BLADDER HYPERREFLEXIA WITH resultant incontinence

Transcription

1 136 Detrusor and Blood Pressure Responses to Dorsal Penile Nerve Stimulation During Hyperreflexic Contraction of the Bladder in Patients With Cervical Cord Injury Young-Hee Lee, MD, PhD, Graham H. Creasey, MD, Hyunkyo Lim, MD, Jaemann Song, MD, PhD, Kihak Song, MD, Jinweon Kim, MD ABSTRACT. Lee Y-H, Creasey GH, Lim H, Song J, Song K, Kim J. Detrusor and blood pressure responses to dorsal penile nerve stimulation during hyperreflexic contraction of the bladder in patients with cervical cord injury. Arch Phys Med Rehabil 2003;84: Objective: To investigate the immediate effect of dorsal penile nerve (DPN) stimulation on detrusor pressure (P det ) and blood pressure during hyperreflexic contractions of the bladder in patients with cervical spinal cord injury (SCI). Design: Blood pressure and P det monitoring during cystometry with and without DPN stimulation. Setting: Urodynamic laboratory in a university hospital in Korea. Participants: Eight men (age range, 20 55y) with cervical SCI that was incurred from 4 months to 10 years before this study. Intervention: During water cystometry, blood pressure was monitored with an intra-arterial catheter introduced percutaneously into the radial artery and was recorded simultaneously with the P det. Blood pressure was also measured manually with an electronic blood pressure cuff. Electric stimulation was applied to the DPN by using surface electrodes each time a bladder contraction was detected. Stimulation intensity was twice the threshold of the pudendal-anal reflex. Main Outcome Measures: P det, systolic blood pressure, and diastolic blood pressure. Results: As P det increased, the blood pressure increased in all cases. All the reflex contractions of the bladder were effectively suppressed by DPN stimulation, and as the P det decreased during stimulation, radial arterial pressure also decreased immediately and significantly. Conclusions: DPN stimulation can decrease P det and the increased blood pressure associated with it. Key Words: Autonomic dysreflexia; Bladder, neurogenic; Blood pressure; Electric stimulation; Rehabilitation; Spinal cord injuries by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation From the Department of Rehabilitation Medicine, Wonju Christian Hospital, Wonju, Korea (Lee); Departments of Rehabilitation Medicine (Lee, Kim), of Anesthesiology (Lim), and of Urology (Song, Song), Yonsei University Wonju College of Medicine, Wonju, Korea; and Veterans Affairs Medical Center and Case Western Reserve University, Cleveland, OH (Creasey). Supported by the Regional Research Center program of the Ministry of Science and Technology and the Korea Science and Engineering Foundation. No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the author(s) or upon any organization with which the author(s) is/are associated. Reprint requests to Young-Hee Lee, MD, PhD, Dept of Rehabilitation Medicine, Yonsei University Wonju College of Medicine, 162 Ilsan-Dong, Wonju, , Korea, lee02@wonju.yonsei.ac.kr /03/ $35.00/0 doi: /apmr BLADDER HYPERREFLEXIA WITH resultant incontinence is a major problem for suprasacral spinal cord injury (SCI) patients. Clean intermittent catheterization (CIC) is commonly used to treat the condition. Pharmacologic treatment with anticholinergic agents helps prevent incontinence, but some patients cannot tolerate the side effects of the drugs. 1 Moreover, surgical treatment by bladder augmentation commits the patient to catheterization for life. 2 Another management option for incontinence is electric stimulation. To inhibit hyperreflexic contraction, this has been applied to SCI patients in 2 ways. One expects a therapeutic effect to continue after a treatment period, and the other expects an immediate, direct suppressive effect on hyperreflexic contraction of the bladder. Some reports about therapeutic effects showed favorable results in urodynamic studies after 4 to 16 weeks of stimulation, 3,4 but complete continence was achieved in less than 20% of the cases. Another group of studies that examined the direct immediate effect of sacral afferent nerve stimulation showed a consistent suppressive effect on reflex contraction. 5 The stimulation effectively inhibited unwanted detrusor contractions and increased cystometric capacity in SCI patients. 