Stenosis Characterization and Identification for Dialysis Vascular Access.

Vascular access dysfunction is the leading cause of hospitalization for hemodialysis patients and accounts for the most medical costs in this patient population. Vascular access flow is commonly hindered by blood vessel narrowing (stenosis). Current screening methods involving imaging to detect stenosis are too costly for routine use at the point of care. Noninvasive, real-time screening of patients at risk of vascular access dysfunction could potentially identify high-risk patients and reduce the likelihood of emergency surgical interventions. Bruits (sounds produced by turbulent blood flow near stenoses) can be interpreted by skilled clinical staff using conventional stethoscopes. To improve the sensitivity of detection, digital analysis of blood flow sounds (phonoangiograms or PAGs) is a promising approach for classifying vascular access stenosis using non-invasive auditory recordings. Here, we demonstrate auditory and spectral features of PAGs which estimate both the location and degree of stenosis (DOS). Auditory recordings from nine stenosis phantoms with variable DOS and hemodynamic flow rate were obtained using a digital recording stethoscope and analyzed to extract classification features. Autoregressive modeling and discrete wavelet transforms were used for multiresolution signal decomposition to produce 14 distinct features, most of which were linearly correlated with DOS. Our initial results suggest that the widely-used auditory spectral centroid is a simple way to calculate features which can estimate both the location and severity of vascular access stenosis.

Neuroanatomic and behavioral correlates of urinary dysfunction induced by vaginal distension in rats.

The aim of the present study was to use a model of simulated human childbirth in rats to determine the damage to genitourinary structures and behavioral signs of urinary dysfunction induced by vaginal distension (VD) in female rats. In experiment 1, the length of the genitourinary tract and the nerves associated with it were measured immediately after simulated human delivery induced by VD or sham (SH) procedures. Electroneurograms of the dorsal nerve of the clitoris (DNC) were also recorded. In experiment 2, histological characteristics of the bladder and major pelvic ganglion of VD and SH rats were evaluated. In experiment 3, urinary parameters were determined in conscious animals during 6 h of dark and 6 h of light before and 3 days after VD or SH procedures. VD significantly increased distal vagina width (P < 0.001) and the length of the motor branch of the sacral plexus (P < 0.05), DNC (P < 0.05), and vesical nerves (P < 0.01) and decreased DNC frequency and amplitude of firing. VD occluded the pelvic urethra, inducing urinary retention, hematomas in the bladder, and thinness of the epithelial (P < 0.05) and detrusor (P < 0.01) layers of the bladder. Major pelvic ganglion parameters were not modified after VD. Rats dripped urine in unusual places to void, without the stereotyped behavior of micturition after VD. The neuroanatomic injuries after VD occur alongside behavioral signs of urinary incontinence as determined by a new behavioral tool for assessing micturition in conscious animals.

LONG-TERM EVALUATION OF A NON-HERMETIC MICROPACKAGE TECHNOLOGY FOR MEMS-BASED, IMPLANTABLE PRESSURE SENSORS.

This paper reports long-term evaluation of a micropackage technology for an implantable MEMS pressure sensor. The all-polymer micropackage survived 160 days when subjected to accelerated lifetime testing at 85 °C in a 1% wt. saline solution. The package shows minimum effect on sensors' sensitivity and nonlinearity, which deviated by less than 5% and 0.3%, respectively. A 6-month in vivo evaluation of 16 MEMS-based pressure sensors demonstrated that the proposed micropackage has good biocompatibility and can protect the MEMS pressure sensor. To the best of our knowledge, these results establish new lifetime records for devices packaged using an all-polymer micropackaging approach.

Neural pathways of somatic and visceral reflexes of the external urethral sphincter in female rats.

