Introduction
Lower urinary tract dysfunction describes various problems related to the bladder’s ability to store or empty urine. Voiding dysfunction refers specifically to bladder emptying problems. Urinary retention is the inability to complete the voiding phase of the micturition cycle, and oftentimes represents the end stage of voiding dysfunction. Abnormal bladder emptying can occur as a result of dysfunction of the bladder or the outlet, and sometimes both. Voiding dysfunction manifests clinically in lower urinary tract symptoms (LUTS), which may be associated with voiding or emptying symptoms (decreased force of stream, incomplete emptying, hesitancy, straining to void, and urinary retention) or storage symptoms (frequency, urgency, nocturia, and urgency incontinence). Because symptoms do not always correlate with the underlying pathology, and numerous conditions may present similarly, it is a challenging task to determine the specific etiology involved. In many cases, voiding dysfunction can be explained by neurologic disease, learned behavioral patterns, or congenital, acquired, or iatrogenic bladder outlet obstruction. At other times the cause may not be readily apparent, such as in cases of idiopathic detrusor underactivity (DU). In this chapter, we discuss normal voiding and the pathophysiologic events that lead to abnormal lower urinary tract function, as well as the evaluation, management, and treatment of women with specific types of voiding problems.
Neurophysiology of micturition
Normal voiding is accomplished by activation of the “micturition reflex” ( Fig. 34.1 ). This is a coordinated event characterized by, in order: (1) relaxation of the striated urethral sphincter, (2) contraction of the detrusor, (3) opening of the vesical neck and urethra, and (4) onset of urine flow ( Fig. 34.2 ). This reflex is normally controlled by the pontine micturition center (PMC) located in the rostral brainstem. A separate sacral micturition center is located at S2 to S4, through which the bladder can contract independent of cortical and pontine input. The PMC, through its neural pathways to the sacral micturition center, is responsible for coordinated and voluntary voiding. Both the autonomic and somatic nervous systems play a crucial role in lower urinary tract function. Normal voiding occurs when the bladder responds to threshold tension via its mechanoreceptors. To avoid a random occurrence, central nervous system inhibitory and facilitatory pathways are involved in coordination of urine storage and micturition.
Micturition depends on a spinobulbospinal reflex that is relayed through the PMC, which receives input from the cerebral cortex, cerebellum, basal ganglia, thalamus, and hypothalamus, and is the final common pathway to the bladder motor neurons. Much of the input from suprapontine centers is inhibitory, although some facilitatory influences are involved. The central facilitatory areas are the anterior pons and the posterior hypothalamus, and the inhibitory areas include the cerebral cortex, basal ganglia, and cerebellum. The cerebellum also is implicated in the maintenance of tone in the pelvic floor striated musculature and coordination between bladder contraction and periurethral striated muscle relaxation. Because the suprapontine input to the PMC is mostly inhibitory, interruption of this input (e.g., cerebrovascular accident, cerebral atrophy, Parkinson disease, brain tumor, or trauma) often results in uncontrolled detrusor activity, or involuntary contractions, but the “micturition reflex” is left intact. The typical presentation of a suprapontine lesion is loss of voluntary control of micturition. Uninhibited detrusor contractions may result in urinary frequency, urgency, and urgency incontinence. Little risk is present for developing renal deterioration because voiding is coordinated, even if not always voluntary.
Anatomically, the two areas of the spinal cord responsible for transmitting afferent input from the lower urinary tract are the lateral spinothalamic tracts and the posterior columns. The lateral spinothalamic tracts contain ascending routes responsible for transmitting bladder sensation and triggering voiding. Proprioceptive sensory impulses generated in bladder muscle and periurethral striated muscle travel in the posterior columns. The PMC controls efferent input to the bladder and external sphincter via two separate regions. The medial region is responsible for motor input to the bladder detrusor muscle via the reticulospinal tracts to the sacral intermediolateral cell groups, which contain preganglionic parasympathetic neurons that form the motor supply of the bladder detrusor muscle. Electrical stimulation of this region results in a prompt decrease in pelvic floor electromyography (EMG) and urethral pressure followed by an increase in intravesical pressure (normal voiding). The lateral region has specific projections via the corticospinal tracts to the nucleus of Onuf in the sacral cord that contains motor neurons innervating the pelvic floor, including the urethral and anal sphincters. Electrical stimulation of this region results in a rapid increase in urethral pressure and pelvic floor EMG but little increase in intravesical pressure (normal storage).