6 This method showed favorable results not only in the laboratory, but also after discharge to home. We 7 reported a case that involved the useful application of self-controlled stimulation of the dorsal penile nerve (DPN) for bladder hyperreflexia in SCI. The patient had incomplete tetraplegia and managed his bladder with intermittent selfcatheterization and medication. However, he continued to have reflex bladder contractions that he could feel, but he could not catheterize himself in time to prevent incontinence. During cystometry, the suppressive effect of electric stimulation on hyperreflexic contractions proved both reliable and reproducible. The patient could start the stimulation when sensing a bladder contraction, and after the brief stimulation was stopped, suppression of the reflex contraction lasted several minutes. When the patient used stimulation at home, the rate of leakage between catheterizations decreased, and the catheterized volume increased significantly. This technique has the potential to minimize fluid intake restriction, to avoid unnecessary catheterization, and to reduce the need for urine-collection devices. A risk of electric stimulation in SCI patients with high neurologic level is the possible occurrence of autonomic dysreflexia (AD). AD occurs when a nociceptive stimulus distal to the level of the SCI triggers an excessive sympathetic discharge, resulting in hypertension, sweating, headache, and reflex bradycardia. 8 The most common causes of AD are bladder and bowel distension. It may, however, be caused by any painful or irritating stimulus below the level of the lesion. Functional electric stimulation (FES) assisted training or therapeutic interventions may sometimes induce AD in high-level SCI patients. 9 Although severe hypertension during electroejaculation with a rectal probe has been reported, 10 there are no

2 BLOOD PRESSURE RESPONSES TO DPN STIMULATION, Lee 137 Subject No. Table 1: Patient Characteristics and Volume of Infusion (V inf ) at the First and the Last Reflex Contraction Age (y) Duration Since Injury (mo) Neurologic Level ASIA Classification Method of Voiding V inf at First Contraction (ml) V inf at Last Contraction (ml) C6 A PC, CIC C5 B PC, CIC C6 B PC C4 C PC, Self C6 A PC, CIC C5 B PC C6 C PC, Self C8 A PC Abbreviations: ASIA, American Spinal Injury Association Impairment Scale; PC, percussion and Credé; Self, inconsistent, occasional, voluntary voiding. reports about hypertension and AD caused by sacral afferent stimulation to inhibit bladder contraction in SCI patients. In this study, we investigated the immediate effects of DPN stimulation on detrusor pressure (P det ) and blood pressure during hyperreflexic contraction of the bladder in patients with cervical SCI. METHODS Eight men (age range, 20 55y) with cervical SCI and an injury duration of 4 months to 10 years participated in the study (table 1). Reflex voiding was the method used for bladder emptying in all patients, and this was combined with CIC in 3 patients. None of the patients had nephrolithiasis, upper tract dilatation, or vesicoureteral reflux. All had negative urine cultures before the urodynamics testing. Any medication for bladder dysfunction was discontinued at least 72 hours before testing, and no subject took antihypertensive medication routinely. All subjects had 1 or more symptoms of AD, such as headache, nasal congestion, facial flushing, or sweating, when the bladder was full and drainage was delayed. Test Settings Simultaneous measurements of the intravesical pressure, intrarectal pressure, and subtracted P det were performed with the Menuet standard water cystometry a with the patient in the supine position. The bladder was filled through a urethral catheter with normal saline at room temperature at a rate of 30mL/min. Blood pressure was monitored with an intra-arterial catheter introduced percutaneously into the radial artery. The arterial catheter was connected to a pressure transducer, and blood pressure and the P det were recorded simultaneously. Blood pressure was also measured manually with an electronic blood pressure cuff on the contralateral arm during the important stages of the test: before infusion without and with electric stimulation and during the reflex bladder contractions without and with electric stimulation. Electric stimulation was applied with the Empi FOCUS portable neuromuscular stimulator. b The DPN was stimulated with circular 1-cm diameter surface electrodes. The cathode was placed proximally and the anode distally on the dorsum of the penile shaft 2cm apart. Nonconductive paper tape 1cm wide was placed between the cathode and the anode to prevent their contact. Stimulation parameters were biphasic rectangular pulses of 25-Hz frequency, with a 250- s pulse width. The stimulation intensity was twice the threshold of the pudendalanal reflex. 11 The threshold was defined as the current at which visible reflex contraction of the anal sphincter by electric stimulation occurred. The threshold was determined before cystometry by using the same stimulator and parameters for DPN stimulation. The first DPN stimulation was applied before infusion to record the blood pressure response to the stimulation. After measuring blood pressure without and with electric stimulation, the infusion began. The stimulation was repeated on every subsequent reflex contraction during the cystometry. Each stimulation was applied after detrusor contraction was identified by observing 2 or more typical oscillations in the P det curve and after manual measurement of blood pressure. The test protocol was designed to stop infusion if (1) electric stimulation did