coauthors (2011) showed an improvement in urinary incontinence episodes for up to 36 weeks. The Cochrane meta-analysis did not address urgency. Okamura and associates (2011) reported that in patients treated with 100 U of BTXA, the frequency of urgency did not decrease significantly. Studies that allowed concurrent use of oral anti-cholinergic medications also assessed changes in the amount of oral medication used. Ehren and colleagues (2007) reported lower consumption of oral medication in patients treated with 500 U BTX-A.

Most studies used urodynamic variables to confirm changes seen in symptom scores. The variables addressed include mean cystometric capacity (MCC) and maximal detrusor pressure (MDP). Multiple studies reported increased MCC and decreased MDP at doses ranging from 100 U (A1Taweel et al., 2011) to 500 U (Ehren et al., 2007). Post-void residual volume (PVR) was also measured to determine the occurrence of adverse events (Duthie et al., 2011).

In most studies, researchers established a cause-and-effect relationship between urodynamic improvements and injection with BTX-A. However, in studies that allowed participants to continue taking oral anticholinergics while undergoing BTX-A treatment, researchers could not establish which drug was responsible for the improvements (Ehren et al., 2007). To date, no study has compared BTX-A combined with oral medication to BTX-A alone or to oral medication alone. Such a study would be useful in practice to decide whether patients receiving BTX-A should continue or discontinue their oral medications. The majority of the reviewed studies did not provide a power analysis for their sample size. Many of the earlier studies had a very small number of participants. As the medication's efficacy became more evident, larger studies were conducted. However, much of the funding for these studies came from Allergan, the company that produces BTX-A. This puts researchers at risk for biased results. Support for the efficacy of BTX-A is shown using a wide variety of instruments. The findings from QOL, urodynamic measurements, and symptom scores tend to support each other, and thus support the validity of the instruments.

Research about botulinum toxin led to approval of BTX-A for treating overactive bladder in patients with neurogenic overactive bladder (FDA, 2011). Further research is needed for the drug to be approved for treatment of idiopathic overactive bladder. An important goal of continuing research is to determine the most effective dosage of BTX-A. Reviewed studies used a range of 50 U (Rovner et al., 2011) to 500 U (Ehren et al., 2007) of botulinum toxin-A. Rovner and co-authors (2011) reported doses of 100 U or more were superior to the placebo. The level of improvement seen in MCC and urinary incontinence episodes was dose dependent (Rovner et al., 2011). Al Taweel and associates (2011) reported no significant difference in symptom improvement, urodynamics, or QOL between 100 U and 200 U dosages. Yokoyama and colleagues (2012) reported that in two phase III clinical trials, no significant difference was found in the results from 200 U and 300 U. Cruz and associates (2011) reported no additional benefit beyond 300 U, and minimal additional benefits beyond 150 U. Adverse effects related to urinary retention appear to be dose dependent (Yokoyama et al., 2012). Cruz and associates (2011) also reported a dose-dependent response for PVR-related safety parameters. However, it is difficult to compare data related to urinary retention because studies use different PVR values to define retention as an adverse event (Duthie et al., 2011).

Nursing Implications

Nursing care for patients undergoing botulinum toxin A injections should be similar to preparations for patients undergoing pre-operative cystoscopy or prostate biopsy in a surgical clinic (Lajiness, 2009). The nurse should confirm completion of the consent form and any relevant laboratory studies needed prior to the procedure. The patient should be asked to void prior to transport to the operating room. Mso, time of urination and output volume should be documented to rule out residual urine in the bladder (Marley, 2011). Specifically, for botulinum toxin injections, the patient should not have contraindications such as a urinary tract infection and/or hypersensitivity to the medication (Wilson et al., 2012). Patients should be assessed for concurrent use of anticoagulants due to slight risk of bleeding from needle insertion for injection. Prior to scheduling the procedure, patients are advised to talk with the health care provider regarding management of anticoagulants (Lajiness, 2009). Patients should be assessed for possible drug-drug interactions. Aminoglycosides and neuromuscular blocking agents (e.g., succinylcholine and pancuronium) may potentiate the effects of neuromuscular blockade. Chloroquine may antagonize the neuromuscular blocking effects (Wilson et al., 2012).

Allergan, the manufacturer of Botox, provides a warning the toxin may spread from the area of injection and produce symptomatic adverse effects, which include asthenia, general muscle weakness, double vision, blurred vision, difficulty swallowing, and trouble breathing (Allergan, 2012; Lajiness, 2009; Wilson et al., 2012). Patients should be reminded they should not drive or operate heavy equipment when symptoms of this nature occur. Symptoms brought about by muscle weakness may be life threatening, such as dysphagia, dysphonia and dysarthria, and dyspnea. Patients with pre-existing symptoms of this nature would be more at risk (Allergan, 2012). Patients must be warned dysphagia may last for several months. The FDA requires health care providers offer patients the Botox medication guide every time the medication is given (Lajiness, 2009). As there is a risk for urinary retention after injection (Chuang et al., 2010), patients should be assessed for willingness to learn procedures for clean intermittent catheterization (Lajiness, 2009). After the injection, patients are reminded to call their health care provider should they experience symptoms consistent with urinary tract infection (burning, frequency, and increased incontinence) or inability to urinate (Lajiness, 2009).

Lastly, patients should be taught improvement in OAB symptoms does not occur immediately after injection. Initial improvement of symptoms often occurs several days to a couple of weeks after injection, and should last for 3 to 4 months. Repeat treatments may be given to control urological symptoms after the effects of the injection have eroded (Wilson et al., 2012).


From a bacterial toxin that could cause death from food poisoning to an unexpected treatment for multiple conditions involving neuromuscular conditions, botulinum toxin A provides prolonged relief to patients suffering from overactive detrusor activity due to neurological conditions. The health care team should provide pursue patient safety and continuous support to promote medication effectiveness and prevent development of life-threatening adverse effects.


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Rhea Faye D. Felicilda-Reynaldo, EdD, RN, is Assistant Professor, Department of Nursing, Missouri State University, Springfield, MO; and a MEDSURG Nursing Editorial Board Member. She may be contacted at

Kaitlin Backes is Student Nurse, BSN-Genedc Program, Department of Nursing, Missouri State University, Springfield, MO.

Note: Information in this article is based on an evidence-based paper written by Ms. Backes while mentored by Dr. Felicilda-Reynaldo in an undergraduate nursing research course.
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Title Annotation:CNE SERIES: Nursing Pharmacology; continuing nursing education
Author:Felicilda-Reynaldo, Rhea Faye D.; Backes, Kaitlin
Publication:MedSurg Nursing
Article Type:Report
Geographic Code:1USA
Date:Jan 1, 2014
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