The external urethral sphincter (EUS) plays a crucial role in maintaining urinary continence. The activity of the EUS is modulated by bladder and urethra sensory neurons. However, a complete understanding of the somatic or visceral sources that modulate the EUS is lacking. The aims of the present study were to characterize the response of the EUS to perineal skin, genital, rectal, and urethral mechanical stimulation, as well as to determine the peripheral neural pathways of the reflex. EUS reflex electromyographic activity (EMG), innervation of pelvic and perineal structures, and the anatomy of afferent and efferent nerves were determined in anesthetized female rats. The EUS responds to cutaneous as well as genital and rectal stimuli. However, the EUS EMG response is significantly larger when induced by genital stimulation. The dorsal nerve of the clitoris and the cavernous nerve both innervate the distal urethra and the distal vagina, as well as the clitoris and perigenital skin and are the main afferent pathways for the genito-sphincteric reflex. Efferent axons travel through the pudendal nerve and the lumbosacral trunk and converge in the motor branch of the lumbosacral plexus, which innervates the EUS. Because the nerves are located on the vaginal walls, they are susceptible to damage during childbirth. Physiology and anatomy of the different neural pathways that regulate EUS activity are important to consider when inducing nerve damage to create models of urinary incontinence.

Induced Regenerative Elastic Matrix Repair in LOXL1 Knockout Mouse Cell Cultures: Towards Potential therapy for Pelvic Organ Prolapse.

Impaired elastic matrix remodeling occurs in reproductive tissues after vaginal delivery. This has been linked to development of pelvic organ prolapse (POP) for which there currently is no pharmacologic therapy. Hyaluronan oligomers and transforming growth factor beta 1 (termed elastogenic factors, EFs) have been shown to significantly enhance tropoelastin synthesis, elastic fiber assembly, and crosslinking by adult vascular smooth muscle cells (SMCs). The goal of this study was to ascertain if these factors similarly improve the quantity and quality of elastic matrix deposition by vaginal SMCs (VSMCs) isolated from lysyl oxidase like-1 knock out (LOXL1 KO) mouse model of POP. Cells isolated from whole vagina of a LOXL1 KO mouse (multiparous, stage 3 prolapse) were cultured and identified as SMCs by their expression of various SMC markers. Passage 2 vaginal SMCs (VSMCs; 3×104/10 cm2) were cultured for 21 days with EFs. Cell layers and spent medium aliquots were assessed for elastin content and quality. EF-treated VSMCs proliferated at a similar rate to untreated controls but synthesized more total elastin primarily in the form of soluble matrix elastin. Elastin mRNA was also increased compared to controls. The elastic matrix was significantly denser in EF-treated cultures, which was composed of more mature, non-interrupted elastic fibers that were absent in controls. The results are promising towards development of a therapy to enhance regenerative elastic matrix repair in post-partum female pelvic floor tissues.

Comparison of air-charged and water-filled urodynamic pressure measurement catheters.

AIMS: Catheter systems are utilized to measure pressure for diagnosis of voiding dysfunction. In a clinical setting, patient movement and urodynamic pumps introduce hydrostatic and motion artifacts into measurements. Therefore, complete characterization of a catheter system includes its response to artifacts as well its frequency response. The objective of this study was to compare the response of two disposable clinical catheter systems: water-filled and air-charged, to controlled pressure signals to assess their similarities and differences in pressure transduction. METHODS: We characterized frequency response using a transient step test, which exposed the catheters to a sudden change in pressure; and a sinusoidal frequency sweep test, which exposed the catheters to a sinusoidal pressure wave from 1 to 30 Hz. The response of the catheters to motion artifacts was tested using a vortex and the response to hydrostatic pressure changes was tested by moving the catheter tips to calibrated heights. RESULTS: Water-filled catheters acted as an underdamped system, resonating at 10.13 ± 1.03 Hz and attenuating signals at frequencies higher than 19 Hz. They demonstrated significant motion and hydrostatic artifacts. Air-charged catheters acted as an overdamped system and attenuated signals at frequencies higher than 3.02 ± 0.13 Hz. They demonstrated significantly less motion and hydrostatic artifacts than water-filled catheters. The transient step and frequency sweep tests gave comparable results. CONCLUSIONS: Air-charged and water-filled catheters respond to pressure changes in dramatically different ways. Knowledge of the characteristics of the pressure-measuring system is essential to finding the best match for a specific application.

Increased duration of simulated childbirth injuries results in increased time to recovery.

