Bladder and bowel dysfunction commonly occurs in individuals undergoing rehabilitation. In keeping with the objectives of this book, the goal of this chapter is to provide general principles of assessment for a learner, rather than an in-depth review of the subject. The chapter is divided into two sections, the first on neurogenic bladder and the second on neurogenic bowel, with the focus on assessment of the bladder and bowel.
Although evaluation and management usually focuses on a person’s “neurogenic bladder,” it is important to remember that changes in the lower tracts, such as poor drainage or high bladder pressures, often have a direct impact on the kidneys. Therefore, an understanding of the entire urinary tract function, neurophysiology, and urine transport is essential when planning optimal assessment and treatment. The urinary tract is divided into the upper and lower urinary tracts. The upper tracts are composed of the kidneys and ureters. The lower urinary tracts are composed of the bladder and urethra.1,2
The kidney consists of two parts: the renal parenchyma and collecting system. The renal parenchyma secretes, concentrates, and excretes urine into the collecting system. Once urine drains through the multiple renal calyces, it collects in the renal pelvis. Active forces of urine transport then occur due to peristalsis of the calyces, renal pelvis, and ureter. Once the urine bolus arrives at the bladder, it travels through an important structure, the ureterovesical junction (UVJ).3 The UVJ is where the ureters traverse obliquely sandwiched between the muscular and submucosal layers of the bladder wall for a distance of 1 to 2 cm before opening into the bladder. This submucosal tunnel is designed as a one-way valve to allow urine flow into the bladder, but prevents reflux backward up into the ureter2 (Fig. 5–1). A common misconception is that high pressures in the bladder will cause vesicoureteral reflux, but the reverse is true. Sustained high intravesical pressures will inhibit drainage from the kidney and can over time cause upper tract damage.
Figure 5–1
The ureterovesical junction : Normal ureterotrigonal complex. (A) Side view of ureterovesical junction. Waldeyer’s muscular sheath invests the juxtavesical ureter and continues downward as the deep trigone, which extends to the bladder neck. The ureteral musculature becomes the superficial trigone, which extends to the verumontanum in the male and stops just short of the external meatus in the female. (B) Waldeyer’s sheath is connected by a few fibers to the detrusor muscle in the ureteral hiatus. This muscular sheath, inferior to the ureteral orifices, becomes the deep trigone. The musculature of the ureters continues downward as the superficial trigone. (Reprinted with permission from Tanagho EA, Pugh RCB. The anatomy and function of the ureterovesical junction. Br J Urol. 1963;35(2):151–165.)
Anatomically, the bladder is divided into the detrusor and the trigone. The detrusor is composed of smooth muscle bundles that freely crisscross and interlace with each other. The trigone is located at the inferior base of the bladder and extends from the ureteral orifices to the bladder neck.
Traditionally, the urethra has been thought to have two distinct sphincters: the internal and the external, or rhabdosphincter. The internal sphincter is not a true anatomic sphincter. Instead it refers to the junction of the bladder neck and proximal urethra. This area is considered to be a functional sphincter because there is a progressive increase in tone with bladder filling so that the urethral pressure is greater than the intravesical pressure.2,3
Bladder storage and emptying are a function of interactions between the peripheral parasympathetic, sympathetic, and somatic innervation of the lower urinary tract. Additionally, there is modulation from the central nervous system (CNS).
The importance of the afferent innervation of the bladder and sphincter is often neglected. There are two types of afferents: small myelinated A-delta and unmyelinated (C) fibers innervating the bladder. The small myelinated A-delta fibers respond in a graded fashion to bladder distention and are essential for normal voiding. The unmyelinated (C) fibers have been termed “silent C-fibers” because they do not respond to bladder distention and therefore are not essential for normal voiding. However, these silent C-fibers do exhibit spontaneous firing when they are activated by chemical or cold temperature irritation at the bladder wall. More importantly, the unmyelinated (C) fibers, have been found to “wake up” and respond to distention and stimulate bladder contractions in those with suprasacral spinal cord injury (SCI). Therefore, C fiber afferents play an important role in involuntary bladder contractions (bladder overactivity) in those with suprasacral injuries. This helps explain the mechanism of action of intravesical lidocaine and topical oxybutynin at quieting an overactive bladder. It is possible that a major mechanism of onabotulinum toxin is suppression of the bladder fiber afferents4 (Fig. 5–2).
