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The Role of Urodynamics in Assessing Symptomatic Benign Prostatic Hyperplasia

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For Our Fathers

Ian K. Walsh, MD, FRCS; Anthony R. Stone, MD, FRCS

Symptomatic benign prostatic hyperplasia (BPH) usually represents a combination of voiding and storage symptoms.

•     Relieving bladder outlet obstruction may worsen global symptoms.

•     Symptom scoring systems cannot reliably predict treatment outcome.

•     Uroflowmetry and residual urine measurement cannot quantify bladder storage.

•     Filling cystometry objectively quantifies the storage function of the lower urinary tract.

•     Pressure-flow studies demonstrate and quantify bladder outlet obstruction.

•     Full urodynamic study is mandatory when symptomatic BPH coexists with significant storage symptoms, incontinence,

      neurological disease, repeated episodes of urinary retention or long-term indwelling catheters.

•     In the investigation of symptomatic BPH, urodynamic study of lower urinary tract emptying and storage behavior remains

      the only reliable method for providing accurate functional diagnosis.

Introduction

Benign prostatic hyperplasia predominantly affects men beyond their fifth decade and accounts for approximately 115,000 surgical procedures in the United States alone.1  Symptomatic BPH occurs when microscopic adenomatous and stromal hyperplasia results in macroscopic benign prostatic enlargement, which may cause lower urinary tract symptoms (LUTS).  Lower urinary tract symptoms are further subdivided into voiding (“obstructive”) symptoms such as hesitancy, poor urinary flow and terminal dribbling, and storage (“irritative”) symptoms such as frequency, nocturia, urgency and urge incontinence.  This subclassification of LUTS is important, since the pathophysiology of symptomatic BPH is not merely the result of bladder outlet obstruction, but rather encompasses other factors such as overt or occult detrusor instability and/or impaired detrusor contractility. 

Pathophysiologically, the presence of bladder outlet obstruction (BOO) is initially compensated  for by detrusor hypertrophy.  Over the course of time, pathological deposition of, and replacement of detrusor fibers with collagen occurs.2  In addition to impairing detrusor contractility and reducing bladder compliance, this process may also be associated with denervation hypersensitivity of the bladder’s neuro-musculature, a process which is yet to be accurately defined.2,3  While current approaches to treat symptomatic BPH are directed toward relieving BOO, this may not relieve the oftentimes more bothersome filling LUTS, and may even worsen them.4

The caveat of accurate diagnosis leading to more effective treatment, whether conservative, medical or surgical, is therefore particularly sanguine when applied to the management of symptomatic BPH.  Some methods of diagnosis are, however, complex and suitable only for tertiary referral.  While relatively simple and affordable office investigations may provide useful information, formal urodynamic investigation, commonly perceived as being appropriate only at the tertiary referral level, may play a pivotal role in clinical decision making.5  Absolute and relative indications for urodynamic study in symptomatic BPH are outlined in Tables 1 and 2, respectively.

Symptom Scoring Systems

Table 1. Absolute Indications for Urodynamic Study in Symptomatic Benign Prostatic Hyperplasia

•     Storage symptoms more bothersome than voiding symptoms.

•     History of incontinence.

•     Significant history and/or clinical evidence of neurological disease or injury.

•     Repeated episodes of urinary retention.

•     Longstanding indwelling urinary catheter.

•     Post-void residual urine volume exceeding 500 cc.

Table 2. Relative Indications for Urodynamic Study in Symptomatic Benign Prostatic Hyperplasia

•     Storage symptoms present, although voiding symptoms more troublesome.

•     Presenting complaints at variance with formal symptom score results.

•     Symptom score results at variance with free uroflowmetry.

•     Previous history of bladder outlet surgery.

•     History of diabetes (risk of occult neuropathy).

•     Young patient (<50 years old).

•     Insignificant post-void residual (obstruction unlikely).

