Section-1
A Cesarean scar defect (CSD), also referred to as an isthmocele or niche, is a pouch-like defect
in the lower uterine segment at the site of a previous Cesarean section. The reported rate of
CSD varies greatly (24% to 88%) in women with a previous Cesarean section, highlighting the
variability in diagnosis and imaging approaches [1] [2]. Many women are asymptomatic with
respect to the CSD, however, it can present with abnormal uterine bleeding, pelvic pain, and
secondary infertility [1] [2]. CSD is an increasingly relevant topic in reproductive medicine due
to the increasing global prevalence of cesarean section and the need to understand the
pathophysiological mechanisms that lead to CSD, as well as its clinical consequences on fertility,
for better diagnostics, management, and prevention.
CSD is defined as a hypoechoic or anechoic triangular or semicircular defect in the myometrium
at the site of a healed cesarean incision; although a CSD will usually be identified on a
transvaginal ultrasound or hysterosonography [3]. A CSD may present as a niche (a shallow
indentation) or a diverticulum (a deep pouch extending towards the bladder). These defects
may occur due to incomplete healing of the myometrium leading to fibrotic remodeling, which
can be affected by surgical technique, method of closure of the uterus, and healing conditions
after delivery [4] [5]. Clinically, CSD is associated with a variety of expressions that include
abnormal bleeding, pelvic pain, and even infertility [6].
CSD has been strongly associated with chronic endometritis (CE), which is a persistent
inflammatory state of the endometrium that compromises the uterine microenvironment.
Symptomatic CSDs, particularly those with postmenstrual spotting, have been found to have
significantly higher rates of CE compared to asymptomatic CSDs [7]. Infiltration by inflammatory
cells can alter normal endometrial receptivity, reducing implantation potential and clinical
pregnancy rates [2]. There is preliminary evidence to suggest that treating CE in women with
CSD with antibiotics improves early pregnancy performance demonstrating a modifiable
mechanism.
The pouch-like nature of a cerebrospinal device (CSD) may serve as a repository for menstrual
blood, which can lead to hydrometra—an abnormal accumulation of serosanguinous fluid in
the uterine cavity [1] [8]. This retained fluid not only has the potential to inhibit sperm travels,
alter endometrial pH, and bulk release inflammatory factors that are unfavorable for embryo
survival, but hydrometra has also been associated with lower implantation rates in both natural
conception and assisted reproductive technology (ART) settings.
Successful implantation requires a coordinated and receptive endometrium. CSD can disrupt
this normal process due to prolonged inflammation, altered vascularity, retained blood or fluid,
etc. [7] [2]. In addition to ongoing physiologic processes affecting implantation, scarring can
also have structural consequences, such as localized fibrosis and remodeling of tissues at the
location of the previous scar, where gene expression changes may modify or influence
Aboriginal patterns skewed for implantation, such as adhesion molecules and cytokines [7].
These structural and biochemical changes may make successful implantation less likely,
particularly in symptomatic patients.
Decidualization is the progesterone-functional change of endometrial stromal cells for embryo
implantation and placentation. CSD may obstruct decidualization by also converting normal
myometrial and stromal tissue into fibrotic poorly vascularized scar tissue, and it has been
demonstrated in histopathological studies that CSD sites have fewer myometrial cells with
some examples of endometriosis, both of which impact decidual transformation [9] [10].
Deficient decidualization can result in implantation failure or subsequent pregnancy loss.
CSD is an underrecognized but still relatively meaningful contributor to secondary infertility.
CSD actions are through chronic inflammation, hydrometra, and impaired endometrial
receptivity in addition to deficient decidualization [1] [2] [7] [8] [9] [10]. Detecting and directly
treating CSD can help to improve reproductive outcomes regardless of when the tissue was
available for treatment. As Cesarean delivery becomes more prominent, CSD should be
assessed and directly managed or treated whenever possible in the overall management of
reproductive health development protocols.
References
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aged Women. J Minim Invasive Gynecol. 2016 Sep-Oct;23(6):893-902. doi:
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