Figure 5–2
Ascending and descending innervation of the bladder and its sphincters. (Reproduced with permission from Disorders of the Autonomic Nervous System, Respiration, and Swallowing. In: Ropper AH, Samuels MA, Klein JP, eds. Adams & Victor’s Principles of Neurology, 10e New York, NY: McGraw-Hill; 2014.)
The parasympathetic (PS) efferent supply originates from a distinct detrusor nucleus located in the intermediolateral gray matter of the sacral cord at S2–S4. Sacral efferents emerge as preganglionic fibers in the ventral roots and travel through the pelvic nerves to ganglia immediately adjacent to or within the detrusor muscle to provide excitatory input to the bladder. After impulses arrive at the ganglia, they travel to the smooth muscle M2 or M3 muscarinic receptors. Stimulation of these parasympathetic M2 and M3 receptors results in bladder contractions.5,6 Therefore, the parasympathetic system can be thought of as being responsible for bladder emptying.
The sympathetic efferent nerve supply to the bladder and urethra begins in the intermediolateral gray column from T11 through L2 and provides inhibitory input to the bladder.5,6 Sympathetic stimulation facilitates bladder storage because of the strategic location of the adrenergic receptors. Beta-3 adrenergic receptors predominate in the superior portion of the bladder. Stimulation of beta-3 receptors causes smooth muscle relaxation of the bladder wall. Sympathetic alpha receptors have a higher density near the base of the bladder and prostatic urethra; stimulation of these receptors causes smooth muscle contractions and therefore increases the outlet resistance of the bladder and prostatic urethra.5–7 Therefore, sympathetic stimulation results in urine storage by simultaneous relaxation of the bladder and tightening of the outlet (see Fig. 5–2).
The external urethral sphincter (EUS) classically has been described as having somatic innervation, allowing the sphincter to be closed at will. Somatic efferents originate from a pudendal nucleus of sacral segments from S1–S4. Then they travel through the pudendal nerve to the neuromuscular junction of the striated muscle fibers in the EUS.
The internal urethral sphincter has been described as being under control of the autonomic system. This area has a large number of sympathetic alpha receptors, which cause closure when stimulated8,9 (see Fig. 5–2).
The distinction between the internal and external sphincter is less clear. Crowe and associates reported a substantial invasion of adrenergic nerve fibers in smooth and striated muscle in the urethra in individuals with SCI with lower motor neuron lesions.10
Micturition has two phases: the filling (storage) phase and emptying (voiding) phase. The filling phase occurs when a person is not trying to void. The emptying phase is defined as when a person is attempting or told to void.
During filling, there should be very little rise in bladder pressure. As filling continues, low intravesical pressure is maintained by a progressive increase in sympathetic stimulation of the beta-3 receptors located in the body of the bladder that cause relaxation and stimulation of the alpha receptors located at the base of the bladder and urethra that causes contraction. Sympathetic stimulation also inhibits excitatory parasympathetic ganglionic transmission, which helps suppress bladder contractions. During the filling phase, there is a progressive increase in urethral sphincter electromyographic (EMG) activity.11 Increased urethral sphincter activity also reflexively inhibits bladder contractions. When a bladder is full and has normal compliance, intravesical pressures are normally between 0 and 6 cm H2O and should not rise above 15 cm H2O. Filling continued past the limit of the viscoelastic properties of the bladder results in a steady progressive rise in intravesical pressure.12 This part of the filling curve usually is not seen in a person with normal bladder function, because this much filling would cause significant discomfort and not be tolerated.
When a patient is told to void (voiding or emptying phase), there should be cessation of urethral sphincter EMG activity and a drop in urethral sphincter pressure and funneling of the bladder neck. There is no longer reflex inhibition to the sacral micturition center from the sphincter mechanism. This is followed by a detrusor contraction. The urethral sphincter should remain open throughout voiding, and there should be no rise in intraabdominal pressure during voiding. In younger individuals, there should be no post-void residual (PVR), although PVRs may increase with aging.
