Introduction
The primary functions of the urinary bladder are storage and emptying, which are mediated by a combination of parasympathetic, sympathetic, and autonomic signaling (see Chapter 3 ). Bladder compliance is the ability of the bladder to accommodate changes in urinary volume during the storage phase, without a significant change in bladder pressure. Changes in compliance can result in a loss of bladder distensibility during bladder filling, as well as increases in intravesical pressures and/or decreased capacity during this phase.
Bladder compliance is a urodynamic measurement that is calculated by the change in detrusor pressure ( P det ) during the change in bladder volume, and is expressed as ΔV (in mL)/Δ P det (in cm H 2 O) ( ). This can be calculated using a volume/cystometric pressure curve during urodynamic evaluation. Ultrastructural changes within the detrusor muscle, defects in the nervous system, and compromise or changes in bladder anatomy can all contribute to impaired bladder compliance through a loss of viscoelastic properties, replacement of bladder wall constituents by fibrosis, and/or changes in bladder muscle tone. Specifically, studies have demonstrated loss of bladder compliance with deposition of collagen within the extracellular matrix of the bladder as a result of chronic outlet obstruction, as well as radiation, pelvic/bladder injury, and so on ( ). This incites damage on the cellular level, including hypoxia, hypertrophy of myocytes causing thickening of the bladder wall, and decreases in neural density ( ; ). Pathologic conditions associated with impaired bladder compliance include radiation, chronic infection/inflammation including tuberculosis and schistosomiasis, outlet obstruction (urethral stricture, pelvic organ prolapse, benign prostatic hyperplasia, etc.), neurologic conditions (multiple sclerosis [MS], Shy–Drager syndrome, spinal cord injury [SCI], cauda equina), and surgical denervation (abdominoperineal resection, radical hysterectomy) ( ).
Compliance and changes in bladder neurophysiology
Normal bladder storage and emptying occur via a coordinated reflex arc involving the somatic and autonomic nervous systems. The sympathetic nervous system, through stimulation of efferent nerve fibers originating from T10 to L2 via the hypogastric nerve, allows for bladder storage (relaxation of the detrusor muscle and contraction of bladder neck/proximal urethra), while the parasympathetic nerves (S2–S4 efferents) are suppressed. In addition, the somatic efferents stimulate the contraction of the external urethral sphincter via the pudendal nerve, allowing for distensibility of the bladder at low pressures without urinary incontinence/leakage. This system, coupled with the ultrastructure of the bladder (the layers of the bladder wall, including urothelium, lamina propria, smooth muscle, and serosa), allows for bladder filling with low intraluminal pressures. See Chapter 3 for more details.
Disruption of the nervous system and/or bladder structure can result in impaired compliance ( ). SCIs, congenital disorders (i.e., spina bifida, myelomeningocele), vascular disease, diabetes, and demyelinating disorders (i.e., MS) can cause varying levels of neurologic injury, and ultimately neurogenic bladder. Injury to the various nervous systems can cause a disruption in signaling patterns between the bladder and the brain via the pontine micturition center (PMC), which plays a role in inhibition of bladder contractility. A disruption of the PMC can impair the bladder’s ability to fill at low pressures, ultimately decreasing elasticity and bladder compliance. In addition, damage to the sympathetic nerves above the level of T10 results in bladder and sphincter spasticity, increased detrusor tone, and muscle hypertrophy, and contributes to loss of bladder compliance ( ; ).
Types of neurogenic bladder
Several neurologic diseases, including SCIs, spina bifida, MS, Parkinson disease, stroke, and dementia, can result in neurogenic bladder with a variety of characteristic changes in bladder physiology and urodynamic parameters, which are summarized in Table 33.1 .
| Location of Disease | Neurologic Pathology | Bladder Pattern/Dysfunction |
| Brain (pons, cortex, etc.) | Stroke a Parkinson disease Dementia Closed head injury/traumatic brain injury a Frontal lobe lesion Normal pressure hydrocephalus b Multiple sclerosis | Detrusor overactivity ± Pseudodyssynergia ± Impaired contractility |
| Suprasacral (C1–L2) | Spinal cord injury c Tumors, infarction, infection of spinal cord Disc disease Spinal stenosis Tethered cord syndrome | Detrusor overactivity ± Detrusor sphincter dyssynergia |
| Lower lumbar and sacral | Peripheral nerve injury Pelvic plexus injury/trauma d Cauda equina syndrome Myelomeningocele e | Areflexic bladder Impaired contractility |
a Initial insult results in urinary retention with temporary detrusor areflexia, which is replaced with detrusor overactivity with possible impaired contractility in the stable phase.
