INTRODUCTION
Although the lower uterine segment usually heals well after Caesarean
section (CS), any loss of muscle during the repair, which can be
substantial even after one CS, leads to niche formation (1). Niche
formation has been linked to a number of modifiable surgical factors
including single layer closure and use of locking sutures. Both niche
prevalence and depth increase with number of CS, prevalence rising from
62% after one to 78% after three CS depending on method of evaluation
(2). The nearer the scar is to the level of the internal os the higher
the likelihood of a niche and the larger the defect (2). Niche
development may be accompanied by formation of new vascular connections
within the scar area, which along with in-migration of a variety of
inflammatory cells contributes to healing (3).
During future pregnancies the niche has the potential to become an
isthmocele leading to complications including uterine rupture and
placenta accreta spectrum disorders (PASD). As the niche deepens, the
residual myometrial thickness (RMT) gets less, with the RMT further
thinning during pregnancy as the niche widens. The longer and deeper the
initial scar area, the larger the decrease in RMT seen in pregnancy and
the larger the resultant defect (4). The likelihood of developing
complications in future pregnancy is related to the RMT, as it reflects
the amount of muscle remaining. An RMT of less than 2mm carries a
significant risk of scar rupture (5).
The frequency of PASD has markedly increased over the last few years
because of the increased Caesarean section rate. The risk is higher when
placenta praevia complicates a pregnancy following previous CS,
especially if the primary indication mandated a higher uterine scar, and
rises with each subsequent CS (6). Historically treatment options
centred round intentional retention of the placenta (IRP) with or
without hysterectomy but latterly several techniques have been developed
aimed at conserving the uterus including the Triple P (7) and Naussica
(8) procedures.
Recent evidence of PASD being a
disorder of defective decidua and uterine dehiscence rather than
destructive trophoblastic invasion (9) suggests that a conservative
approach with effective manual removal of placenta, when combined with
peri-operative prophylactic haemostatic measures can be an optimal
approach.
We have previously described a technique (Siraj et al) for repair of the
myometrial defect or isthmocele at the site of the previous scar at the
time of repeat Cesarean section (10). The repair increases the RMT and
reinforces the posterior uterine wall which is often thin in these
cases. We now describe how this technique can be extended for use in
cases of suspected PASD with focus on control of the major hemorrhage,
in part due to the neovascularization around the scar which can be
offered as an alternative to peripartum hysterectomy in women who
request uterine conservation. This approach has the added advantage of
offering opportunity to reconstitute the uterine wall by contemporaneous
correction of the niche, potentially allowing future pregnancy and
avoiding other niche-related complications.