The bladder may be described as overactive, underactive, or normal. The bladder is described as being overactive during the filling phase of urodynamics if the bladder has involuntary contractions (which may or may not cause incontinence, depending on the sphincter activity). If this is due to a neurogenic cause, it is called neurogenic detrusor overactivity (NDO). If no cause is known, it is called idiopathic detrusor overactivity (IDO). During the voiding phase the bladder may be normal or abnormal. Abnormal bladder function can be further subdivided into detrusor underactivity (if there are weak contractions causing poor emptying) or an acontractile detrusor (no bladder contractions). The sphincter during the filling phase is referred to as normal urethral closure mechanism or abnormal urethral closure mechanism (one that allows leakage in the absence of a bladder contraction). The point at which this occurs is known as the detrusor leak point pressure. The abnormal urethral closure mechanism may be due to anatomic urethral hypermobility, intrinsic sphincter damage (such as fibrosis from radiation, prolonged excessive stretching of the urethra with a Foley catheter), or spinal cord (lower motor) injury.
The sphincter during the voiding phase may be described as normal or abnormal. Normal sphincter function refers to the sphincter relaxing before the bladder contraction and remaining open during voiding. Abnormal sphincter function refers to the sphincter not relaxing appropriately. In those with suprasacral SCI, detrusor sphincter dyssynergia (DSD) is defined as a detrusor contraction concurrent with an involuntary contraction of the urethral and/or periurethral striated muscle (Fig. 5–3).
Figure 5–3
Example of a urodynamic study with simultaneous recording of intravesical and urethral pressure in a person with a supra sacral SCI with neurogenic detrusor overactivity and detrusor sphincter dyssynergia. Note the subtle dyssynergia of the bladder (Pdet) and sphincter (Pura). This resulted in a weak intermittent urinary stream (Flow). (Reproduced with permission from Lue TF, Tanagho EA. Chapter 28. Neuropathic Bladder Disorders. In: McAninch JW, Lue TF, eds. Smith and Tanagho’s General Urology, 18e New York, NY: McGraw-Hill; 2013.)
Those with lower motor injuries and those who are in pain or nervous may have a nonrelaxing sphincter.13 A variety of voiding dysfunctions can occur after SCI and other disorders. These are outlined in Table 5–1. This table is helpful in getting a general idea of a person’s voiding issue. However, there are significant variations in the predicted patterns of bladder and sphincter function (such as amount of detrusor overactivity or degree of DSD) so that further assessment is necessary.
Level of Injury | Predicted Voiding Pattern |
Suprapontine (from cerebrovascular disease, hydrocephalus, intracranial neoplasms, traumatic brain injury, Parkinson’s disease, and multiple sclerosis) | Bladder detrusor overactivity |
Sphincter synergy | |
Suprasacral SCI (from cervical SCI, cervical metastasis) | Bladder detrusor overactivity |
Sphincter dyssynergia | |
Sacral SCI | Bladder detrusor – underactive or acontractile (sometimes poor bladder wall compliance) |
Sphincter underactivity |
Studies have shown that a patient’s history cannot accurately determine the type and reason for a person presenting with a voiding dysfunction.14,15 However, a careful history should always be obtained, as it plays an important role in developing an evaluation and eventual treatment strategy. The history is also helpful in establishing the individual’s voiding pattern and urologic history prior to current rehabilitation issues.
Similar to the approach for individuals with neurogenic bowel, one should determine the person’s voiding pattern, the duration and frequency of voiding symptoms, impact of the person’s current voiding dysfunction, satisfaction and concerns with their current bladder management, and future expectations. The physiatric history is particularly significant for voiding dysfunction. One should ask about hand function, dressing skills, sitting balance, ability to perform transfers, and ability to ambulate. These factors are important considerations when developing bladder management strategies.
The first and easiest part of the evaluation and management of a person in a rehabilitation setting with a voiding dysfunction is to determine if there are any reversible causes. A helpful pneumonic that can be used to evaluate the most common, potentially reversible causes of urinary incontinence is “DIAPPERS.”16 Although this was initially used in reference to reversible causes of incontinence, it can also be used for reversible causes of urinary retention. A modification to this pneumonic to also include urinary retention is seen in Table 5–2. Correction of reversible causes may result in a resolution of the voiding dysfunction so that a further evaluation is not needed.
