Conclusions and future directions
PETER PETROS (*) - MICHAEL SWASH (**)
(*) Royal Perth Hospital, University of Western Australia
(**) Dept of Neurology, The Royal London Hospital, London, UK
INTRODUCTION
The Theory states: "Anorectal dysfunction in the female is mainly caused by lax suspensory ligaments inactivating anorectal
muscle forces".
The aim of Part 2 was to directly challenge the Theory
by repairing specific ligaments, pubourethral only (Study
No. 9), pubourethral and uterosacral (Study No. 10), pubourethral,
uterosacral, ATFP, cardinal, and perineal body
(Study No. 11), and uterosacral and perineal body only
(Study No. 12). We used the pictorial algorithm (Fig. 1)
to guide which zone to repair, anterior, middle or posterior.
Clinical results from Studies 9-12 appeared to validate
these assumptions.
Accurate diagnosis of structural damage
The first step in understanding causation is the appreciation
that all structures work together inextricably as a
system. Though our results indicated that laxity in the pubourethral
and/or uterosacral ligaments appeared to be the
main cause of the idiopathic fecal incontinence, these cannot
be the only causes. It is theoretically possible for any of the
structures in Fig. 1, red lettering, to contribute to the genesis
of fecal incontinence. All these structures work synergistically,
and each structure may contribute a different weight to
the system. The varying size of each bar (Fig. 1), expresses
this variation pictorially.
Though external anal sphincter damage was specifically
excluded from this study, it needs to be diagnosed and
repaired where present. The EAS has a key role in our
theory. With reference to Fig. 1, EAS is a tensor of the perineal
body, and the inferior insertion point of the downward
rotating muscle force 'LMA' (arrow). Inability to tension
the perineal body may invalidate backward stretching of the
posterior vaginal wall by LP (backward arrow), with similar
consequences to those reported in Study No. 12.
One consequence of the theory is that there has to be a
critical mass below which a severely damaged muscle will
not have sufficient contractile force to effect organ closure.
Even tenotomy muscles can atrophy to a point of no return.
Severe muscle damage may explain the lower cure rate in
Study No. 10, which we consider was the worse affected
group. At present we have no method for diagnosing severe
muscle damage.
Surgery
One biomechanical consequence of our theory, which has
surgical implications, is that the ligaments and fascia require
a critical length and tension for optimal muscle contraction.
The advent of the TFS provides a tool which can, for the
1st time, restore tension as part of the ligament/fascia reconstruction.
The results of Study No11 are encouraging, but
far more data will be required to fully assess the effects of
surgical tensioning on restoration of function.
Finally there is the consequence of operating on damaged
tissues. Study No 10 reports instances where repair of
one ligament may divert the pelvic forces to stretch another
(subclinically damaged) ligament to cause de novo symptoms.
For this reason, it may be prudent to consider routinely
repairing both the pubourethral and uterosacral ligaments
and in patients with idiopathic fecal incontinence, and the
uterosacral ligaments, perineal body and rectovaginal fascia
in patients with 'obstructed defecation'.
Correspondence to:
Prof. Peter Petros,
E-mail: kvinno@highway1.com.au