Storage and evacuation of urine depend on neural integration at the peripheral, spinal cord, and central levels. Normally, bladder distension will cause low-level firing of afferent nerves. This will cause a reflex inhibitory response to the bladder via the hypogastric nerve and a stimulatory response to the external sphincter from the pudendal nerve. With further distension, myelinated A delta fiber afferents are activated. Afferents travel up the spinal cord to the PMC. Here, central input, mostly inhibitory, is received from suprapontine centers. If voiding is not desired, the voiding reflex can be suppressed or interrupted. If voiding is desired, efferent output to the pelvic plexus at S2–S4 via the spinal cord is initiated. Ultimately, the stimulatory message is sent to the bladder via the pelvic nerve. At the same time, inhibitory messages are sent via the hypogastric and pudendal pathways to allow for relaxation of the urethral sphincter mechanisms and coordinated voiding.
Peripheral innervation to the bladder and to the internal and external sphincters is provided by the pelvic, hypogastric, and pudendal nerves. Parasympathetic efferent input to the bladder arises from the intermediolateral cell column of S2–S4 and travels as preganglionic fibers via the pelvic nerve to the pelvic plexus located on both sides of the rectum, from which postganglionic fibers innervate the bladder. Efferent sympathetic nerves to the bladder and urethra arise from the intermediolateral cell column of T10 to L2 as preganglionic fibers that travel to ganglia located in the superior hypogastric plexus, from which arises the hypogastric nerve that contains the postganglionic sympathetic efferents to the bladder and urethra. The pudendal nerve carries the somatic input from S2–S4 to the external sphincter. Injury to any one of these nerves or their branches can result in a partial or complete denervation to the involved end organ.
In addition to the neurophysiologic pathways, other pharmacologic factors are responsible for normal voiding. The lower urinary tract is rich in both cholinergic and adrenergic receptors. Muscarinic receptors are located in the body of the bladder, and they are activated by parasympathetic release of acetylcholine to induce bladder contraction. Also, β-adrenergic receptors in the detrusor cause relaxation in response to increasing levels of cyclic adenosine monophosphate. In the bladder neck and urethra, α-adrenergic receptors are responsible for the increase in urethral tone and rise in intraurethral pressure during sympathetic stimulation via the hypogastric nerve. Each of these receptor types have been the basis for pharmacologic therapy of the lower urinary tract.
Anticholinergic medications can cause bladder relaxation by inhibiting parasympathetic pathways; β-adrenergics also treat bladder overactivity by stimulating adrenoreceptors and causing detrusor relaxation. α-Agonist medications have been used to treat stress incontinence, whereas α-blockers can facilitate emptying by relaxation of bladder neck smooth muscle.
Classification of voiding dysfunction
Many complex classification systems for voiding dysfunction have been proposed; however, they failed to be diagnostically and therapeutically oriented. We have found the functional classification system proposed by to be the most useful. This simple and practical classification system can be applied easily to our diagnostic criteria (e.g., urodynamics). Of equal importance is that treatment options can be chosen based on the classification.
The functional classification is based on a simple understanding of urine storage and micturition. For normal urine storage and voiding to occur, there must be proper and coordinated functioning of the bladder and the bladder outlet. Therefore, in simple anatomic terms, voiding dysfunction can be divided into the following categories:
- 1.
Bladder dysfunction
- 2.
Bladder outlet dysfunction (bladder neck, urethra, external sphincter)
- 3.
Combined bladder and outlet dysfunction
Similarly, the effects of these problems can be classified as follows:
- 1.
Failure to properly store urine
- 2.
Failure to properly empty urine
- 3.
Failure to store and empty urine
Voiding dysfunction can be characterized as neurogenic or nonneurogenic. Furthermore, nonneurogenic voiding dysfunction related to outlet obstruction can be classified as functional or anatomical. Bladder outlet obstruction is characterized by a reduced urine flow rate and/or a raised postvoid residual (PVR) associated with an elevated voiding detrusor pressure. It is usually diagnosed by studying the synchronous values of urine flow rate and detrusor pressure and any PVR measurements. Common anatomic causes of female bladder outlet obstruction include advanced pelvic organ prolapse, stress incontinence surgery, and urethral stricture ( ). Neurogenic obstruction is functional and the result of dyscoordination of the external and/or internal sphincter during voiding.