b Triad of gait disturbances, dementia, and urinary incontinence (additionally urinary frequency, urgency, and nocturnal enuresis). Treatment with neurosurgery consultation for shunt placement.
c Initial phase/spinal shock: detrusor areflexia, flaccid paralysis. Recovery of detrusor activity often coincides with return of reflexes below the level of the lesion.
d Hypogastric nerve injury resulting in incomplete bladder neck closure, pelvic nerve injury causing impaired detrusor contractility, and pudendal nerve injury rendering external sphincter incompetent.
e Areflexic, poorly compliant bladder with high storage pressures because of external sphincter hypertonicity (failure to relax during voiding) and incompetent/open bladder neck.
Detrusor overactivity
Neurogenic detrusor overactivity (DO), sometimes called detrusor hyperreflexia, results in the inability of the bladder to store urine secondary to unsolicited bladder contractions and, over time, can lead to impaired compliance. DO has been attributed to bladder denervation supersensitivity and hypertrophy, which in turn increase the collagen content of the bladder wall, ultimately leading to decreased viscoelasticity and impaired compliance ( ). This is commonly seen in patients with MS, SCI, Parkinson disease, or stroke.
Detrusor areflexia
A bladder pattern seen in SCI, MS, peripheral nerve injury, and occasionally stroke is detrusor areflexia/acontractile and hypocontractility. During the storage/filling phase, this is often associated with a decrease in or lack of sensation/urge to void, in addition to increased storage capacity. Over time this can contribute to impaired bladder compliance, especially when associated with elevated detrusor leak point pressures (DLPPs) and/or storage pressures greater than 40 cm H 2 O.
Detrusor sphincter dyssynergia
Detrusor sphincter dyssynergia (DSD) in SCI and MS is a loss of coordination between the bladder and sphincter during the voiding phase. Normal physiology dictates sphincter relaxation before bladder contraction and micturition; DSD results in an involuntary contraction of the sphincter (periurethral striated external sphincter, and possibly smooth muscle of the internal sphincter) during an involuntary detrusor contraction. This discoordinated contraction should raise concern for risk of increased intravesical pressures causing reflux, urinary tract infection, hydronephrosis, renal failure, etc. ( ).
Intrinsic sphincter deficiency
Intrinsic sphincter deficiency (ISD) results from deinnervation of the external/internal sphincters as the result of a lower motor neuron disorder such as a low-level SCI, spina bifida/myelomeningocele, cauda equina, or peripheral injury ( ). ISD often coexists with an areflexic bladder with impaired compliance, and is best studied with the use of video urodynamics (VUDs) to demonstrate incompetent/open sphincter during filling phases.
Urodynamics and bladder compliance
A standardized definition of bladder compliance has been established by the International Continence Society, which states that “compliance is calculated by dividing the change in volume by the change in detrusor pressure, reported in mL/cm H 2 O” ( ). This value can be calculated through the use of urodynamics, specifically during filling cystometry, and it is recommended that bladder volume and P det be measured at the start of filling and at capacity. Normal bladder compliance is typically defined as greater than 40 mL/cm H 2 O, with the lower limit of normal being 20 to 30 mL/cm H 2 O, and impaired compliance ranging from 1 to 20 mL/cm H 2 O ( ). The criteria for defining impaired compliance are not well established, and have varied widely ( Table 33.2 ). However, studies have demonstrated loss of compliance with transmission to the upper urinary tract at ranges of 5 to 12.5 mL/cm H 2 O ( ; ).
| Reference | Summary of Findings |
| Normal compliance ratio >30.3 cc/cm H 2 O at 100 cc bladder volume | |
| Normal compliance ratio >12.5 cc/cm H 2 O | |
| Normal compliance in nonneurogenic >40 mL/cm H 2 O and >30 mL/cm H 2 O in neurogenic Low compliance (women) <30 mL/cm H 2 O in nonneurogenic and <10 mL/cm H 2 O in neurogenic | |
| Normal compliance 6–10 cm H 2 O | |
| Low compliance 5 cm H 2 O Normal compliance 50 cm H 2 O High compliance 150 cm H 2 O |
During filling cystometry, early increases in P det with increasing volume are seen in abnormal compliance instead of the normal bladder distensibility, yielding low storage pressures throughout the bladder filling phase ( Fig. 33.1 ). Leakage of urine during the filling phase can also reflect a loss of compliance, and is known as the DLPP, which is the P det at which leakage occurs in the absence of both a bladder contraction and an increase in intraabdominal pressure. A DLPP greater than 40 cm H 2 O has been shown to transmit intravesical pressures to upper tracts as vesicoureteral reflux and ureteral dilation. ( ). Impaired compliance can also be seen with sustained bladder contractions, as storage of urine during these contractions occurs at high pressure, and risk of damage to upper urinary tracts should be considered.