      It is impossible to diagnose BOO from symptoms alone.6  Several symptom scoring systems have been devised in an effort to quantify the severity of symptomatic BPH.  The most commonly used system at present is the AUA symptom score, which can classify patients into mild, moderate or severe symptomatic categories.  Men with moderate to severe scores and those with bothersome symptoms usually require therapeutic intervention to provide relief and avoid complications of untreated symptomatic BPH.1  There are, however, correlative issues associated with the AUA score.  Several studies have reported a poor correlation with the results of objective urodynamic study.7,8  Other authors have highlighted the shortcoming that the AUA scoring system is misleadingly weighted towards evaluating voiding LUTS, when, in fact, storage LUTS are the ones that have the most adverse impact upon most patients’ quality of life.9  The addition of bother and quality of life questions to the AUA questionnaire has failed to rectify this inherent weakness.10  Attempts have therefore been made to address the problem by designing symptom scores that evaluate storage LUTS and can correlate well with urodynamic diagnosis in the hope that the questionnaires themselves will indicate the need for further investigation or predict the likely outcome of surgical intervention.  Symptom scoring systems such as the International Continence Society Male and Quality of Life questionnaires and Danish Prostate Symptom Scores are weighted more toward storage symptoms and the global degree of bother.9,11  While these systems are validated and reportedly provide a more clinically applicable assessment of LUTS, the problem remains that the results still fail to correlate well with objective urodynamic findings and cannot, therefore, be considered reliable in predicting treatment outcome.12

Urodynamic Studies
As our understanding of lower urinary tract structure and function continues to evolve, the technology and expertise associated with urodynamic studies (once termed “the neurourologist’s reflex hammer”) have advanced rapidly in concert.  An exhaustive review of recent advances is beyond the scope of this text, but attention will be paid to the urodynamic parameters relevant to quantifying BOO.

Any urodynamic investigation consists essentially of:  1) free-flow rate assessment; 2) measurement of post-void residual urine; 3) filling cystometry; and 4) pressure-flow study.  These should proceed in the order described and each part of the study should be considered an integral part of the investigation,  information provided from each section being collated with all others to give an accurate, objective evaluation of lower tract function.

The Relevance of Urodynamic Studies to the Management of Symptomatic Benign Prostatic Hyperplasia

Free-Flow Rate Assessment
Free-flow rate assessment can be considered an initial tool for evaluating male patients presenting with LUTS, particularly symptomatic BPH.  Uroflowmetry can provide valuable information over symptoms alone in diagnosing the cause of lower tract dysfunction, providing performance statistics for maximum and average flow rate (Qmax and Qave, respectively) with respect to BOO.  This may obviate the need for formal urodynamic study in routine clinical practice.13  Useful information can also be obtained by observing the flow pattern itself—the characteristic bell-shaped curve in the normal male, converting to the prolonged, oscillating trace pathognomonic of BOO or the low amplitude plateau, suggesting urethral stricture.  Free-flow rate assessment is limited, however, by an inability to discriminate between low flow due to BOO or impaired detrusor function.14

Post-Void Residual Urine
Post-void residual urine is usually performed either by catheterization or ultrasonic scanning.  When investigating BOO, a residual urine volume exceeding 100 cc to 150 cc is considered significant.  It must be borne in mind, however, that the presence of residual urine is not caused only by BOO per se and that patients with BOO may present insignificant residual urine because of compensatory mechanisms, such as detrusor hypertrophy or abdominal straining to facilitate bladder emptying.15

Filling Cystometry
The filling cystometry method objectively quantifies the storage function of the lower urinary tract.  Earlier methods employing bladder insufflation with gas have been superseded by infusing isotonic fluids at fill rates ranging from 30 cc/min to 120 cc/min.  Urodynamic parameters provided by this method include subjectively perceived volumes at first sensation of bladder filling, first desire to void, strong desire to void, urgency and maximum cystometric capacity.  These perceived sensations may occur at lower volumes in men with symptomatic BPH for a variety of reasons.  The intravesical intrusion of an enlarged prostate can effectively reduce functional bladder capacity, and in the case of a significantly enlarged middle lobe, trigonal irritation can cause a disturbance of sensory effector mechanisms, predominantly via unmyelinated c-afferent fibers responsive to noxious stimuli.

