Neurogenic Bladder Dysfunction

Pathophisiology of Neurogenic Bladder

All types of bladder dysfunction caused by an interruption of normal bladder innervation by the nervous system are referred to as neurogenic bladder.

Neurogenic bladder dysfunction can create intolerable discomfort and embarrassment and may also result in other serious physiological problems as well as recurring urinary tract infections.

A Special Concern: Spinal Shock

Immediately after spinal injury the person experiences a temporary condition of flaccid paralysis that is characterized by a loss of all reflex activity below the level of the lesion. This is referred to as spinal shock.

The signs of spinal shock related to the urinary tract mirror the signs of autonomous neurogenic bladder—that is, reflexes are absent, perception of fullness is absent, and the bladder becomes overdistended. Urinary retention Opens in new window is a common problem in patients who have a neurological impairment and associated disability.

As spinal shock resolves, it is critical to recognize the signs of resolution in order to correctly determine the type of neurogenic bladder that results, either reflex or autonomous. During this time the priority in care planning and urinary management is to prevent urinary retention, maintain low pressure within the bladder, empty the bladder regularly to completion and avoid reflux at all times.

Neurogenic bladder dysfunction is the most common form of bladder impairment seen in rehabilitation settings. Neurogenic lower tract urinary dysfunction is “due to a disturbance of neurological control mechanisms” (Stoher et al., 1999). Neurogenic bladders are classified into five types and are labeled according to the underlying pathological process:

1. uninhibited,
2. reflex or spastic,
3. autonomous or flaccid,
sensory paralytic, and
4. motor paralytic neurogenic bladders.

Most neurogenic bladders represent a combined motor and sensory impairment. For ease of description, the types of neurogenic bladder are described in Table X according to the schema proposed by Lapides and Diokno (1976).

1. Uninhibited Neurogenic Bladder

The uninhibited neurogenic bladder results from a disruption of the corticoregulatory tract or a malfunction of the supraspinal center that regulates voiding. Frequent uninhibited contractions occur, but the bladder usually empties completely, resulting in no residual urine. The micturition reflex remains intact. Sensation is present as is the bulbocavernous reflex.

A CMG will demonstrate strong, uninhibited contractions as the bladder is filled. The capacity of the bladder is decreased, and involuntary voiding will take place almost as soon as the urge is perceived.

Persons with uninhibited neurogenic bladder frequently complain about the urgency and frequency of urination and nocturia. After the urge is perceived, they cannot inhibit flow. When the external sphincter is voluntarily contracted, partial control of urination, even with strong voiding contractions, is possible. The intravesical pressure, however, remains high because of the force of detrusor contractions.

Anticholinergic medication may be recommended to decrease bladder contractility and increase bladder capacity. These patients may be able to avoid incontinence by voiding before the bladder is full enough to trigger the micturition reflex.

Therefore an important part of nursing intervention is scheduled voiding, habit training, and attention to fluid intake, to anticipate the need to void before the urge becomes too strong. For those patients who can follow three-step commands and volitionally start and stop their urinary stream, bladder training is a nursing intervention that may lead to continence.

2. Reflex Neurogenic Bladder

The reflex neurogenic bladder is referred to as an upper motor neuron, suprasacral, spastic, or central neurogenic bladder. This type of bladder dysfunction occurs when both the sensory and motor tracts of the spinal cord, which send messages between the bladder and the supraspinal center, are disrupted. Bladder overdistention can also predispose the individual to autonomic dysreflexia, a life-threatening complication.

The reflex arc remains intact, and voiding is involuntary because of the lack of cerebral control and may be incomplete because of uncoordinated bladder contractions. The bulbocavernous reflex is present and hyperactive. A CMG shows uninhibited contractions with decreased bladder capacity. The detrusor muscle frequently hypertrophies, which can lead to vesicoureteral reflux, hydronephrosis, and permanent renal damage.

The person with reflex neurogenic bladder is unable to sense fullness and is unable to void volitionally; therefore micturition cannot be started or stopped in the normal manner.

If the detrusor contraction and external urinary sphincter are coordinated, spontaneous voiding will occur when the micturition reflex arc is stimulated. If the two events are uncoordinated, however, pressure within the bladder wall will increase as the detrusor attempts to contract against the contracted external urinary sphincter. The resulting dysfunction is termed detrusor-sphincter dyssynergia. This pattern causes increased resistance to outflow with high intravesical pressure, high residual urine volumes, and poor bladder emptying (Erickson, 1980).