Urodynamic findings in neurogenic bladder
The use of contrast urodynamics with fluoroscopy (VUDS) is recommended in patients with neurologic disorders that would place them at high risk for neurogenic bladder, to provide further insight into the anatomical function/dysfunction of the urinary system ( ).
DO appears on the urodynamics study (UDS) tracing as a rise in P det in conjunction with an increase in intravesical pressure and unchanged abdominal pressure. Phasic DO is seen throughout the study, and may or may not be associated with incontinence during this involuntary bladder contraction. Terminal DO is an involuntary detrusor contraction at capacity that results in bladder emptying/incontinence and cannot be suppressed by the patient. DO is typically associated with suprasacral causes of neurogenic bladder.
Detrusor external sphincter dyssynergia (DSD) can be diagnosed with the assistance of electromyography (EMG; via perineal surface electrodes) and fluoroscopy during contractions on VUDS. It is characteristically demonstrated as increased activity of the pelvic floor/sphincter complex via the EMG tracing in conjunction with bladder contractions. In addition, a voiding cystourethrogram can be helpful because in the setting of DSD, it may demonstrate concomitant urethral narrowing during the voiding phase with increased sphincter activity on EMG. DSD may also appear as a dilated proximal urethra and open bladder neck, secondary to an obstructing/contracting sphincter, during the voiding phase ( ).
ISD can be difficult to diagnose on urodynamics because there is no standardized definition. However, ISD may be suspected in cases where maximal urethral closing pressure is less than 25 to 30 cm H 2 O, and/or Valsalva leak point pressure is less than 60 cm H 2 O ( ; ). VUDS may demonstrate “funneling” of the bladder neck during voiding cystourethrogram ( ).
Additionally, in the setting of a neurogenic bladder resulting in the loss of bladder compliance or increased storage pressures, VUDS can aid in the diagnosis of vesicoureteral reflux. If this is identified on VUDS, it is imperative to further evaluate the upper genitourinary tract with renal ultrasound and nuclear renal scan, as well as assess renal function with 24-hour creatinine clearance and serum creatinine.
Patient evaluation
The evaluation for compliance abnormalities and neurogenic bladder should begin with history and physical examination to ascertain the causes of the urinary tract dysfunction ( Box 33.1 ). A careful history can provide insight into possible causes, including prior surgeries, chronic inflammation, anatomic abnormalities, neurologic symptoms, infectious etiology, prior urologic disease, and so on. Physical examination should not only include a complete genitourinary examination, but also focus on patient ambulatory status, manual dexterity, or other neurologic changes such as paresthesias or gait abnormalities. In addition, it is recommended that patients complete self-administered questionnaires that focus on bladder dysfunction and corresponding symptoms, such as the Urogenital Distress Inventory-Short Form and the Incontinence Impact Questionnaire-Short Form. Completion of these questionnaires can aid in establishing baseline symptoms and allow for monitoring of subjective improvement during the treatment period.
History
Sequential progression of urinary symptoms
Neurologic symptoms (vision, gait, coordination, parasthesias, weakness, etc.)
Bowel habits/constipation/fecal incontinence
Sexual history
Prior urologic disease
Diabetes
Thyroid disease
Herpes simplex virus infection
Back pain or disc disease
Pelvic, anorectal, or spinal surgery
Previous therapies, including medications
Physical Examination
Ambulatory status
Manual dexterity
Back: skin or spinal cord anomalies
Abdomen: scars, mass, tenderness
Pelvic and vagina: pelvic organ prolapse, enlarged uterus, pelvic or vaginal mass
Sacral neurologic examination: sensation, perineal reflexes, pelvic floor contraction
Anal sphincter tone and squeeze
Neurologic examination – sensation, motor, deep tendon reflexes
Urinalysis
Postvoid residual
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