not suppress reflex contraction, (2) the infused volume reached 450mL, (3) systolic blood pressure (SBP) increased to 40mmHg above baseline, or (4) the subject could not tolerate the test. The test protocol was also designed to empty the bladder if the SBP or diastolic blood pressure (DBP) remained above 180 or 110mmHg, respectively, with electric stimuluation. The first typical increase of P det by reflex contraction was defined as the first contraction, and the last typical increase of P det, which was suppressed effectively by DPN stimulation, was defined as the last contraction. An experienced anesthesiologist monitored blood pressure change and vital signs throughout the study. Rapid-acting antihypertensive agents were available in case of uncontrolled blood pressure. Approval of the study was given by the local ethics committee, and all patients gave informed consent to participate. Data Collection and Statistical Analysis Manually measured SBP and DBP were compared before infusion, during the first contraction, and during the last contraction without and with electric stimulation. Peak P det during the first and last contractions was measured. The average P det of the last 30 seconds of electric stimulation was measured during the first and last contractions and was considered representative of P det when suppressed by electric stimulation. Data were analyzed by using the SPSS software, version 8.0, c for Windows. Comparisons were made by using the Wilcoxon signed-rank test. The level of significance was set at.01. RESULTS Subject characteristics and volume of infusion at the first and the last reflex contractions are summarized in table 1. There were3to5reflex contractions during cystometric examination, and those contractions were effectively suppressed by DPN stimulation. The concurrent arterial and P det graphs showed

3 138 BLOOD PRESSURE RESPONSES TO DPN STIMULATION, Lee Fig 1. P det and radial arterial blood pressure responses to DPN stimulation during hyperreflexic contraction of the bladder in subject 8. Electric stimulation suppressed both P det and blood pressure. consistent elevation of blood pressure with the increase of P det. A typical case of changes in blood pressure and P det is shown in fig 1. Fig 3. Changes of blood pressure with electric stimulation before infusion, during the first reflex contraction, and during the last reflex contraction. The bottom brackets in the graph refer to DBP; the upper brackets refer to SBP. *P<.01. P det Response The first reflex contraction of the bladder occurred when the infused volume reached 35 to 140mL (avg, 74.4mL) (fig 2). The peak P det during the first contraction was cmH 2 O. This first contraction was effectively suppressed by DPN stimulation in all cases. The P det during suppression by electric stimulation was cmH 2 O. From 2 to 4 more reflex contractions occurred during the procedure. The infused volume of saline when the last reflex contraction occurred was 150 to 340mL (avg, 196.3mL). Peak P det during the last contraction was 80.7cmH 2 O, which did not differ significantly from that of the first contraction. The P det suppressed with DPN stimulation tended to increase as the infused volume increased. The P det during suppression by electrical stimulation during the last contraction was cmH 2 O, which was significantly higher than that suppressed by the first contraction (P.01). Fig 2. Changes of P det with DPN stimulation (ES) during the first and the last reflex contraction. *P<.01. Blood Pressure Response Initial blood pressures measured manually before infusion or electric stimulation were mmHg (SBP) and mmHg (DBP) (fig 3). The SBP and DBP seemed to increase slightly with electric stimulation before infusion, to mmHg and mmHg, respectively, but these changes were not statistically significant. The radial arterial recording of SBP and DBP increased as P det increased in all cases. SBP and DBP during the first contraction were mmHg and mmHg, respectively, which were significantly higher than those before infusion (P.01). As the P det decreased on DPN stimulation, radial arterial pressure also decreased in all cases. The mean SBP and DBP during the first contraction were decreased to mmHg and mmHg, respectively, by electric stimulation; these pressures were significantly lower than those without electric stimulation (P.01). SBP during the last contraction without electric stimulation was further increased to mmHg, which was significantly higher than during the first contraction (P.01). However, DBP during the last