Evaluation of female voiding dysfunction
The evaluation of LUTS and potential voiding dysfunction in women begins with a thorough history focusing on the type and duration of symptoms and voiding habits over time. Historically, women have fewer reported classic voiding (obstructive) symptoms and have more commonly presented with storage symptoms and recurrent urinary tract infections. Two studies showed that, with a high index of suspicion and careful questioning, voiding symptoms were noted in 71% to 76% and storage symptoms were present in 79% to 92% of women with obstruction; therefore, voiding symptoms should not be overlooked when evaluating a woman who complains primarily of storage symptoms. A complete medical, surgical, obstetric-gynecologic, neurologic, and urologic history may uncover possible causes of voiding dysfunction. Any inciting events, such as surgeries to treat stress urinary incontinence (SUI) or any other procedures in the lower urinary tract or vagina, must be recorded. Other relevant information that may aid in the diagnosis of obstruction include history of urogenital trauma, history of falls, back injury, or surgery, and other medical conditions, such as diabetes, neurological disease, or psychiatric conditions.
A complete physical examination including a pelvic examination is required. An abdominal examination is performed to evaluate for abdominal masses or a palpable distended bladder. A pelvic examination then is performed, and one should first inspect the vagina and the epithelium for atrophic changes, signs of prior surgery, and possible foreign body. Attention should be paid to the positions of the urethra, bladder neck, and bladder at rest and with Valsalva by visualizing the amount of anterior, apical, and posterior compartment prolapse. One should inspect the anterior vaginal wall for existing scars or hypersuspension or urethral kinking caused by prior surgery. The posterior blade of a small vaginal speculum is helpful in visualizing the anterior vaginal wall. The cotton swab test can be used to quantify urethral hypermobility when needed. The patient also should be assessed for SUI. Vaginal apex support and position are important, as uterine or apical prolapse are potential causes of obstruction. After examination of the anterior vaginal wall is completed, the blade of the speculum is rotated, and the posterior wall and apex are inspected. Similar to other forms of prolapse, posterior vaginal wall prolapse, including rectocele and posterior enterocele, can cause obstruction and voiding dysfunction. Bimanual examination with palpation of the uterus and cervix should be done to determine uterine size and position, and to identify the presence of any pelvic masses, including fibroids, which may cause or contribute to voiding dysfunction.
In patients with LUTS, a focused neurologic examination should also be performed. Attention should be paid to the sensory and motor functions of the sacral nerves, including anal sphincter tone, perineal sensation, bulbocavernosus and anal wink reflexes, strength of lower extremities, and deep tendon reflexes (knee and ankle). A careful neurologic examination may help to confirm suspected disease or uncover an unknown lesion, and a formal neurologic consultation may be appropriate.
Simple office-based tests can give insight to the cause of LUTS. Urine analysis (and culture, if indicated) is done routinely. Intake and voiding diaries are helpful in quantifying fluid consumption, symptoms, voiding habits, and urine production. Diaries log the number of incontinence episodes and type (stress, urgency, insensible). Noninvasive uroflowmetry and PVR volume determination are good methods to screen for disorders of bladder emptying. A PVR assessment can be performed initially as a safety measure to rule out significant retention of urine, and later to monitor changes in bladder emptying ability, especially in neurologic conditions, as some patients may develop bladder dysfunction at any point in their disease process. There is no standard definition as to what constitutes a clinically significant PVR; however, recent studies have commonly used 100 or 150 mL as limits. No data suggest that higher residuals indicate pathological conditions. Absolute volumes, proportion of bladder capacity, or presence of relevant symptoms are all used in some contexts ( ).
Acute urinary retention is defined as a relatively sudden inability to pass urine associated with bladder distension. Chronic retention is less specifically defined but usually presents as an elevated PVR of at least 250 mL without pain. Individuals with chronically elevated PVR may be at increased risk of ongoing voiding dysfunction, recurrent urinary tract infections, and stone disease, but often are asymptomatic or minimally symptomatic and may not require intervention. Although uroflowmetry and PVR cannot determine why voiding or emptying are abnormal (e.g., DU vs. obstruction), they may prompt more thorough evaluation with urodynamics. Thus, we consider uroflowmetry and PVR to be good screening tests for a woman with LUTS. A single elevated PVR should not be considered the sole assessment of bladder emptying ability and should be confirmed with a repeat measurement on a follow-up visit. PVR volume should be interpreted with respect to LUTS, urinary tract infections, and other symptoms.