Stress urinary incontinence (SUI) development is strongly correlated with vaginal childbirth, particularly increased duration of the second stage of labor. However, the mechanisms of pelvic floor injury leading to SUI are largely unknown. The aim of this study was to determine the effects of increased duration of vaginal distension (VD) on voiding cystometry, leak point pressure testing, and histology. Sixty-nine virgin female rats underwent VD with an inflated balloon for either 1 or 4 h, while 33 age-matched rats were sham-VD controls. Conscious cystometry, leak point pressure testing, and histopathology were determined 4 days, 10 days, and 6 wk after VD. The increase in abdominal pressure to leakage (LPP) during leak point pressure testing was significantly decreased in both distension groups 4 days after distension, indicative of short-term decreased urethral resistance. Ten days after VD, LPP was significantly decreased in the 4-h but not the 1-h distension group, indicating that a longer recovery time is needed after longer distension duration. Six weeks after VD, LPP was not significantly different from sham-VD values, indicating a return toward normal urethral resistance. In contrast, 6 wk after VD of either duration, the distended rats had not undergone the same increase in voided volume as the sham-VD group, suggesting that some effects of VD do not resolve within 6 wk. Both VD groups demonstrated histopathological evidence of acute injuries and tissue remodeling. In conclusion, this experiment suggests pressure-induced hypoxia as a possible mechanism of injury in vaginal delivery.

Effect of vaginal distension on blood flow and hypoxia of urogenital organs of the female rat.

Vaginal delivery of children causes traumatic injury to tissues of the pelvic floor and is correlated with stress urinary incontinence; however, the exact mechanism of organ and tissue injury leading to incontinence development is unknown. The purpose of this project was to test the hypothesis that vaginal distension results in decreased blood flow to, and hypoxia of, the urogenital organs responsible for continence, which would suggest an ischemic and/or reperfusion mechanism of injury. Thirteen female rats underwent vaginal distension for 1 h. Thirteen age-matched rats were sham-distended controls. Blood flow to the bladder, urethra, and vagina were determined using a microsphere technique. Hypoxia of these organs was determined by immunohistochemistry. Blood flow to all three organs was significantly decreased just before release of vaginal distension. Bladder blood flow decreased further immediately after release of vaginal distension and continued to be significantly decreased 15 min after the release. Blood flow to both the urethra and vagina tripled immediately after release, inducing a rapid return to normal values. Vaginal distension resulted in extensive smooth muscle hypoxia of the bladder, as well as extensive hypoxia of the vaginal epithelium and urethral hypoxia. Bladders from sham-distended rats demonstrated urothelial hypoxia as well as focal hypoxic areas of the detrusor muscle. We have clearly demonstrated that vaginal distension results in decreased blood flow to, and hypoxia of, the bladder, urethra, and vagina, supportive of hypoxic injury as a possible mechanism of injury leading to stress urinary incontinence.

Early structural effects of oestrogen on pudendal nerve regeneration in the rat.

OBJECTIVE: To determine the early effects of oestrogen on the ultrastructure of the pudendal nerve and distal nerve fascicles near the external urethra sphincter (EUS) after a pudendal nerve crush injury. The pudendal nerve is one of the pelvic floor tissues injured during vaginal delivery, possibly contributing to the development of stress urinary incontinence (SUI) in women, the symptoms of which often do not appear until menopause, implicating hormonal factors. MATERIALS AND METHODS: Twenty-seven virgin female Sprague-Dawley rats were anaesthetized and underwent ovariectomy. Three days later, they had one of four procedures: bilateral pudendal nerve crush plus implant of a subcutaneous oestrogen-containing capsule (NC+E); nerve crush plus implant of a sham saline-containing capsule (NC+S); no nerve crush with an oestrogen capsule; or no nerve crush with a sham capsule. After 2 weeks the pudendal nerves and urethral tissues were prepared for light and electron microscopy. The number of axons, myelin figures and endoneurial nuclei in the pudendal nerve segment distal to the lesion were counted. Nerve fascicles near the EUS were also counted and categorized as normal or showing signs of degeneration and/or regeneration. The location of each nerve fascicle was specified as either ventral or dorsal. RESULTS: As there were no significant differences between the two control groups they were combined to form a single control group. In the distal pudendal nerve there were significantly fewer myelinated axons and large myelinated axons in the NC+E and NC+S groups than in the control group. There were three times as many large unmyelinated axons in the NC+E group than in either the NC+S or control groups (P < 0.05). There were only half as many nerve fascicles near the ventral side of the EUS in the NC+S group than in both the control and NC+E groups (P < 0.05). CONCLUSION: Oestrogen appears to affect large unmyelinated axons in both the injured pudendal nerve and at the denervated EUS target. After pudendal nerve crush, nerve fascicles with evidence of degeneration or regeneration near the EUS appear to be spared with oestrogen treatment, particularly in the ventral region. These observations may reflect the early stages of a neuroregenerative effect of oestrogen. Additional studies are needed to confirm these results at later periods and with functional methods.

