Bladder Emptying: Contractility

where V t = volume of noncontracting bladder wall tissue [7].

Although some studies report WF and WFmax, no consensus has been made regarding normative values particularly in female patients [6, 8, 9]. A WFmax of <12 μW/mm2 for males and <5 μW/mm2 for postmenopausal females has been used in some studies to define detrusor underactivity [8, 10, 11]. Use of WF may not be suitable for practical use due to complexity of the calculation, poor reproducibility, and lack of standardized cutoff values [6, 8].

Schafer simplified the approach to classify contractile strength based on relationship of detrusor pressure and urine flow rates in men with bladder outlet obstruction [1, 12]. Bladder contractility index (BCI) is based on detrusor pressure at maximum flow rate (P det @ Q max) and maximum flow rate (Q max):

$$ \mathrm{B}\mathrm{C}\mathrm{I}={P}_{det}@\kern0.24em {Q}_{max}+5{Q}_{max} $$

In men, BCI > 150 suggests strong contractility; BCI 100–150 suggests normal contractility and BCI < 100 suggests weak contractility [1, 3].

To address the limitation that BCI was based on men with BOO, Tan modified the BCI calculation and proposed a new formula of contraction strength for elderly women (mean age 70.1 years) with urge incontinence, known as the projected isovolumetric detrusor pressure (PIP) [2]:

$$ \mathrm{P}\mathrm{I}\mathrm{P}={P}_{det}@\kern0.24em {Q}_{max}+{Q}_{max}. $$
With this modified formula, normal contractility in this cohort was defined as PIP = 30–75 [2].

The relationship between detrusor contractility and urine flow in the form of a pressure versus flow rate (p/Q) plot can be helpful in the understanding of detrusor function and outflow obstruction [12]. In efforts to better clarify this relationship, further calculations such as passive urethral resistance relation (PURR), linear PURR, detrusor-adjusted mean PURR factor (DAMPF) have been proposed and can be helpful in the assessment of patients with outflow obstruction taking into account their detrusor contractility which could otherwise be overlooked [12].

Detrusor Underactivity

Detrusor underactivity is defined by the ICS as “detrusor contraction of reduced strength and/or duration, resulting in prolonged bladder emptying within a normal time span” [13]. It is unclear if bladder contractility diminishes with age, though the most recent data suggests that this may indeed be the case [1418]. What is clear is that merely the presence of a weak detrusor contraction during voiding itself may not lead to a diagnosis of detrusor underactivity, since the definition implies some sequelae occur (altered or prolonged voiding) as a result of this urodynamic finding. Both myogenic failure and bladder wall ischemia have been proposed as underlying pathophysiological mechanisms responsible for detrusor underactivity [17, 1921].

Causes and predisposing factors of detrusor underactivity include medications, psychogenic factors, neurologic conditions, end-stage BOO, extensive pelvic surgery, or idiopathic. Urodynamic studies are helpful to diagnosis detrusor underactivity and rule out other causes of voiding dysfunction [17]. Urodynamically, detrusor underactivity is commonly found in a low pressure/low flow state. It also may be diagnosed mistakenly in women who void primarily by urethral relaxation, in which case urinary flow rates may be normal, voiding is not prolonged, and as a result underactivity cannot be truly diagnosed even in the setting of a weak detrusor contraction. In a similar way, a weak detrusor contraction may be associated with intrinsic sphincteric deficiency (ISD) with both men and women, though the presence of relatively normal voiding in these instances argues against the diagnosis of detrusor underactivity, which implies an insufficient contraction. Again, it is important to stress that the urodynamic finding of a minimally contracting detrusor muscle may have no clinical relevance, particularly in women, who void efficiently and effectively by urethral relaxation or have chronically reduced outlet resistance due to ISD. Post-prostatectomy incontinence with compromised bladder outlet is another common situation where a relative detrusor underactivity occurs, in the absence voiding dysfunction or other sequelae.