Filling cystometry also measures detrusor pressures throughout the filling phase.  With longstanding BOO, collagen deposition may restrict the normal receptive relaxation which accommodates bladder filling.  Urodynamically, this reduced bladder compliance is evidenced by a linear increase in detrusor pressure with progressive filling.  If such patients are to proceed to surgical relief of the primary obstructive pathology, they should understand that their storage LUTS may become more predominant postoperatively, perhaps necessitating additional pharmacotherapy with agents such as imipramine or tolterodine postoperatively.

Detrusor instability secondary to BOO is a well-recognized clinical phenomenon.  This is thought to reflect the denervation hypersensitivity secondary to collagen deposition described above.2,3  Loss of  normal excitatory neural input leads to increased coupling between smooth muscle cells, allowing the entire detrusor musculature to behave as an overexcited, autonomous syncytium.  This is represented during the filling phase by phasic rises in detrusor pressure while the patient is attempting to inhibit micturition, which, if severe, may be associated with involuntary urinary leak.  If post-void residual volumes are insignificant and pressure-flow studies (see below) demonstrate efficient voiding, it is reasonable to initiate treatment by dampening bladder overactivity with anticholinergic or antimuscarinic agents such as oxybutinin, tolterodine or dicyclomine hydrochloride.  If ineffective, then bladder outlet surgery is probably indicated, the proviso being that the patient must realize that storage LUTS may worsen in 25% of patients, necessitating long-term pharmacotherapy for symptomatic relief.3

In patients with longstanding BOO, the stage of lower urinary tract decompensation may have already been entered by the time urodynamic studies are performed. Typically, the patient will initially demonstrate poor, low-volume free-flow rate with significant post-void residual.  Cystometry will then reveal late perceived sensations during filling with a flat detrusor trace, and maximum cystometric capacity may approach or exceed 1000 cc.  Little is to be gained in offering such patients bladder outlet surgery.  The overriding pathology by this stage is one of detrusor failure, which is best managed by establishing the patient on a clean intermittent catheterization regimen.

Pressure-Flow Studies
Pressure-flow studies are the final aspect of a complete urodynamic evaluation of lower urinary tract function and the one on which most attention has been focused regarding the investigation of BOO.  An often encountered practical limitation of pressure-flow studies is that many patients are unable to void in the laboratory setting, obviously rendering such study impossible.  If performed, however, this phase of the study provides valuable, clinically applicable information.  The urodynamic parameters of relevance during the voiding phase include maximum urinary flow rate (Qmax); average urinary flow rate; time to reach Qmax and detrusor pressure at various corresponding flow rates, particularly the detrusor pressure at Qmax (PdetQmax).  From such parameters, the degree of BOO can be classified.16 The Abrams-Griffiths nomogram and number (>1.5 = obstruction) classify patients as being either unobstructed, obstructed or equivocally obstructed (Figure 1).  The latter patient grouping has created some confusion and results from either a low-volume void or an inherent inability to accurately classify the borderline patient.  Other authors have focused on measuring linear passive urethral resistance in an attempt to objectively quantify the degree of BOO, results being broadly consistent with the Abrams-Griffiths nomogram.6  The Schafer nomogram both detects the presence of BOO and strictly stratifies its severity (Figure 2).  The difficulty with this method is that “the gray zone” (grade II - III obstruction) still exists and predicting the outcome of bladder outlet surgery may still not be completely reliable.6

Figure 1.

Abrams-Griffiths Nomogram Plot:  Unequivocal Bladder Outlet Obstruction


 

Again, as for free-flow rate, the pattern of voiding is important.  For example, poor or absent detrusor contraction may be augmented by intermittent abdominal straining to facilitate voiding.  Compensatory mechanisms such as these may serve to accomplish voiding, and typically these patients fall into the “equivocally obstructed” category in pressure-flow nomogram classification.  It is unlikely that a patient exhibiting this voiding behavior will respond well to surgery directed towards relieving BOO.   Such a patient is best managed by intermittent self-catheterization, since the problem at this stage is essentially one of secondary detrusor failure.  If the typical obstructed voiding pattern of high-pressure, low-flow dynamics is present, the clinical problem is fairly clear (Figure 3).  Often, however, this pattern is accompanied during the filling phase with evidence of secondary detrusor instability.  Preoperative patient education is all important in this scenario and such patients should be warned that attempts to relieve their BOO may well unmask or worsen their coexistent storage LUTS, perhaps necessitating life-long pharmacotherapy.