Effects of vaginal distension on urethral anatomy and function.

OBJECTIVE: To determine the effect of repeated and prolonged vaginal distension on the leak-point pressure (LPP) and urethral anatomy in the female rat, as prolonged vaginal distension has been clinically correlated with signs of stress urinary incontinence (SUI). MATERIALS AND METHODS: Sixty female rats were placed into one of five groups; four groups underwent one of four vaginal distension protocols using a modified 10 F Foley catheter, i.e. prolonged (1 h), brief (0.5 h), intermittent (cycling inflated/deflated for 0.5 h) or sham distension. All animals had a suprapubic bladder catheter implanted 2 days after and were assessed urodynamically 4 days after vaginal distension. The fifth group of rats acted as controls and did not undergo vaginal distension, but did have a suprapubic bladder catheter placed and urodynamics assessed. To measure LPP the rats were anaesthetized with urethane, placed supine and the bladder filled with saline (5 mL/h) while bladder pressure was measured via the bladder catheter. LPPs were measured three times in each animal by manually increasing the abdominal pressure until leakage at the urethral meatus, when the external abdominal pressure was rapidly released. Peak bladder pressure was taken as the LPP and a mean value calculated for each animal. Immediately after measuring LPP the urethra was removed and processed routinely for histology (5 micro m sections, stained with haematoxylin/eosin and trichrome). The means (sem) were compared using a Kruskal-Wallis one-way anova on ranks, followed by a Dunn's test, with P < 0.05 indicating a significant difference. RESULTS: Both LPP and the external increase in abdominal pressure were significantly lower after prolonged distension, at 31.4 (1.7) and 19.8 (1.2) cmH2O, than in the sham group, at 41.1 (3.2) and 32.0 (4.7) cmH2O, respectively. There were no significant differences in LPP or in the increase in abdominal pressure between the brief, intermittent and sham groups. Qualitative histology showed that prolonged distension resulted in extensive disruption and marked thinning of urethral skeletal muscle fibres. Brief and intermittent distension showed mild and focal disruptions, respectively. CONCLUSIONS: As observed clinically, prolonged vaginal distension results in a lower LPP, greater anatomical injury and increased severity of SUI. These results suggest that ischaemia is important in the development of SUI after prolonged vaginal distension.

Effects of anesthesia on cystometry and leak point pressure of the female rat.

Anesthetics operate by different mechanisms and are often used to perform urodynamics in animals. The objective of this study was to compare the effects of ketamine/xylazine and urethane anesthetics on filling, voiding, and leak point pressure (LPP) in female rats. Nineteen rats underwent awake cystometry 2 days after suprapubic bladder catheter implantation. Bladders were filled with saline (5 ml/hr), while bladder pressure was measured. Half the rats were then anesthetized with urethane i.p. and half were anesthetized with ketamine and xylazine i.p. (K/X). All rats then underwent cystometry and LPP testing under anesthesia. Spontaneous nonvoiding contractions were analyzed and capacity was determined by voiding or leakage. Capacity was significantly higher in awake rats (0.55 +/- 0.06 ml) than with either K/X (0.21 +/- 0.06 ml) or urethane (0.30 +/- 0.05 ml). The pressure just prior to voiding in awake cystometry (15.6 +/- 1.7 cm H2O) was not significantly different from that with either anesthetic (K/X: 10.1 +/- 1.0 cm H2O; urethane: 13.3 +/- 2.0 cm H2O). Spontaneous nonvoiding contractions occurred in 4 rats with urethane and 3 rats with K/X. The volume at which the first contraction occurred was significantly lower with K/X (0.05 +/- 0.02 ml) than urethane (0.19 +/- 0.04 ml). There was no significant difference in the frequency of spontaneous nonvoiding contractions between K/X (4.58 +/- 0.30/min) and urethane (5.16 +/- 2.66/min), nor was there a difference in LPP between anesthetics (K/X: 40.4 +/- 2.4 cm H2O; urethane: 36.2 +/- 3.9 cm H2O). The results suggest that urethane is preferable to K/X for anesthetized cystometry studies since it more closely simulates normal physiological responses.