Drugs such as baclofen (Lioresal) may be valuable in decreasing the spasticity of skeletal muscle, including that of the external sphincter. Recently botulinum toxin type A (Botox) has been used to provide short-term relaxation of the urethral sphincter in patients with SCI and detrusor-sphincter dyssynergia (Petit et al., 1998) as well as others with pelvic floor dysfunction (Phelan et al., 2001). Botox injections produce effects similar to those of a sphincterotomy but are short term in nature.

Anticholinergic medications used in combination with these antispasmodic medications may reduce the voiding pressures enough to allow low-pressure reflex voiding (40 cm H₂O). This bladder program requires incontinence management because these individuals may have intermittent episodes of incontinence associated with reflex voiding.

An alternative for those with good hand function is to increase the anticholinergic medications, allowing the person to stay dry and to empty the bladder by intermittent catheterization every 4 to 6 hours (Lloyd, Giroux, & Toth, 1988), in which case the nursing intervention is urinary retention management (NIC).

3. Autonomous Neurogenic Bladder

The autonomous neurogenic bladder is referred to as a lower motor neuron, flaccid, or areflexic bladder. It is difficult to determine when spinal shock subsides for a patient who has an autonomous neurogenic bladder, because the characteristics are similar.

Damage occurs to the conus medullaris or cauda equine (lesions involving the reflex arc), disrupting pathways that carry sensory impulses from the bladder to the spinal cord, motor impulses from the spinal cord to the detrusor muscle, and motor impulses from the spinal cord to the external sphincter. Autonomous neurogenic bladder is the most common neurogenic bladder dysfunction seen in children with congenital disabilities such as spina bifida and myelomeningocele.

Voiding is involuntary and occurs when the bladder overflows. Peripheral reflexes and the bulbocavernous reflex are absent or hypoactive. Sensation and motor control are absent. Findings from a CMG demonstrate the absence of uninhibited contractions, a bladder capacity above normal (600 to 1000 ml), decreased intravesical pressure, and residual urine.

As with reflex neurogenic bladder, the patient with autonomous neurogenic bladder cannot sense fullness, or cannot void volitionally, and therefore cannot start or stop voiding in a normal manner.

The bladder can be partially emptied with manual pressure (Crede’s method) and straining (Valsalva maneuver). Two patterns of external sphincter activity may occur:

1. no motor activity or
2. some uncontrollable activity.

In both patterns the amount of residual urine depends on how well the individual can expel urine by applying pressure, the tone of smooth muscle and elasticity of the bladder wall, and the amount of muscle resistance offered by the internal and external urinary sphincters (Peschers, Jundt, & Dimpfl, 2000).

Recently there has been increasing concern about the safety of Credé’s methods because of the potential risk of the complications of high-pressure voiding, vesicoureteral reflux, hydronephrosis, and permanent renal damage (Vickrey et al., 1999).

An alternative method of bladder emptying is intermittent catheterization every 4 to 6 hours as the management program.

The most appropriate program for children with spina bifida or myelomeningocele takes into account the type of neurogenic bladder, functional and cognitive levels, and the child’s developmental level. Typically children as young as 3 to 5 years of age are able to learn and perform intermittent catheterization with adult supervision.

4. Sensory Paralytic Bladder

The sensory paralytic bladder occurs when the afferent or sensory side of the micturition reflex arc is damaged. This condition is most often seen in persons with diabetes who have sensory neuropathy.

The patient with sensory paralytic bladder is able to void volitionally, but the sensation of bladder fullness and emptiness is absent. Findings from the CMG demonstrate the absence of uninhibited contractions with an increased bladder capacity. Because of the lack of the sensation of emptiness, the presence of residual urine is variable, as is the presence of the bulbocavernous reflex and perineal sensation.

The patient senses no fullness, pain, or temperature but is able to initiate voiding unless the bladder has become markedly atonic because of prolonged periods of retention and overdistension. A loss of bladder wall tone may develop because of the large volumes of urine that collect in the bladder between voids. This urinary retention can lead to overflow incontinence. Because persons with sensory paralytic bladder retain motor control, they can avoid incontinence by utilizing a timed voiding program (Lloyd et al., 1988).

5. Motor Paralytic Bladder

The motor paralytic bladder occurs when the efferent or motor side of the micturition reflex arc is damaged. Voluntary control of urination is variable, and sensation is normal. The bulbocavernosus reflex is absent. The CMG demonstrates no uninhibited contractions with increased bladder capacity. Residual urine is markedly increased.