Clinical scenario 1 (Fig. 16.1 ):


Fig. 16.1
Urodynamic tracing of urethral relaxation in a female. Note decreased EMG activity during voiding. Permission to void denoted by red arrow

Urethral relaxation

A 69-year-old female with recurrent urinary tract infections but no bladder storage or emptying complaints. Her PVR is zero. Cystoscopy is unremarkable. She has no prior history of urologic pelvic surgery or neurological disease. Her urodynamics are interesting because the PFS demonstrates urethral relaxation. Note the decrease abdominal pressure and the lack of significant rise in either P ves or P det . Despite an apparent P det Q max of only 13 cm H 2 O (actual P det value may be even lower due to drop in P abd ), she completely empties her bladder by urethral relaxation, voiding 651 mL, with a maximum flow rate of 27 mL/s and normal bell-shaped flow curve. This is due to urethral relaxation at the time of voiding—as detected by the diminished sphincteric activity noted on EMG monitoring.

Clinical scenario 2 (Fig. 16.2 ):


Fig. 16.2
Urodynamic tracing demonstrating low pressure voiding in a female with SUI. Note the presence of a compromised outlet due to SUI can result in lower voiding pressure. Stress urinary incontinence denoted by black arrows. Permission to void denoted by red arrow

Reduced outlet resistance, low pressure voiding in woman with SUI

A 62-year-old female with symptomatic stress urinary incontinence. She reports voiding with a normal flow. She is noted to have SUI on her study at 114 mL with differential VLPP of approximately 39 cm denoted by first two arrows. The low VLPP is consistent with intrinsic sphincter dysfunction. Bladder compliance is normal and there was no evidence of detrusor overactivity. Her MCC was 251 mL.

During the PFS, the detrusor contraction is relatively weak, but adequate to allow her to empty her bladder to completion with a bimodal flow curve (Q max 15 mL/s). The presence of a compromised bladder outlet has been associated with both lower valsalva leak point pressure (VLPP) and voiding pressures in women with SUI.

The quality of the UDS is good. A cough at the end of the study confirmed catheters were in appropriate position with adequate zeroing. Her voided volume was not marked on the tracing.

Clinical scenario 3 (Fig. 16.3 ):


Fig. 16.3
Urodynamic tracing of a female with sensation of difficulty urinating due to detrusor underactivity. Permission to void denoted by red arrow

Detrusor underactivity/Crede voiding

An 82-year-old female with recurrent UTIs, urinary frequency and sensation of difficulty emptying her bladder. First sensation is at 176 mL. No stress incontinence was seen with cough or Valsalva maneuver. MCC is 365 mL. Compliance is normal. No detrusor overactivity is noted. On pressure-flow component of study, the patient was noted to apply external pressure to her suprapubic region, or crede, to assist with voiding. She voids with a prolonged stream to completion without a residual volume, and a notably weak detrusor contraction.

EMG shows appropriate relaxation as voiding starts though increased EMG activity during void may reflect straining. In this case, due to the presence of abnormal voiding, the term detrusor underactivity should be applied.

The quality of this urodynamic tracing is fair. After permission to void (denoted by red arrow), a subtle rise in the P abd is noted with crede maneuver which is also reflected in P ves tracing. Q max of 21 mL/s is not representative of her flow curve as she does a crede maneuver to achieve that reading. Average flow rate is considerably lower and more representative of her altered voiding function.

Clinical scenario 4 (Fig. 16.4 ):


Fig. 16.4
Urodynamic tracing of a male who is 4 years post-radical prostatectomy with incomplete bladder emptying and elevated residual. The BCI is <100 consistent with detrusor underactivity. Permission to void given twice, and noted with increases in both abdominal and vesical catheters and corresponding small volume voids

Idiopathic detrusor underactivity following radical prostatectomy

A 71-year-old man underwent a radical prostatectomy 4 years prior to the study. His PSA is still undetectable. He complains of a weak prolonged stream, urinary frequency, nocturia (3/night), and sensation of incomplete emptying over the past year. Cystoscopy was unremarkable. First sensation occurred at 103 mL. He experiences strong urge at 201 mL but is ultimately able to attain a normal MCC of 348 mL.