Development of a mathematical model for the prediction of the area of venous leak.

Erectile dysfunction (ED) is an increasingly prevalent medical problem, affecting up to 50% of men aged between 40 and 70-y-old. Many cases are vasculogenic and some of these stem from the inability of the penis to store blood during erection due to leak into the venous system, termed corporo-venocclusive dysfunction (CVOD). The area of leakage during erection could be the most direct measure of erectile function but has not been investigated before. We have developed a simple mathematical model to determine the area of leak during erection and have tested it on data from both normal men (n=3) and men with venogenic impotence (n=16) undergoing dynamic infusion cavernosometry (DIC). The area of leak in the impotent group is significantly greater than in normal men at intracorporal pressures above 30 mmHg and reaches a plateau between 60 and 90 mmHg. Based on this study, we suggest that it may be necessary only to perform DIC at intracorporal pressures between 60 and 90 mmHg.

Neuroregeneration and voiding behavior patterns after pudendal nerve crush in female rats.

Since the pudendal nerve innervates the external urethral sphincter, pudendal nerve injury and resultant neuroregeneration should affect voiding behavior. In this study, neuroregenerative activity of pudendal nerve was correlated to the changes in urinary behavior in female rats. Eighteen female rats underwent bilateral pudendal nerve crush, and 17 to 21 age-matched rats were used as unoperated controls. Urinary volume and frequency were recorded 6 and 13 days post-operatively (dpo). Initiation of pudendal nerve regeneration was indicated by an upregulation of beta(II) tubulin mRNA in the dorsolateral motoneurons (DLM), as measured at 7 and 14 dpo by in situ hybridization with radio-labeled beta(II) tubulin cDNA. At 6 dpo, mean volume voided by the crush group was significantly decreased compared to the control group during the light cycle (P < 0.05). At 7 dpo, the DLM mRNA level was significantly increased in the nerve crush group compared to the control group (P < 0.05). At 13 dpo, there were no differences in volume or frequency between the two groups, suggesting a return to normal voiding behavior. At 14 dpo, there was no significant difference in DLM mRNA levels between crush and control groups. Initiation of nerve regeneration occurs before normalization of voiding behavior after pudendal nerve crush. This data suggest that treatments to accelerate nerve regeneration would improve functional recovery of neurologically based incontinence.

Comparative physiology and biochemistry of rat and rabbit urinary bladder.