D Delirium or other cognitive causes I Infection/inflammation of the urinary tract A Atrophic vaginitis (elderly women and those of estrogen antagonists) P Pharmaceuticals P Pain E Endocrine (Diabetes) R Restricted mobility S Stool impaction |
The neuro-urologic physical examination should focus on the abdomen, external genitalia, and perineal skin. When performing the rectal examination, it is important to understand that the size of the prostate does not determine if a person has prostate obstruction. Prostate obstruction is determined by the amount of prostate tissue growing inward and constricting the urethra, which cannot be determined by a rectal examination. Therefore, urodynamic study rather than rectal examination is needed to objectively diagnose outflow obstruction. In women, one should examine for the location of the urethral meatus and whether there is a cystocele or rectocele. An intravaginal urethra may make intermittent catheterization a difficult option. A cystocele or rectocele may predispose to urinary incontinence. Evaluation of the perineum is important to assess if there are any rashes or skin breakdowns from those with chronic urinary incontinence.
Anal sphincter tone also should be evaluated. Decreased or absent tone suggests a cauda equina or peripheral nerve lesion, whereas increased tone suggests a suprasacral lesion. Voluntary contraction of the anal sphincter tests sacral innervation, suprasacral integrity, and the ability to understand commands. The bulbocavernosus reflex has been reported as present only 70% to 85% of the time in neurologically intact people. A false negative often is due to a person being nervous and already having their anal sphincter clamped down at the time of the examination. The cremasteric reflex is elicited by lightly stroking or poking the superior and medial (inner) part of the thigh, regardless of the direction of stroke. The normal response is an immediate contraction of the cremaster muscle that pulls up the ipsilateral testis (on the same side of the body). The anal or anocutaneous reflex causes a contraction of the anal sphincter in response to pinprick stimulus of the perineum. This reflex is evidence of normal motor function at S4–S5.
Evaluation of the perineum is important to assess if there are any rashes or skin breakdowns, particularly in those with chronic urinary incontinence.
It is best to obtain a baseline urine for culture and sensitivity. It is important to know that a large number of individuals with a neurogenic bladder are colonized with one or more organisms. Therefore, a bladder infection in a person with SCI is defined as having bacteria in the urine—pyuria—and, most importantly, a new onset of symptoms.17–19 A serum creatinine is easy to obtain; however, it is not particularly helpful as a year-to-year screening test. It is helpful, particularly if elevated, to monitor change. This is because a significant amount of kidney damage (greater than 50%) must occur prior to the appearance of changes in the serum creatinine. A “normal” serum creatinine may be elevated due to poor renal function in a person with significant loss of muscle mass. A 24-hour creatinine clearance gives a better assessment of renal function.
No evaluation at all may be necessary if a reversible cause is identified and treatment is successful. A more extensive evaluation with a voiding diary and PVR to confirm a clinical impression may be useful in a person with an acute onset of a disability without an obvious neurogenic bladder (hip fracture, post-op pain). A more extensive lower tract evaluation (urodynamics) is needed in a person with significant and potentially long-term disability, such as SCI, multiple sclerosis (MS), or spina bifida; if previous treatment has not been satisfactory; or if a more invasive procedure is being considered (such as suprapubic tube or onabotulinum toxin bladder injections). A decision on whether or not to also evaluate the upper tracts depends on identified risk factors of upper tract damage (high intravesical pressures, detrusor sphincter dyssynergia, recurrent urinary tract infections [UTIs]). Those with a history of traumatic SCI, MS, spina bifida, and other spinal cord disorders are at more risk of upper tract damage because of detrusor overactivity, poor bladder wall compliance, and poor coordination of the bladder and sphincter (DSD).
A variety of tests are designed to evaluate the upper tracts. Some tests are better at evaluating renal function, whereas others are more superior at evaluating renal anatomy. Usually a test to evaluate anatomy is sufficient. However, if there are significant concerns of the impact of a voiding issue (high voiding pressures, such as very poor bladder wall compliance) or if abnormal anatomy is identified such as hydronephrosis, then a test that evaluates renal function is indicated.
An important noninvasive tool to help assess bladder function is an intake and output (I&O) voiding diary. It has been found that a three-day (72-hour) diary gives the best results. The diary should list fluid intake, type of fluid, time of day volume voided (or catheterized), and incontinent episodes. This gives an excellent idea of a person’s voiding pattern in their usual environment. It also gives the person an insight into their fluid intake and voiding pattern. This may allow a person to effectively adjust their fluid intake and voiding pattern. If so, no further urologic evaluation may be needed.