Figure 2.  Schafer Nomogram Plot:  Severe Bladder Outlet Obstruction

Figure 3. Pressure-Flow Study in Bladder Outlet Obstruction:  High Detrusor Pressure (pdet) Augmented by Voluntary Abdominal Contraction (pabd) to Generate High Intravesical Voiding Pressure (pves).  Corresponding Flow (Q) is Low and Intermittent.

When Should Urodynamic Studies Be Performed in the

Investigation of Bladder Outlet Obstructions?

This long-debated issue remains largely unresolved.  For patients with straightforward symptomatic BPH whose complaints are clearly of voiding LUTS, it is reasonable to rely upon investigation by symptom scores, free-flow rate assessment and measurement of post-void residual urine.  These evaluations lend themselves very well to the office setting.  After discussing the natural history of BPH, the treatment options of watchful waiting,  a-blockade and bladder outlet surgery can then be discussed with the patient to allow him to make a well-informed decision which should reliably improve his quality of life.1,9

In clinical practice, however, the situation is often not so clearly defined.  The patient with symptomatic BPH who presents with significant storage LUTS, such as urgency, should proceed to full urodynamic investigation.  This may reveal detrusor instability as the primary or secondary cause of symptoms.  Detrusor instability secondary to BOO is not a contraindication for bladder outlet surgery, but if this is associated with demonstrable urge incontinence, the patient should be primarily initiated on antimuscarinic therapy with or without self-catheterization. 

Patients complaining of incontinence against a background of symptomatic BPH should also be studied.  The reason for this is that incontinence coexisting with BOO indicates either:  1) detrusor failure secondary to BOO, which will not respond well to simply relieving the obstruction; 2) detrusor instability secondary to BOO, which should be managed as above; 3) idiopathic detrusor instability masquerading as BOO, which can only be worsened by bladder outlet surgery; or 4) detrusor hyper-reflexia secondary to overt or occult neurological disease.  For the same reasons, young men (<50 years old) with this complaint should also arouse suspicion, since they may harbor previously unsuspected lower urinary tract abnormalities or occult neuropathology. 

Patients with a history of neurological disease or injury, or symptoms/clinical findings suggesting such, are undoubtedly candidates for urodynamic study.  The diagnostic possibilities are legion in this setting, and include neuropathic bladder overactivity; impaired detrusor compliance or dyscoordination of detrusor and sphincter activity; or an acontractile detrusor which empties mainly by overflow.  Outlet surgery in this patient group will serve only to provoke or initiate urinary incontinence. 

Another group of patients who merit further study are those with longstanding symptomatic BPH who have had more than one episode of acute urinary retention.  Further questioning often reveals a long history of BOO, which may suggest chronic urinary  retention.  This should raise the possibility of detrusor decompensation as described above.  A particular patient who should alert suspicion is the one who has suffered one or more episodes of acute urinary retention and presents with a urinary catheter in situ.  The prolonged presence of an indwelling catheter effectively defunctionalizes bladder activity, represented by abnormal perceived sensations during filling cystometry and reduced bladder compliance with a steady, linear rise in detrusor pressure as filling proceeds.  If such a patient proceeds to bladder outlet surgery, the results may be disastrous.  It is best in such a case to facilitate voiding with a combination of self catheterization and a-blockade to relieve obstruction, in the hope that adequate bladder voiding function will return in the course of time.  If not, the patient can then undergo further urodynamic study to accurately categorize his voiding efficiency and thus predict whether relief of obstruction will significantly improve his symptoms and quality of life.