Because sensory nerves are intact, the patient will sense fullness and emptiness. Motor loss, however, will be partial or complete. When the onset of a motor paralytic bladder is slow and left untreated, the detrusor muscle may stretch and lose tone, resulting in large residual urine volumes. The patient may complain of difficulties in initiating voiding, decreased force of the urinary stream, and a need to strain to void.

These signs and symptoms result from loss of motor function and decreased muscle tone. The person may experience overflow incontinence, but distention may be prevented by intermittent catheterization. Persons with motor paralytic bladder may learn to empty the bladder by using a Valsalva maneuver, Credé’s method (if permitted), or intermittent catheterization.

Management of complications arising from the various neurogenic bladders are an immediate priority.

One of the most common problems seen in patient today is vesiculo-ureteral reflux (VUR). Vesiculo-ureteral reflux is a condition where urine in the bladder flows back into the ureters and eventually backs up into the kidney parenchyma itself. This causes urinary tract infections and eventually results in acute or chronic pyelonephritis (Smith 1975). In most patients the valve that prevents backflow located at the uretero-vesicular junction is incompetent. The uretero-vesicular (UV) junction has the physiological value that permits urine to empty into the bladder by ureter peristalsis while preventing a reflux or backing up into the ureter. There are three components of the physiological value:

1. There are bundles of detrusor muscle fibers where the ureter passes through the wall into the bladder. The ureters are compressed during the voiding process when the bladder muscle contracts.
2. Within the bladder wall and at the point where the ureter passes into the bladder, there is an increase in elastic tissue within the ureters.
3. There is a Waldeyer’s (named after an anatomist in Berlin, Dr. Wilhelm Von Waldeyer’s (named after an anatomist in Berlin, Dr. Wilhelm Von Waldeyer) sheath or a protective surrounding structure or body along the outer longitudinal muscle layer, which consists of detrusor fibers. Thus, when the bladder contracts during voiding, the Waldeyer’s sheath prevents reflux by kinking the lower end of the ureters against the bladder wall.

The oblique course of the ureter through the bladder wall and under the mucosal flap is the valvular mechanism to prevent reflux. The firm attachment of the ureter within the trigone area helps provide fixation during bladder filling and micturation and is another mechanism to prevent vesiculo-ureteral reflux (Pearman 1973).

Many authors agree (Cook and King 1979; Guttmann 1976; Pearman and England 1973; Smith 1975) that chronic infection of the neurogenic bladder is associated with VUR and, consequently, renal disease. There is some debate, however, as to which is cause and which is effect. Fellows and Silver (1976) reported on some researchers who found that when infection is treated, reflux ceases. More often, though, reflux persists and infection is difficult to eradicate in the neurogenic bladder.

Guttman (1963) concluded that “infection of the bladder plays a very important etiological role in the development of vesiculo-ureteral reflux in causing impairment or destruction of the elasticity and valve-like action of the ureteric orifices, as a result of ureteritis and peri-ureteritis following bladder infection” (p. 185). Reflux has been produced experimentally by injecting saline into the tissues surrounding the intravesical ureter, thus mimicking the inflammation of the mucosa and submucosa that is associated with cystitis. Reflux has also been induced by placing foreign bodies in the bladder or renal pelvis in order to promote infection and edema of the UV junction (Cook and King 1979).

Conversely, reflux contributes to the occurrence of urinary infection because it provides a reservoir of residual urine, but more commonly when the UV junction is only marginally competent (Cook and King 1979).

Obstruction at either the bladder neck or external sphincter level has also been deemed a probable contributing cause of VUR. The tight, spastic sphincter is believed to cause a large residual volume to accumulate in the bladder, increasing the intravesical pressure and eventually causing weakness and hypertrophy of the trigone musculature at the UV junction.

Saccules or diverticuli develop at the weak points and result in a shortening of the intravesical segment of the ureter, allowing reflux to occur (Smith 1975). Cystitis, which leads to vesical wall edema, may also lead to VURs in the neurogenic bladder. The edema seems to affect the trigone and intravesical ureter and may impair valvular function. Once the infection is eradicated, however, cystography usually reveals no reflux. Studies on ureteric peristalsis and how VUR affect it have shown that where reflux was present, peristaltic activity was markedly depressed or completely absent, and free reflux occurred (Scott 1963).