OBJECTIVE: To compare directly the biochemistry and contractile responses of rat and rabbit bladder to different stimuli. Materials and methods Sexually mature male New Zealand White rabbits and Sprague Dawley rats were compared. Each bladder was excised while the animal was anaesthetized; longitudinal bladder strips were cut and then mounted in an organ bath. Tension (2 g) was placed on all strips and each underwent field stimulation (FS) for a total of 20 s at 1-32 Hz, 1 ms and 80 V and was exposed to carbachol (100 micromol/L), ATP (2 mmol/L) and KCl (120 mmol/L). The tension was monitored continually using a polygraph and data stored digitally in a computer. The responses to each stimulus were determined as the maximum tension generated, maximum rate of tension generation and duration to a maximum response. The Ca2+- ATPase activity of the rat and rabbit bladder was determined. Bladder pressures were then predicted from the strip data using Laplace's law and compared with published values. RESULTS: Contractile responses (per unit tissue mass) of rat bladder strips were significantly greater than those of rabbit bladder strips at all frequencies of FS and to carbachol, KCl and ATP. The rate of contractile force generated by rat bladder strips in response to all stimuli were significantly greater than that generated by rabbit strips. Rabbit bladder strips took significantly longer to generate maximum tension than did rat bladder strips in response to pharmacological stimuli. In response to FS, rat strips took significantly longer than rabbit strips to generate maximum tension. Although the predicted rat bladder pressures were significantly greater than those for rabbit, the predicted pressures for both the rat and rabbit were significantly lower than the pressure responses of the isolated whole bladder model. The contractile data correlated well with the Ca2+-ATPase activity data; rat bladder had seven times the enzyme activity of rabbit bladder. CONCLUSION: Per unit mass, rat bladder is capable of generating more than five times the tension of rabbit bladder. Similarly, the rate of tension generation by rat bladder is three to five times greater than that by rabbit bladder. The duration to maximum tension generated in response to FS compared with pharmacological stimuli was affected by the inherent difference in the rate of contractile response to electrical activation compared with agents which diffuse through tissue, and by the difference in size between rat and rabbit bladder smooth muscle cells.

Effects of pudendal nerve injury in the female rat.

To test a neurogenic hypothesis for external urethral sphincter (EUS) dysfunction associated with urinary incontinence, the proximal pudendal nerve was crushed in anesthetized retired breeder female rats (n = 5) and compared with a sham lesion group (n = 4). Outcome measures included concentric needle electromyograms (EMGs) from the target EUS, voiding patterns during a 2-hour dark period, and micturition data over a 24-hour period. Fast Blue (FB) was introduced to the crush site at the time of injury and Diamidino Yellow (DY) to the EUS at the time the rats were killed (3 months post-operative), when histological analysis of the nerve and urethra was also performed. EMG records indicated the EUS motor units undergo typical denervation changes followed by regeneration and recovery. Voiding patterns from the crush group show a significant increase of small urine marks in the front third of the cage. At 1-2 weeks post-op, the frequency of voids was significantly increased in the crush group compared to pre-op and late post-op time periods. The mean volume voided in the light phase at the early post-op time was significantly increased in the sham group. Light and electron microscopic patterns seen in nerve and muscle suggest the regenerating motor units maintain a structural integrity. Motoneurons in the lower lumbar cord were labeled with either DY (14. 5 +/- 6.8), FB (31.7 +/- 23.7), or both (35.0 +/- 17.5) tracers, indicating approximately 54% of the crushed pudendal neurons regenerated to the EUS. In conclusion, several measures suggest this reversible crush lesion induces mild urinary incontinence. This animal model is promising for further development of hypotheses regarding neural injury, the pathogenesis of incontinence, and strategies aimed at prevention and treatment. Neurourol. Urodynam. 19:53-69, 2000.

Whole bladder mechanics during filling.

In addition to molecular and cellular properties, elemental and whole bladder properties are important to the function of the bladder during filling. The bladder pressure volume filling relation is dependent on all aspects of bladder tissue. Elemental mechanics properties include elasticity, viscoelasticity, and plastic deformation of bladder tissue. Whole bladder properties include bladder shape, mass, and distension. This paper reviews work on mathematical model aimed at determining the effect of whole bladder properties on bladder filling mechanics and outlines directions for the future.

Filling mechanics of obstructed and de-obstructed rat urinary bladders.