Urodynamic testing can be an important part of the evaluation of female voiding dysfunction. It should be performed in patients for whom additional information is needed to make an accurate diagnosis and to guide therapy and/or counseling, and in those patients whose condition has the potential to have deleterious and irreversible effects on the upper urinary tract. Urodynamic findings inconsistent with patient symptoms or events occurring during testing that are uncharacteristic for patients during normal activity should be interpreted with caution. This is especially true for uroflowmetry, where it is very important to correlate catheterized uroflow with what is normal or characteristic for the patient. Multichannel urodynamics with simultaneous measurement of vesical and abdominal pressure and “subtracted” detrusor pressure during filling and voiding (see Fig. 34.2 ) is the standard. The filling phase (cystometry) evaluates the ability of the bladder to effectively store urine by assessing bladder stability, compliance, and capacity. Pressure-flow analysis during voiding assesses bladder contractility and bladder outlet resistance. EMG may be added to assess the pelvic floor musculature and external sphincter. Videourodynamics is the addition of simultaneous fluoroscopy during urodynamics, and is particularly helpful in confirming and localizing anatomic or functional obstruction. It can discover an obstruction that would not have been found on the basis of multichannel urodynamics alone. If videourodynamics are not available, then a separate voiding cystourethrogram that examines the bladder, bladder neck, and urethra during voiding can be helpful in localizing obstruction.
The final component of the evaluation is cystourethroscopy, when indicated. Scarring, kinking, or deviation of the urethra, especially after previous surgery, may be responsible for incomplete emptying. Rarely, a urethral lesion responsible for obstruction may be found. Examination of the bladder may uncover a lesion, such as a tumor or stone, and may identify some of the changes associated with obstruction or retention.
Diagnosis and management
Treatment of voiding dysfunction is dictated by several factors. First is the potential danger to the upper urinary tract associated with high storage pressures or urinary retention, which can lead to renal deterioration. Although this is less common in nonneurogenic voiding dysfunction, any evidence of upper tract decompensation (hydronephrosis, renal insufficiency, recurrent pyelonephritis) should be given immediate attention. Second is the degree of bother of the patient’s symptoms. In many cases, empiric therapy is an appropriate first step for patients with symptoms caused by voiding dysfunction. In patients without neurologic disease whose primary complaints are storage symptoms, that is, urgency incontinence without emptying disorder, behavioral modification with pelvic floor muscle exercises or oral pharmacotherapy is effective in relieving overactive bladder symptoms. In cases in which the diagnosis is not clear, or when abnormal emptying and storage coexist, a more comprehensive workup is necessary. When empiric therapy fails, or if voiding dysfunction is associated with neurologic disease, further investigation with urodynamic testing is usually indicated. In these instances, the specific cause for the voiding dysfunction will direct treatment. On the other hand, if a patient presents with an incidental finding of an elevated PVR, no further testing may be necessary. For example, if an asymptomatic woman presents after routine pelvic ultrasound that showed a PVR of 200 mL, there is no compromise of the upper urinary tract, and she remains asymptomatic, further diagnostic studies are usually unnecessary, and monitoring of PVR may be sufficient.
Distinguishing neurogenic from nonneurogenic voiding dysfunction is important. The distinguishing feature is a known neurological disease. In most cases, neurogenic voiding dysfunction is related to either neurogenic DU or acontractility, or functional obstruction from detrusor-sphincter dyssynergia (DSD). Nonneurogenic voiding dysfunction can also be caused by DU or obstruction, which can be functional, as in the case of dysfunctional voiding and primary bladder neck obstruction (PBNO), or anatomic, as in the case of pelvic organ prolapse, urethral stricture, postsurgical obstruction, etc. A complete list of causes for bladder outlet obstruction in women is shown in Table 34.1 .
| Anatomic Obstruction | Functional Obstruction |
|---|---|
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Neurogenic voiding dysfunction
Pathophysiology
A wide range of neurological diseases can affect the complex central and peripheral neural networks that regulate the function of the lower urinary tract, resulting in storage and voiding dysfunction. This can have a profound effect on the urinary system, and the pattern of voiding dysfunction depends on the extent, the evolution, and the site of the neurological dysfunction ( ). The term neurogenic bladder is often used loosely by clinicians to describe a bladder that is not functioning normally. It is critical to be more precise in assessment and classification for diagnostic and therapeutic purposes. Thus, the goals in assessing patients with neurogenic voiding dysfunction are to determine the effects of the neurologic disease on the entire urinary tract in such a way that treatment can be implemented to relieve symptoms and prevent damage to the upper and lower urinary tracts. For the patient with neurologic disease, global symptoms do not always indicate the magnitude to which the disease is affecting the urinary tract.