P det does not rise substantially with his void, and a prolonged flow curve is noted. Q max is 10 mL/s with P det Q max of 14 cm H 2 O. His BCI (P det Q max+ 5(Q max ) is 64 (<100) which represents detrusor underactivity. He also was catheterized for 90 ml at the end of the study.

The quality of this tracing is fair. At the beginning of the study, P det is below zero, which is physically implausible. Vesical and rectal catheter position should be assessed to insure accuracy in situations such as this. Often the catheters may be against the wall of the bladder or rectum and instilling more fluid (or releasing) in the rectal balloon or initiating bladder filling will move the pressure detector from the luminal wall and correct the problem. Prior to voiding, there are corresponding increases of P ves and P abd which represent patient movement and hiccups. It is important to annotate the study with findings such as this to facilitate interpretation.

Clinical scenario 5 (Fig. 16.5 ):


Fig. 16.5
Urodynamic tracing of a male with post-prostatectomy incontinence and relative detrusor hypocontractility. Similar to women with SUI, a compromised bladder outlet in a male can also be associated with low voiding pressures. Stress urinary incontinence denoted by black arrow. Permission to void denoted by red arrow

Relative detrusor underactivity associated with sphincteric deficiency in man status-post radical prostatectomy.

A 68-year-old man 3 years out from radical retropubic prostatectomy is noted to have three pads per day leakage. Otherwise, he feels well, has had no bladder infections, and voids with a strong stream. In this urodynamic study, there is a reasonable bladder capacity (360 mL), an absence of detrusor overactivity during filling, stress incontinence (noted at first arrow), and a relatively weak detrusor contraction supplemented by straining. Since he empties to completion, and in the absence of a prolonged flow, this finding would not be consistent with the term “detrusor underactivity” but rather represents a reduced detrusor contraction, possibly related to loss of outlet resistance over time.

Treatments for Detrusor Underactivity

A limited understanding of causes and a dearth of effective treatments for detrusor underactivity suggests that further innovative research and treatment strategies are warranted [22]. Optimization of voiding in patients with detrusor underactivity is attempted by avoiding/treating constipation, discontinuing/limiting medications that can impact detrusor contractility, such as narcotics and medications with anticholinergic properties, and aggressive ambulation. Bethanechol and other parasympathomimetic agents have shown limited efficacy in clinical trials, and thus their use is largely discouraged [23, 24]. TURP in men with detrusor underactivity is controversial with lower success rates compared to those without detrusor underactivity, but may have a role in select patients by reducing outflow resistance or undiagnosed BOO after careful preoperative counseling [2426]. Intermittent catheterization and indwelling catheterization are the remaining options for those with a symptomatic impaired bladder emptying secondary to underactivity.

Acontractile Detrusor

An acontractile detrusor is defined as “the detrusor cannot be observed to contract during urodynamic studies resulting in prolonged bladder emptying and/or a failure to achieve complete bladder emptying within a normal time span [13].” Detrusor acontractility may be a more severe form of detrusor underactivity, and is thought to be caused by the similar underlying pathophysiologic mechanisms in many instances. Neurogenic causes (i.e., sacral cord injury), fixed chronic obstruction (prolonged untreated benign prostatic growth), and functional causes (non-neurogenic neurogenic bladder/Hinman syndrome, non-relaxing pelvic floor) may all be associated with detrusor acontractility. As with detrusor underactivity, detrusor acontractility can be transient or permanent depending on the clinical circumstance. Also, the terminology implies not only to the finding of absent detrusor contraction, but to a resultant impact on voiding as well. In certain clinical scenarios, such as voiding by urethral relaxation, the detrusor contraction may be absent, but voiding remains normal.