4 BLOOD PRESSURE RESPONSES TO DPN STIMULATION, Lee 139 contraction did not differ significantly from that during the first contraction. SBP and DBP during the last contraction decreased significantly by electric stimulation. However, suppressed SBP during the last contraction was higher than suppressed SBP during the first contraction (P.01). There were no cases of hypertension after the bladder was emptied that required a rapidly acting antihypertensive medication. DISCUSSION We conducted this study to identify risks of hypertension while suppressing reflex contraction of the bladder with DPN stimulation in cervical SCI patients. Study subjects showed a favorable response of blood pressure to DPN stimulation. It has been known for many years that detrusor instability can be improved by electric stimulation of pudendal afferent fibers. 12,13 Stimulation of large sacral afferents has produced acute inhibition of detrusor hyperreflexia by pudendal-pelvic spinal reflex pathways. 14 Moreover, this technique is now used to ameliorate many symptoms, such as urge incontinence, that are related to detrusor instability. 15,16 Experience with electric stimulation in the treatment of SCI neurogenic bladder is limited. Stimulation conducted to facilitate a direct immediate response effectively inhibits unwanted detrusor contractions and increases cystometric capacity in SCI patients. 5,6,17 This method has shown favorable results not only in the laboratory, but also in home use, as we have previously reported. 7 There is a chance of hypertension associated with AD when SCI patients with high neurologic levels receive electric stimulation. Usually, AD is precipitated by noxious stimuli below the level of the spinal cord lesion in persons with injuries at or above the midthoracic level. Because DPN stimulation might be an irritating stimulus, AD was considered a potential risk, although no cases of AD in association with DPN stimulation have been reported in the literature. There was a report 10 that described severe hypertension in patients with high SCI who were undergoing electroejaculation. There has been another case report 18 of AD followed by new-onset atrial fibrillation during electroejaculation in a patient with C6 tetraplegia. Electroejaculation typically uses a high-intensity stimulating current, usually above 45 to 100mA. 19,20 The current intensity used in this study was less than 20mA. Increases in blood pressure and concomitant bradycardia, suggestive of AD, have also been documented during FES in individuals with a high SCI. 9 Stimulation of skin nociceptors by FES might be a possible cause of AD. However, Matthews et al 21 reported that these responses were unaffected by the use of topical anesthetic cream on the skin at the stimulation site. They postulated that mechanisms other than skin nociception were operative in FES-induced AD. Other nociceptive triggers for FES-induced AD may come from the muscle afferents, or FES nociception could be the result of stimulation of 1 of, or a combination of, the following: electric activation of pain fibers of the skin or muscle, isometric muscle contraction and its resultant ischemia metabolites, or musculotendinous stress. 22 In contrast to the cases of electroejaculation or FES, electric stimulation alone did not increase blood pressure significantly before infusion was started in our study. The different stimulation site and parameters could explain this difference from those reports. During bladder contraction, DPN stimulation actually decreased the increased blood pressure, probably by suppressing detrusor contraction. Before infusion, none of our subjects showed any symptoms of AD in response to electric stimulation. During the first detrusor contraction, 6 subjects reported 1 or more symptoms of AD in the absence of electric stimulation, and SBP increased 20mmHg more than the initial value in 5 patients. Electric stimulation relieved symptoms and reduced the increased blood pressure in all 6 subjects. During the last contraction, all subjects experienced symptoms of AD with blood pressure elevation, and electric stimulation did not resolve AD in 2 subjects. These findings suggested that electric stimulation might be less effective in relieving the AD at larger bladder volumes, although it could suppress the bladder contraction. One limitation of our study is that we did not measure pulse rates during the experiment; this is an important parameter in identifying AD. CONCLUSION This study showed that DPN stimulation, performed to inhibit reflex bladder contraction, did not produce blood pressure increases. On the contrary, DPN stimulation decreased the increased blood pressure in AD. This study did not include a large or diverse group of subjects. Acute hypertension can be potentially dangerous and can have grave consequences, including stroke onset. Careful monitoring of blood pressure and symptoms of AD should be a routine part of DPN stimulation for patients with SCI above the midthoracic level in both research and clinical settings. Acknowledgment: We thank Michael D. Craggs, PhD, University College of London, for his help with the methods; John Chae, MD, Case Western Reserve University, for his review of the manuscript; and Soonmoo Hong, Wonju Christian Hospital, for his help with urodynamic tests. References 1. Cardenas DD. Neurogenic bladder: evaluation and management approach. 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