Fig. 12.1
(a) Calculating compliance. A = 495 ml/3 cm H2O A = 165 ml/cm H2O (b) Calculating Compliance. B = 400 ml/62 cm H2O B = 6.5 ml/cm H2O
When analyzing compliance on an urodynamic tracing, the International Continence Society (ICS) recommends choosing two standard points for comparison: “the detrusor pressure at the start of bladder filling and the corresponding bladder volume (usually zero), and the detrusor pressure (and corresponding bladder volume) at cystometric capacity or immediately before the start of any detrusor contraction that causes significant leakage (and therefore causes the bladder volume to decrease, affecting compliance calculation). Both points are measured excluding any detrusor contraction” [1].
Low bladder compliance is consistent with an abnormal increase in detrusor pressure between these two given points. Over the past few decades there have been several studies attempting to define “normal compliance.” Unfortunately, however, there has never been an agreed upon absolute value for bladder compliance. Topercer and Tetreault [2] attempted to define abnormal compliance in their 1979 study comparing asymptomatic women to women with stress urinary incontinence, but could not establish a definitive value due to the lack of a data pattern among study participants. Weld et al. [3] found that there was a significant change in the risk of upper tract damage between compliance values of 12.5 and 15 cc/cm H2O, and thus recommended using a cut-off value of 12.5 cc/cm H2O to define abnormal compliance. However, Churchill et al. [4, 5] define abnormal compliance as greater than 10 cc/cm H2O.
While there are various measurements used to define abnormal compliance, it is widely agreed upon that a sustained bladder pressure of greater than 40 cm H2O can cause significant risk to the upper tracts [6]. It is also thought that the amount of time that the bladder experiences high pressures is directly proportional to the risk of upper tract deterioration [4]. Thus, a patient whose urodynamic tracing demonstrates a sustained tonic elevation in detrusor storage pressure appears to be more at risk for upper tract complications (see case #1) than a patient who has intermittent, phasic rises in detrusor pressure that return to baseline (see case #7).
Sustained pathologic increases of detrusor pressure which can cause upper tract complications can be measured in two ways. First, consistently high abnormal storage pressures should be approached with caution and may signify upper tract risk [7]. The absolute value of sustained pressure elevation during filling is not standardized, but clinicians should be wary of sustained filling pressures exceeding 25 cm H2O. Second, a widely agreed upon measurement assessing upper tract risk is the detrusor leak point pressure (DLPP). It is defined as the lowest detrusor pressure at which urine leakage occurs in the absence of either a detrusor contraction or increased abdominal pressure [1]. Studies have shown that a sustained Pdet greater than 40 cm H2O is consistent with upper tract deterioration [6].
Many pathologic conditions can result in abnormal compliance. For example, decreased bladder compliance can result from neurogenic causes like multi-system atrophy (MSA), spina bifida, spinal cord injury (SCI), or iatrogenic causes such as resultant nerve damage from pelvic surgery, such as radical hysterectomy or abdominoperineal resection (APR). Other non-neurogenic causes can include bladder outlet obstruction (BOO), chronic cystitis, or a defunctionalized bladder [8, 9].
The measurement of compliance may be misleading in the presence of anatomic variations which may result in a buffering of intraluminal detrusor pressure. In cases such as vesicoureteral reflux or bladder diverticuli in the setting of a poorly compliant bladder, the detrusor pressure may appear falsely low due to a “pressure sink” effect. In these cases, the urine storage pressure is actually being dissipated into the expanding bladder diverticulum or refluxing upper tracts. These are clinical scenarios in which videourodynamics can provide invaluable information [7]. In addition, in severe intrinsic sphincter deficiency, the bladder storage pressures may appear low as a result of urethral loss or urethral leakage. In these cases urethral occlusion is necessary to determine the filling properties of the bladder.
Detrusor overactivity (DO) is an urodynamic observation characterized by involuntary detrusor contractions (IDC) during the filling phase which may be spontaneous or provoked. Phasic DO is defined by a characteristic waveform and may or may not lead to urinary incontinence [1]. Phasic IDC generally have shorter periods of pressure elevations with a return to baseline. Sustained involuntary detrusor pressure elevation caused by continuous bladder tension reflects a tonic increase in bladder pressure. This is indicative of low compliance. Phasic detrusor overactivity can sometimes be misleading and confused for abnormal compliance as well. This can especially occur if it is prolonged and of low amplitude. To differentiate between an IDC and abnormal compliance during filling, simply stop the infusion. If the Pdet returns to baseline, then the rise in Pdet is due to an IDC; if the Pdet remains elevated, then the rise in Pdet is due to a compliance abnormality [8].
This chapter will present urodynamic tracings and discuss the differential diagnosis, clinical interpretation, and treatment options for each given condition with regards to abnormal compliance (Fig. 12.1a, b).
Case Scenarios
Case #1
A 47-year-old male with a 10-year history of transverse myelitis presents with a chief complaint of persistent urinary leakage despite performing clean intermittent catheterization (CIC). He has been catheterizing three times a day for the last 10 years and has been managed with a daily extended release anticholinergic. His urodynamic tracing, shown below in Fig. 12.2, demonstrates an abnormal constant increase in detrusor pressure during the filling phase. This persistent elevation in Pdet can be characterized as a tonic abnormality of filling, representing abnormal compliance. During the filling phase, the patient also demonstrates an early sensation abnormality, followed by superimposed IDC with leakage. The DLPP is 36 cm H2O. While 36 cm H2O is borderline, one can infer that this patient is at higher risk for long-term upper tract deterioration based on the sustained, tonic compliance abnormality as well as further sustained rise in detrusor storage pressure. With the patient’s clinical history and urodynamic tracing, a renal ultrasound would certainly be warranted to establish a baseline and evaluate for hydronephrosis. Initially, treatment options for this patient could include increasing the frequency of CIC as well as increasing anticholinergic therapy as tolerated. The rate-limiting dosage for anticholinergic therapy would be determined by tolerable side effects including dry mouth, constipation, and heat intolerance, most commonly. After a trial of a more aggressive CIC and anticholinergic regimen, further treatment options would include onabotulinum-toxinA injection or even possibly augmentation cystoplasty (Fig. 12.2).
Fig. 12.2
Transverse myelitis. Filling phase
Case #2
A 57-year-old male underwent a laparoscopic proctosigmoidectomy for colon cancer, and, subsequently, developed a neurogenic bladder. His urodynamic tracing in Fig. 12.3 demonstrates a tonic increase in detrusor pressure throughout the filling/storage phase, as with case #1. Neurogenic bladder can develop as a result of a denervation injury during many colorectal, urologic, and gynecologic procedures. Most commonly, neurogenic bladders are seen as a result of APR.
Fig. 12.3
Neurogenic bladder after a laparoscopic proctosigmoidectomy
The fluoroscopic images above in Fig. 12.4 demonstrate the utility of videourodynamic studies. Without imaging, this patient’s Pdet falsely appears much lower than it actually is. When a patient develops poor bladder compliance, due to a decrease in the native viscoelastic properties of the bladder, the intrinsic detrusor pressure can be transmitted to the upper tracts as a “pop-off” type mechanism. This is best demonstrated by videourodynamics to delineate vesicoureteral reflux or bladder diverticuli. This patient’s imaging combined with cystoscopy demonstrates a posterior bladder diverticulum as well as a left hutch diverticulum with grade IV vesicoureteral reflux. The voiding phase of the study is consistent with detrusor areflexia. In this setting of iatrogenic neurogenic bladder, treatment options again include an increase in CIC frequency and anticholinergic therapy, onabotulinum-toxinA injection or an augmentation cystoplasty.