One of the easiest screening tests to evaluate bladder emptying is a post-void residual (PVR). PVRs can be determined with catheterization or bladder ultrasound. A normal PVR has traditionally been considered to be 100 cc. However, no studies show that more than 100 cc will cause increased UTIs. Studies have shown that acute and chronic bladder overdistention and high bladder pressures can cause bladder wall ischemia and UTIs. Therefore, these factors should also be taken into consideration. A normal PVR does not rule out a voiding problem. For example, a PVR may be normal despite significant outflow obstruction (e.g., benign prostate hypertrophy, sphincter detrusor dyssynergia) due to compensatory increase in the strength of detrusor contractions, or with no bladder contractions due to increasing intraabdominal pressure (e.g., Valsalva maneuver, Crede maneuver). Caution also has to be taken in interpreting a large PVR. It may be abnormal because a person did not void prior to the PVR determination, it was not taken immediately after voiding, or there was an abnormal voiding situation (e.g., the patient was given a bedpan at 3:00 A.M.).
The bedside cystometrogram (CMG) is used to evaluate sensation, stability, and bladder capacity. This is accomplished by inserting an indwelling catheter after the person has voided. A bulb syringe is then attached to the end of the catheter, and the bulb is removed so that the syringe acts as a funnel. Sterile water is then poured into the syringe. The height above the bladder represents the bladder pressure when the water stops draining down into the bladder. There are several limitations to the bedside CMG. It is difficult to determine if small rises in the water column are due to intraabdominal pressure (i.e., straining) or a bladder contraction. Most important, the voiding phase cannot be evaluated.
The gold standard for obtaining an objective evaluation of bladder and sphincter function is a water-filled pressure flow multichannel urodynamic study, which has the capability to record bladder filling, bladder pressure, flow rate, and voided volume. More sophisticated urodynamic studies also may incorporate urethral pressure recordings, urethral sphincter or anal sphincter EMG, and videofluoroscopy (videourodynamics). Simultaneous videofluoroscopy and sphincter EMG are useful adjuncts to evaluate sphincter function. Videofluoroscopy can be used to evaluate for vesicoureteral reflux. A cystogram can also be used to evaluate for vesicoureteral reflux. A water-filled pressure flow urodynamic study is necessary to objectively measure both the filling and the emptying phase of micturition. The first is the filling (storage) phase during which water is infused into the bladder. The second portion of the study is the voiding (emptying) phase. The voiding phase is considered to begin when a person is told to void.
Cystoscopy plays an important role when there is a suspected anatomic reason for a person’s voiding dysfunction. Some indications for cystoscopy in those with voiding disorders include hematuria, recurrent symptomatic UTIs, recurrent asymptomatic bacteriuria with a stone-forming organism (i.e., Proteus mirabilis), an episode of genitourinary sepsis, urinary retention, incontinence, pieces of eggshell calculi obtained when irrigating a catheter, and long-term indwelling catheter. Cystoscopy also is indicated when removing an indwelling Foley catheter that has been in place two to four weeks and changing to a different type of management, such as intermittent catheterization (IC)or a balanced bladder. Additionally, cystoscopy is indicated if sand or stones are noted on the catheter during a catheter change because there is an 86% chance that there will be remaining stones within the bladder.20 See Table 5–3 for more cystoscopy indications for those with neurogenic bladder.
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A decision on whether or not to also evaluate the upper tract depends on identified risk factors of upper tract damage (high intravesical pressures, detrusor dyssynergia, recurrent UTIs). Those with traumatic SCI, multiple sclerosis, spina bifida, and other spinal cord disorders are at more risk of upper tract damage because of detrusor overactivity, poor bladder wall compliance, and poor coordination of sphincter relaxation during a bladder contraction and voiding (DSD).
A variety of tests are designed to evaluate the upper tracts. Some tests are better at evaluating renal function and others at evaluating renal anatomy. Those that evaluate anatomy include an abdominal x-ray, and renal ultrasound. More detailed imaging is obtained from an abdominal and pelvic computerized tomography (CT) scan or magnetic resonance imaging (MRI) scan. In those with cancer, an abdominal and pelvic CT scan is recommended and can replace the renal ultrasound study.
Tests that are best to evaluate renal function include a 24-hour urine creatinine clearance and quantitative MAG3 (mercaptoacetyltriglycine) renal scan with effective renal plasma flow (ERPF).21–24 If there is a question of kidney obstruction, a MAG3 Lasix renal scan helps to differentiate between a large collecting system and true obstruction. An obstruction becomes much more obvious when there is a forced diuresis. The author finds a MAG3 renal scan and renal ultrasound very helpful to screen for upper tract function and anatomic problems for those at risk.