0022-5347/03/1693-1011/0

THE JOURNAL OF UROLOGY

Copyright 2003 by AMERICAN UROLOGICAL ASSOCIATION

Vol. 169, 10111012, March 2003

Printed in U.S.A.

DOI: 10.1097/01.ju.0000051323.18096.53

EDITORIAL: BLADDER FAILUREA CONDITION TO RECKON WITH

The 2 preceding articles in this issue of The Journal come
from research groups that are seeking better ways to diagnose urethral obstruction, yet significantly their common
theme is not urethral obstruction but detrusor contractility.
McIntosh et al (page 1003) demonstrate by invasive measurements that the detrusor contraction is not inhibited by
mechanically interrupting the flow. Kranse and van Mastrigt
(page 1007) argue that weak detrusor contraction is a factor
contributing to incomplete bladder emptying. Inability to
empty completely because of inadequate contraction implies
bladder failure as the organ continues to pump but inadequately.
Incomplete bladder emptying is a hidden condition that
does not usually lead directly to complaints but is common,
especially in the elderly in whom it contributes to urinary
frequency and overflow incontinence, and complicates the
management of coexistent urge incontinence.1 Ultrastructural studies in the elderly have shown that incomplete emptying, for long believed to be a sign of obstruction, is linked to
degeneration of the muscle and nerve cells of the detrusor,2
and can occur just as often in women (without obstruction) as
in men.
REASONS FOR INCOMPLETE BLADDER EMPTYING

In most cases bladder emptying is a balance between the

contraction of the detrusor and the resistance of the urethra.
If the detrusor contraction is too weak, the stream will be
slow and the bladder may not be completely emptied. If
emptying is not complete, a premature fading away of the
detrusor contraction is nearly always to blame.3 Kranse and
Van Mastrigt confirm, by an ingenious argument, that weak
detrusor contraction and increased urethral resistance (obstruction) contribute to post-void residual urine. Other recent work supports this conclusion by showing directly that
low values of the so-called detrusor reserve, a numerical
expression of the balance between detrusor contraction
strength and urethral resistance, predict post-void residual
urine.4 Simply expressed, urethral obstruction and detrusor
weakness may lead to a slow stream and residual urine. They
can be distinguished urodynamically by the value of detrusor
pressure. A slow stream with high pressure implies obstruction and a slow stream with low or normal pressure implies
a weak detrusor contraction.
MEASUREMENT OF DETRUSOR CONTRACTION STRENGTH

How to measure detrusor contraction strength has been

the subject of a lively debate. The actual pressure generated
during voiding obviously has some relation to the contraction
strength but it has limitations. When flow is occurring some
of the strength of the contraction is used to generate the flow,
and the pressure is lower than it would be otherwise.5 Two
approaches have been tried. 1) If flow is prevented by blocking the urethra, the detrusor pressure generated (isovolumetric pressure) is a measure of the full contraction strength.
2) The contraction strength can be estimated by calculations
based on the detrusor pressure and the flow rate during
voiding. Care must be taken to use well-founded methods of
calculation5 and a simple nomogram6 or coefficient7 may be
adequate.
McIntosh et al use the first approach. It is already known
that interruption of the flow by mechanically blocking the
urethra gives reliable and consistent estimates of the contraction strength in men8 and women.7 Their new study

reinforces the foundations of this method by showing that the

contraction strength does not change during mechanical interruption, and so one is not trying to hit a moving target. On
the other hand, interruption of flow by voluntarily contracting the sphincter gives less reliable and quite different results,8, 9 presumably because simultaneous reflex inhibition
of the detrusor changes the contraction strength and prevents the full isovolumetric pressure from being attained.9
Kranse and van Mastrigt take the second approach, avoiding the practical disadvantage of having to interrupt voiding
by a mechanical device. From the methods available5 they
choose a sophisticated way of calculating contraction
strength from flow rate and detrusor pressure. It would have
been useful to know if simpler methods led to similar results
but there is no reason to doubt their conclusion that weak
detrusor contraction is associated with post-void residual
urine, especially as it is supported by others.4
THE SPECIFIC AIMS OF THE AUTHORS

The authors objectives are tangential to the theme of this

editorial. Ultimately, McIntosh et al aim to develop a noninvasive method of measuring detrusor contraction strength.
For symptomatic male patients with a slow free flow rate the
isovolumetric pressure would be measured noninvasively. If
high, obstruction would be diagnosed and if low, detrusor
weakness would be diagnosed. McIntosh et al use an external, noninvasive penile cuff to interrupt the flow, combined
with invasive pressure measurements to determine the effect
on the bladder.
A long-term aim of Kranse and van Mastrigt is to perfect
the urodynamic assessment of obstruction. They show that of
the several obstruction or resistance parameters available, 1
particular parameter is best able to predict residual urine.
This is a novel and interesting way of ranking the various
obstruction parameters, which in many other ways are
rather similar.10
BLADDER FAILURE

Detrusor contraction strength tends to decrease11 and

post-void residual urine tends to increase with age. Therefore, bladder failure, the condition in which the bladder is
unable to empty completely because of a failure of the detrusor to contract adequately, is especially common in old age. It
may coexist with urethral obstruction or it may exist independently. It has an anatomical (degenerative) substrate and
can be identified by urodynamic measurements. It complicates the management of coexistent conditions such as urge
incontinence. No good treatment is available, as cholinergic
agonists are usually ineffective and intermittent catheterization is usually unattractive. New therapeutic approaches are
required, for example, new drugs to improve the contraction
of existing detrusor muscle cells, or perhaps implantation of
stem cells to repair the degenerative process. The possibility
of bladder failure has been under-recognized because of a
fixation on urethral obstruction. It is time that this condition
receives serious attention.

1011

Derek J. Griffiths
Division of Geriatric Medicine
University of Pittsburgh
Montefiore Hospital
Pittsburgh, Pennsylvania

1012

BLADDER FAILURE
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