Pathologic processes at each level of innervation must be considered when evaluating neurogenic voiding dysfunction ( Box 34.1 ). For example, suprapontine lesions (e.g., cerebral atrophy, cerebrovascular accident, brain tumor) cause a loss of inhibitory input to the PMC and subsequent uninhibited bladder contractions, a condition known as neurogenic detrusor overactivity (NDO) when evaluated urodynamically. Sphincter reflexes are not affected and coordinated uninhibited voiding can result.
Suprapontine lesions
Cerebrovascular disease
Parkinson disease
Multiple sclerosis
Concussion
Brain tumor
Shy–Drager syndrome
Normal pressure hydrocephalus
Pontine-sacral spinal cord lesions
Spinovascular disease
Spinal cord injury
Multiple sclerosis
Spinal dysraphism
Tabes dorsalis
Spinal stenosis
Disk herniation
Infrasacral/peripheral lesions
Sacral agenesis
Low spinal cord tumor
Spinal cord injury
Cauda equina syndrome
Diabetes
Herpes zoster
Tabes dorsalis
Radical pelvic surgery
Clinically, interruption of the neural pathways connecting the PMC to the sacral micturition center (e.g., spinal cord injuries or lesions) usually results in NDO and a dyscoordination of the bladder and external sphincter (detrusor sphincter dyssynergia [DSD]). DSD is characterized by simultaneous contractions of the detrusor and external (and sometimes internal) urethral sphincter. The involuntary detrusor contractions cause incontinence, and the involuntary sphincter contractions cause bladder outlet obstruction and retention of urine. DSD is commonly seen in suprasacral spinal cord lesions and multiple sclerosis, and, less commonly, in myelodysplasia and lumbosacral lesions. Untreated DSD can result in high storage pressures (loss of bladder compliance) and resultant vesicoureteral reflux, hydronephrosis, urolithiasis, and urosepsis. Suprasacral spinal cord lesions also result in loss of supraspinal input; however, the complexity of the resulting voiding dysfunction depends on the level and completeness of the lesion. Also, input to the sphincters may be disrupted, resulting in DSD. A complete spinal cord lesion will result in the development of a spinal micturition reflex, in which unmyelinated C-fiber afferents excite sacral neurons and trigger a bladder contraction. In addition, incomplete relaxation of the external sphincter results in a contraction against a closed outlet, with subsequent incontinence, retention, and eventual loss of bladder compliance. When the lesion is above the lower thoracic spinal cord, internal sphincter dyssynergia can also develop as the autonomic neural input to the internal sphincter/bladder neck is disrupted. This can occur with spinal cord injury, lesions, or infarction, as well as with multiple sclerosis that affects the suprasacral spinal cord.
Infrasacral cord and peripheral nerve lesions generally result in loss of sensation and contractility, leading to a large, hypercompliant, areflexic bladder. The external sphincter also may be deficient of contractility and tone. Neurologic lesions that interfere with the sacral reflex arc most often are seen in patients with myelodysplasia, diabetic cystopathy, ruptured discs, or low spinal cord tumors. These diminish reflexive voiding and result in various degrees and combinations of detrusor areflexia, intrinsic urethral sphincter deficiency, and paralysis of the external urethral striated sphincter.
Neurologic lesions can be “complete” or “incomplete”; therefore, the exact manifestations of a particular disease or lesion are not absolutely predictable. A complete urologic evaluation for patients with neurogenic voiding dysfunction is always recommended. A single disease process such as multiple sclerosis can affect multiple areas of the central nervous system. Urologic presentations include detrusor overactivity, detrusor overactivity with DSD, and impaired or absent detrusor contractility. The latter two presentations can result in impaired bladder emptying.
Evaluation
The urodynamic evaluation often is integral to the evaluation of patients with suspected neurologic voiding dysfunction, especially when emptying is incomplete and elevated storage pressures are suspected ( Fig. 34.3 ). Incontinence is a common complaint of these individuals and can be secondary to NDO or decreased compliance. Multichannel urodynamics is key to understanding the underlying pathology. The detrusor leak point pressure (DLPP) is the amount of detrusor pressure, in the absence of an increase in abdominal pressure, required to cause incontinence. It is a direct reflection of the amount of resistance provided by the external sphincter; the higher the resistance, as with DSD, the higher the DLPP. The higher the DLPP, the more likely pressure will be transferred to the upper tract. High storage pressures are potentially dangerous to the upper urinary tract. showed that storage pressures of greater than 40 cm H 2 O are associated with upper tract deterioration in myelomeningocele patients. Although this number should not be taken as a definitive cutoff (it was determined in a very specific population), storage pressures that approach or exceed 40 cm H 2 O should prompt an evaluation of the kidneys for hydronephrosis.
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