Dr. DARREN M. GOLD(*)
(*) Senior Lecturer and Colorectal Surgeon St Vincent's Hospital and Clinical School, UNSW Darlinghurst, Sydney Australia
Editorial Note
A number of experts have been invited to submit a commentary on this issue of the journal. Space permits us to publish only one commentary in conjunction with the papers of Petros et al., and this commentary was chosen because it was the first to be completed and returned. More commentaries will be printed in the next issue. Others are invited and will also be considered for publication. The editors of Pelviperineology see this as a wonderful opportunity to open up discussion of anorectal function to the general pelvic floor community. Please consider this opportunity to contribute to the discussion by submitting correspondence for publication.
Invited Comment
Some years ago in an attempt to obtain the Holy Grail
of every medic, the perfect golf swing, I found myself
seduced into buying a set of instructional videos by a small
town American golf instructor, Dalton McRary, who had
by various observations of still images of golfers of yesteryear,
where shutter speeds were not fast enough to prevent
motion blur, come to the conclusion that much of the perceived
and taught theory regarding the golf swing was in
fact incorrect. He based his system for the golf swing on
these observations.1
More importantly in the introduction
booklet to the videos he asks the reader to make a small
mental leap of faith. He asked that although he did not necessarily
expect the reader to automatically believe everything
they were about to read and see, he asked them to
open their minds to the possibility that it may be true. In
other words to give the hypotheses a chance before closing
ones mind to the fact that they went against the currently
accepted wisdom. It was with this in mind that I read the
work by Petros and Swash.
Our understanding of pelvic floor function, at least in
colorectal circles is that the main cause of incontinence and
other disorders is due to a lack of muscle power. Whether
this is due to damaged muscles, damaged innervation or
lack of muscle bulk, it is thought that it is an inherent lack of
contractile strength that contributes to the dysfunction. This
approach is confirmed by the current treatment rationales
to help restore function, namely, muscle repair, sacral nerve
stimulation and biofeedback. The decision as to which mode
of treatment to use is based on the commonly performed
investigations of anorectal physiology, pudendal nerve terminal
motor latency recordings and anal ultrasound to gauge
respectively, muscle power, nerve conduction and muscle
damage.
It would appear that the initial observation made by the
authors, that prompted much of this work was the finding
that the vast majority of patients with concomitant urinary and faecal incontinence treated with a mid-urethral slingplasty
were not only cured of their urinary symptoms but
also their faecal symptoms. No attempt had been made to
correct the muscles themselves. This observation clearly set
the authors thinking about a possible mechanism for such an
outcome and to rethink the current understanding of pelvic
floor function.
The authors have therefore presented the reader with a
new concept of anorectal function they have called "The
Musculoelastic Theory". This concept is supported by the
presentation of 12 papers which act to support the original
concept, support each other and bring together observations
made by other authors in previously published works. The
various presented works involve individual case reports,
which must obviously be taken on their individual merit
only, along with small and large clinical series involving
surgical repair, histological evaluations and radiological
studies.
The basic tenet of The Musculo-Elastic Theory is that
although faecal incontinence is in part contributed to by
muscle damage or nerve conduction abnormalities, it can to
a greater degree be explained by damage to, and weakening
of the ligamentous attachments of the pelvic floor musculature,
which if corrected surgically can produce a significant
improvement in symptoms, without necessarily having
to directly address the actual muscles or nerves themselves.
It is not entirely unreasonable to assume that taut, appropriately
directioned ligamentous attachments are fundamental
to good muscle function. We have all heard the patient who
is convinced her pelvic troubles all started after her hysterectomy.
Theoretically the theory has much to support it. The pelvic
floor muscles are somewhat unique in that they represent a
group of skeletal muscles, under voluntary as well as reflex
control that although arising from bone insert directly into
the soft tissues upon which they act. For the majority of
muscles in the body which connect to bone at their origin as
well as insertion, it is rare that they become stretched and
lax to the point that they are unable to function as intended.
With lack of use, or focal damage these bone oriented muscles
may atrophy and weaken, but as they tend to maintain
their original length can be re-strengthened with physiotherapy
and exercise.
How does a totally snapped hamstring
in an Olympic athlete ever function normally again? When
skeletal muscle inserts into soft tissue only, it is plausible
that when overstretched or torn, especially if this involves
ligamentous damage at the origin, that as normal length
cannot easily be restored that power and function will be
compromised. It is not hard to imagine how such stretching
and damage can occur during pregnancy and childbirth. This
may help to explain why the platysma, with no bony attachments
is such a giveaway to our real age.
There is some evidence to support this. Krochmal et al
studied muscle recovery following tenotomy and reinsertion
of skeletal muscle in rats, by varying the length of the
reinserted tendon.2 In those muscles where the tendon was
shortened, producing greater tension on the muscle fibres,
greater muscle mass, greater muscle length, greater physiological cross-sectional area, greater maximum isometric
force, and greater maximum power relative to the control
tendon length group was achieved. Admittedly the nerve
was left intact but it is difficult to argue with the results. Furthermore,
the other experimental group in this study, where
the tendon was lengthened thereby inducing some laxity did
not necessarily lose contractile power. It would however
have reduced the degree of movement in the related joint.
Our basic understanding of muscle physiology at undergraduate
level should also allow us to accept this without
too much difficulty.
We also know from the work by Malouf et al that external
sphincter repair although producing good initial results has
a significant rate of attrition.3 More interestingly, Malouf
noted that other defaecatory disorders became apparent after
such repair. Can we deduce a possible explanation for this
from the work of Petros and Swash. Perhaps the initial
overlap recreated tension in the muscle to allow an initial
improvement, but as it does not address the main ligamentous
bony attachments of the pelvic floor musculature, is
only short lived. Perhaps the tension produced initially also
has a distracting affect on other pelvic ligaments against
their normal direction of activity thereby producing other
defaecatory effects. Does sacral nerve stimulation work only
by neuromodulation? Does it have some of its effect by
increasing the resting tension of the muscle fibres. Maybe.
I don't know, I'm only guessing. But the whole concept of
a musculoelastic contribution to incontinence will produce
many more questions.
Do we need to re-evaluate our pre-treatment investigations?
Is sphincter physiology really valid? Is identification
of muscle damage a good means for surgical selection? What
does pudendal nerve conduction really tell us? Should all patients with pelvic floor dysfunction of any kind undergo
proctography? Should urodynamics be part of anorectal
investigation? How can we quantify musculoelastic function?
Which are the important ligaments for each disorder?
How can we repair/strengthen them? Should we change our
approach to rectal prolapse?
The list is endless.
I am sure that the authors will agree that works such
as this are rarely the final solution. There are aspects of
the work that may need further consideration. The use of
Poiseuille's formula only applies to laminar flow of an
incompressible liquid through a circular tube of constant
proportions. Its application in helping to explain continence
in a narrowed rectum may not be relevant. That's
not to say that retensioning the rectum doesn't help incontinence.
It's just that it is unlikely to be explained by mere
physics. The papers do however contain much to think
about and will stimulate a huge amount of further study
and research. As readers, if minds are kept open, the pelvic
floor community has been thrown a fertile seed from which
I am sure much will grow.