A radiological study of the effect of elevated intravesical pressures on ureteral calibre and peristalsis in patients with neurogenic bladder dysfunction

Butler, Edmond D.; Friedland, Gerald W.; Govan, Duncan E.

doi:10.1016/s0009-9260(71)80051-x

Cited by 16 publications

(3 citation statements)

References 9 publications

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“…Finally, our results help explain why patients with chronically elevated bladder pressures are more susceptible to ureteral dilation. 22 As shown in Figure 6, elevated bladder pressures increase required peristaltic amplitude for reflux prevention, as well as maximum refluxing volumetric flow rate; therefore, increasing the chance of peristaltic reflux.…”

Section: Discussionmentioning

confidence: 98%

Peristalsis prevents ureteral dilation

Kalayeh,

Fowlkes,

Xie

et al. 2023

Neurourology and Urodynamics

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PurposeThe etiology of ureteral dilation in primary nonrefluxing, nonobstructing megaureters is still not well understood. Impaired ureteral peristalsis has been theorized as one of the contributing factors. However, ureteral peristalsis and its “normal” function is not well defined. In this study, using mathematical modeling techniques, we aim to better understand how ureteral peristalsis works. This is the first model to consider clinically observed, back‐and‐forth, cyclic wall longitudinal motion during peristalsis. We hypothesize that dysfunctional ureteral peristalsis, caused by insufficient peristaltic amplitudes (e.g., circular muscle dysfunction) and/or lack of ureteral wall longitudinal motion (e.g., longitudinal muscle dysfunction), promotes peristaltic reflux (i.e., retrograde flow of urine during an episode of peristalsis) and may result in urinary stasis, urine accumulation, and consequent dilation.MethodsBased on lubrication theory in fluid mechanics, we developed a two‐dimensional (planar) model of ureteral peristalsis. In doing so, we treated ureteral peristalsis as an infinite train of sinusoidal waves. We then analyzed antegrade and retrograde flows in the ureter under different bladder–kidney differential pressure and peristalsis conditions.ResultsThere is a minimum peristaltic amplitude required to prevent peristaltic reflux. Ureteral wall longitudinal motion decreases this minimum required amplitude, increasing the nonrefluxing range of peristaltic amplitudes. As an example, for a normal bladder–kidney differential pressure of 5 cmH2O, ureteral wall longitudinal motion increases nonrefluxing range of peristaltic amplitude by 65%. Additionally, ureteral wall longitudinal motion decreases refluxing volumetric flow rates. For a similar normal bladder pressure example of 5 cmH2O, refluxing volumetric flow rate decreases by a factor of 18. Finally, elevated bladder pressure, not only increases the required peristaltic amplitude for reflux prevention but it increases maximum refluxing volumetric flow rates. For the case without wall longitudinal motion, as bladder–kidney differential pressure increases from 5 to 40 cmH2O, minimum required peristaltic amplitude to prevent reflux increases by 40% while the maximum refluxing volumetric flow rate increases by approximately 100%.ConclusionThe results presented in this study show how abnormal ureteral peristalsis, caused by the absence of wall longitudinal motion and/or lack of sufficient peristaltic amplitudes, facilitates peristaltic reflux and retrograde flow. We theorize that this retrograde flow can lead to urinary stasis and urine accumulation in the ureters, resulting in ureteral dilation seen on imaging studies and elevated infection risk. Our results also show how chronically elevated bladder pressures are more susceptible to such refluxing conditions that could lead to ureteral dilation.

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Section: Discussionmentioning

confidence: 98%

Peristalsis prevents ureteral dilation

Kalayeh,

Fowlkes,

Xie

et al. 2023

Neurourology and Urodynamics

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“…In those patients who underwent sphincterotomy, the characteristic narrowing at the external sphincter was seen on voiding cysto-urethrogram, and perineal muscle EMG revealed an increase rather than a decrease in activity during attempts at voiding (Nanninga et al, 1974). The appearance of the hydronephrosis associated with neurogenic bladder dysfunction has been attributed to the increased intravesical pressure which forces the ureter to pump urine into the bladder at increasingly higher pressures until a state of hydronephrosis is reached (Butler et al, 1971). Somewhat similar conclusions were reached by Thomas et al (1974), who found upper tract deterioration associated with spina bifida patients whose detrusor activity generated high pressures.…”

Section: Discussionmentioning

confidence: 99%

Silent hydronephrosis, a hazard revisited

Rosen¹,

Nanninga²,

O’Conor³

1976

Spinal Cord

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Six patients with neurogenic bladder secondary to spinal cord injury were seen in our Centre for routine follow-up. All of these individuals had attained the catheter-free state by various means and were, by their standards, functioning very well. They had gone from 6 months to 2 1/2 years without genito-urinary re-evaluations. One individual had a normal urogram 1 year after catheter removal and then 2 years later was noted to have bilateral hydronephrosis. Development of silent hydronephrosis in the catheter-free state, its treatment, and a regimen for following patients are discussed.

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“…[1] The appearance of the hydronephrosis associated with neurogenic bladder dysfunction has been attributed to the increased intravesical pressure which forces the ureter to pump urine into the bladder at increasingly higher pressures until a state of hydronephrosis is reached. [2]. Rosen and associates [3] recommend that all spinal cord injury patients functioning in the catheter-free state must be followed regularly at no longer than 6-month intervals.…”

Section: Introductionmentioning

confidence: 99%

Hydronephrosis and renal failure following inadequate management of neuropathic bladder in a patient with spinal cord injury: Case report of a preventable complication

et al. 2012

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BackgroundCondom catheters are indicated in spinal cord injury patients in whom intravesical pressures during storage and voiding are safe. Unmonitored use of penile sheath drainage can lead to serious complications.Case reportA 32-year old, male person, sustained complete paraplegia at T-11 level in 1985. He had been using condom catheter. Eleven years after sustaining spinal injury, intravenous urography showed no radio-opaque calculus, normal appearances of kidneys, ureters and bladder. Blood urea and Creatinine were within reference range. A year later, urodynamics revealed detrusor pressure of 100 cm water when detrusor contraction was initiated by suprapubic tapping. This patient was advised intermittent catheterisation and take anti-cholinergic drug orally; but, he wished to continue penile sheath drainage. Nine years later, this patient developed bilateral hydronephrosis and renal failure. Indwelling urethral catheter drainage was established. Five months later, ultrasound examination of urinary tract revealed normal kidneys with no evidence of hydronephrosis.ConclusionSpinal cord injury patients with high intravesical pressure should not have penile sheath drainage as these patients are at risk for developing hydronephrosis and renal failure. Intermittent catheterisation along with antimuscarinic drug should be the preferred option for managing neuropathic bladder.

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A radiological study of the effect of elevated intravesical pressures on ureteral calibre and peristalsis in patients with neurogenic bladder dysfunction

Cited by 16 publications

References 9 publications

Peristalsis prevents ureteral dilation

Peristalsis prevents ureteral dilation

Silent hydronephrosis, a hazard revisited

Hydronephrosis and renal failure following inadequate management of neuropathic bladder in a patient with spinal cord injury: Case report of a preventable complication

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