Chronic bladder distension occurs after partial outlet obstruction and can lead to decompensation and impaired function. To quantify the degree of chronic bladder distension, we previously defined the zero pressure volume (ZPV), the largest contained volume at zero transmural pressure. In the current study, we investigated the short- and long-term effects of outlet obstruction and de-obstruction on chronic distension and passive bladder filling mechanics. Voiding patterns were measured 10 days (short term) or 6 weeks (long term) after partial bladder outlet obstruction and the bladders were tested in vitro at that time. De-obstructed bladders were obstructed for 6 weeks, and voiding patterns were measured 10 days or 6 weeks after de-obstruction, followed by in vitro testing. Mean voided volume was increased in de-obstructed bladders but not obstructed bladders. The volume of urine in the bladder at euthanasia was greater than mean voided volume in obstructed bladders and less than mean voided volume in de-obstructed bladders, indicating large residual urine in the obstructed bladders. ZPV was significantly increased only after long-term obstruction or de-obstruction. Similarly, intravesical pressure and mean bladder wall stress were increased only after long-term obstruction or de-obstruction. We conclude that tissue remodeling occurs in the bladder wall after long-term obstruction, possibly both as a result of and leading to chronic overdistension and high residual urine. Tissue remodeling occurs in the bladder wall after long-term de-obstruction, possibly due to large voided volumes. Neurourol. Urodynam. 18:659-671, 1999.

Estimating detrusor pressure at home in pediatric patients with myelomeningocele.

PURPOSE: We evaluated a method of estimating detrusor pressure at home in patients with myelomeningocele who perform clean intermittent catheterization to empty the bladder. MATERIALS AND METHODS: Patients with myelomeningocele who perform clean intermittent catheterization underwent cystometry. At home they determined bladder pressure before draining a full bladder and after partial draining with the bladder almost empty. Home estimate of detrusor pressure was calculated using the formula, full bladder pressure - almost empty bladder pressure. RESULTS: A total of 4 boys and 5 girls with a mean age plus or minus standard deviation of 9.6+/-7.9 years who were enrolled in our study made 16.9+/-15.2 home bladder pressure and volume recordings weekly each during a mean of 5.8+/-4.3 months. Mean bladder capacity determined at home was significantly greater than cystometric capacity (354+/-185 versus 250+/-146 ml.). At a mean home and cystometric volume of 190+/-110 ml. full bladder pressure at home was not significantly different from cystometric vesical pressure (31.0+/-8.8 versus 27.5+/-7.5 cm. water). At a mean volume of 23+/-15 ml. mean home almost empty bladder pressure was not significantly different from cystometric abdominal pressure at full and almost empty volumes (14.1+/-5.5 versus 17.0+/-7.4 and 15.5+/-5.8 cm. water). Mean home estimate of detrusor pressure was not significantly different from cystometric detrusor pressure (17.0+/-6.3 versus 10.2+/-9.2 cm. water). CONCLUSIONS: Estimation of detrusor pressure at home is reliable and accurate in patients who perform clean intermittent catheterization. These pressure determinations may be used as a baseline for rapid identification of changes in bladder function.

Home bladder pressure monitoring in children with myelomeningocele.

PURPOSE: We evaluate a pressure gauge used at home for patients with myelomeningocele on clean intermittent catheterization to provide a system for inexpensive frequent monitoring of bladder pressures. MATERIALS AND METHODS: Subjects with myelomeningocele using clean intermittent catheterization underwent cystometry in the laboratory. At home they obtained weekly volumes and bladder pressures before and after emptying. Home estimate of detrusor pressure was defined as full bladder pressure minus empty bladder pressure. Medication changes, subject position and urinary tract symptoms were noted. RESULTS: A total of 11 subjects 10.5+/-7.3 years old have been enrolled and have made 16.7+/-12.6 weekly home bladder pressure and volume recordings in 4.7+/-3.1 months. Bladder capacities measured at home were 132+/-47% of cystometric capacities. At volumes of data overlap home full pressures (31+/-10 cm. water) were not statistically different from cystometric vesical pressures (25+/-9 cm. water). Home empty pressures (7+/-4 cm. water) were similar to cystometric abdominal pressures (14+/-8 cm. water). Home estimates of detrusor pressures (23+/-7 cm. water) magnified differences in full and empty pressures, and were significantly greater than cystometric detrusor pressures (11+/-11 cm. water). In 2 subjects significant increases in home full pressures occurred, which were associated with cessation of anticholinergic medication and infection. CONCLUSIONS: Home monitoring of bladder pressure is a simple, inexpensive and accurate method of obtaining frequent bladder pressures in patients with myelomeningocele. These pressures are consistent over a large range of volumes and times, and could potentially be used to identify quickly changes in patient condition.