Treatments for Detrusor Acontractility

The acontractile detrusor is typically managed by intermittent or indwelling catheterization (urethral or suprapubic), especially if due to a transient cause [27]. In cases of persistent detrusor acontractility, sacral neuromodulation (for non-obstructive causes), intravesical electrostimulation, latissimus dorsi detrusor myoplasty, or continent catheterizable channels have been utilized in differing clinical scenarios [27, 28].

Clinical scenario 6 (Fig. 16.6 ):


Fig. 16.6
Urodynamic tracing of a female with an acontractile detrusor and inability to void. Permission to void denoted by red arrow. Pressure transducers adjusted at this point

Acontractile detrusor in a female

A 26-year-old female presents with complaints of bladder fullness without a typical desire/urge to void. She has noticed that if she tries to urinate the stream only dribbles and may take her several attempts to empty her bladder. She noticed that the stream has worsened with time over the course of 6–8 months. She has also had an increasing number of UTIs. She denies having a known neurological diagnosis but on further questioning reveals that she has experienced some visual changes, and occasional numbness and tingling in her left upper extremity. She has had no prior pregnancy, surgery, or neurological evaluation.

She was subsequently scheduled for urodynamics which revealed delayed first sensation (537 mL) and MCC of 733 mL. No incontinence was observed during filling. Despite having large MCC and desire, with permission, to void (at red arrow), she did not mount any detrusor contraction. An increase in vesical pressure is noted through this long filling curve suggestive of somewhat altered compliance. Given that this occurs over a volume of over 700 mL, the impact of this pressure change can be mitigated by an appropriate catheterization schedule. Urodynamic catheters were removed after the patient was unable to void with reasonable attempts of urination. After the catheter was removed, she only urinated 11 mL.

She has an acontractile bladder on UDS. The differential diagnosis of her acontractile bladder includes an undiagnosed neurologic condition, medication, or idiopathic causes such as Fowler’s syndrome. She has been taught and will perform intermittent catheterization to empty her bladder. A neurological investigation revealed demyelinating lesions on CT suggesting multiple sclerosis.

This tracing is relatively poor quality as it is not perfectly zeroed, movement artifact is present, and the side scale has not been recalibrated to show the entire volume of fluid instilled. Since the patient could not void with the catheter in place a PFS could not be performed. However, detrusor acontractility is diagnosed during her attempt to void.

Clinical Scenario 7 (Fig. 16.7 )


Fig. 16.7
Urodynamic tracing in an elderly male with large capacity bladder, delayed bladder sensation, and inability to urinate. Note no significant increase in detrusor pressure during voiding attempt. Permission to void denoted by red arrow

Acontractile detrusor in elderly male

A 72-year-old male with chronic history of difficulty voiding and post-void dribbling, which was never treated. Noted to have PVR of 650 mL. Urodynamic study shows large bladder capacity, delayed desire to void, a stable bladder during filling, normal compliance, and detrusor acontractility on attempt to void.

Abnormal Detrusor Contractility

Clinical Scenario 8 (Fig. 16.8 )


Fig. 16.8
Urodynamic tracing of a male with post-prostatectomy incontinence and low voiding detrusor pressure. Note the sustained detrusor contraction after he urinates. Permission to void denoted by red arrow. After contraction denoted by black arrow

Detrusor after contraction

A 59-year-old man with post-prostatectomy incontinence. In this urodynamic study, note the sustained detrusor contraction after he urinates, denoted by second arrow. The detrusor after contractions may be an expression of sphincter contraction interrupting an incomplete detrusor contraction. It has been reported mostly in connection with urge incontinence and urge symptoms.

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Jun 20, 2017 | Posted by in UROLOGY | Comments Off on Bladder Emptying: Contractility

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