Conclusions
Formal urodynamic study of lower urinary tract function is invaluable when investigating symptomatic BPH.  Patients with symptoms suggesting that obstruction is the overriding primary pathology (absent or minimal storage symptoms) may be adequately investigated with formal symptom scores, free-flow rate and measurement of post-void residual urine.  In clinical practice, however, such patients are not encountered as frequently as previously thought and we would suggest that if the history indicates a significant degree of storage LUTS, urodynamic investigation is warranted prior to initiating treatment, especially invasive therapies.  Clinical suspicion should also be aroused in the young patient or males with urinary incontinence, neurological disease or injury.  Repeated episodes of urinary retention or the presence of a long-term indwelling catheter should also give cause for concern.  Such patients should proceed to a full urodynamic investigation before embarking on treatment.

In the management of symptomatic BPH, accurate diagnosis is of paramount importance if  treatment is to be effective.  Urodynamic study of lower urinary tract storage and emptying behavior remains the only reliable method for providing accurate functional diagnosis and should not be considered suitable only for tertiary referrals.  Whether all men undergoing surgical relief of outlet obstruction should undergo such study is an issue that is still open to debate.

References

1.   McConnell JD, Barry MJ, Bruskewitz RC.  Benign Prostatic Hyperplasia: Diagnosis and Treatment. Quick Reference Guide for Clinicians. Rockville, Md: Agency for Health Policy and Research, US Public Health Service, Department of Health and Human Services; 1994. AHCPR Publication No. 94-0583. 1994.

2.   Devaud CM, Macarak EJ, Kucich U, Ewalt DH, Abrams WR, Howard PS. Molecular analysis of collagens in bladder fibrosis. J Urol. 1998;160: 1518-1527.

3.   Brading AF, Turner WH. The unstable bladder: towards a common mechanism. Br J Urol. 1994; 73:3-8.

4.   Coolsaet B, Blok C. Detrusor properties related to prostatism. Neurourol Urodyn.  1986;5:435-447.

5.   Griffiths DJ. Pressure-flow studies of micturition.  Urol Clin North Am.  1996;23:279-297.

6.   de La Rosette JJ, Witjes WP, Schafer W, et al.  Relationships between lower urinary tract symptoms and bladder outlet obstruction: results from the ICS-“BPH” study. Neurourol Urodyn. 1998;17:99-108.

7.   Nitti VW, Kim Y, Coombs AJ. Correlation of   the AUA symptom index with urodynamics in patients with suspected benign prostate hyperplasia. Neurourol Urodyn.  1994;13:521-529.

8.   Sirls LT, Kirkemo AK, Jay J. Lack of correlation of the American Urological Association symptom 7 index with urodynamic bladder outlet obstruction. Neurourol Urodyn.  1996;15:447-457. 

9.   Hald T, Nordling T, Andersen JT, Bilde T, Meyhoff HH, Walter S. A patient weighted symptom score system in the evaluation of uncomplicated benign prostatic hyperplasia.  Scand J Urol Nephrol.  1991;138:59-62.

10. Abrams P. Benign prostatic hyperplasia. Poorly correlated with symptoms. BMJ.  1993;307:201.

11. Witjes WP, de la Rosette JJ, Donovan JL, et al.  The International Continence Society “benign prostatic hyperplasia” study: international differences in lower urinary tract symptoms and related bother. J Urol.  1997;157:1295-1300.

12. Pannek J, Berges RR, Haupt G, Senge T. Value of the Danish prostate symptom score compared to the AUA symptom score and pressure/flow studies in the preoperative evaluation of men with symptomatic benign prostatic hyperplasia.  Neurourol Urodyn.  1998;17:9-18.

13. Reynard JM, Peters TJ, Lim C, Abrams P. The value of multiple free-flow studies in men with lower urinary tract symptoms. Br J Urol.  1996;77:813-8.

14. Ather MH, Memon A. Uroflowmetry and evaluation of voiding disorders. Tech Urol. 1998;4:111-117.

15. Wu Z, Wu K, Wang B. Clinical significance of residual urine volume in bladder outlet obstruction with benign prostatic hyperplasia.  Chung Hua Wai Ko Tsa Chih.  1997;35:374-376.

16. Bosch JL. Urodynamic effects of various treatment modalities for benign prostatic hyperplasia. J Urol.  1997;158:2034-2044.