Review Article

Review of Intrauterine Adhesions

Rebecca Deans, MBBS, MRANZCOG,
and Jason Abbott, B MED (Hons), MRCOG, FRANZCOG, PhD*
From the Department of Gynaecology, Royal Hospital for Women, and School of Women’s and Children’s Health, University of New South Wales, Randwick,
New South Wales, Australia.

ABSTRACT This article has been produced to review the literature on symptomatic and asymptomatic intrauterine adhesions. Electronic re-
sources including Medline, PubMed, CINAHL, The Cochrane Library (including the Cochrane Database of Systematic Reviews),
Current Contents, and EMBASE were searched using the Medical Subject Headings (MeSH), including all subheadings, and the
keywords ‘‘Asherman syndrome,’’ ‘‘Hysteroscopic lysis of adhesions,’’ ‘‘Hysteroscopic synechiolysis,’’ ‘‘Hysteroscopy and ad-
hesion,’’ ‘‘Intrauterine adhesions,’’ ‘‘Intrauterine septum and synechiae,’’ and ‘‘Obstetric outcomes after intrauterine surgery.’’
The vast majority of evidence in the literature consists of uncontrolled case series, with only intrauterine adhesion barriers being
assessed in a randomized controlled format. This article reviews epidemiology, pathologic features, classification systems, and
treatments. Seven classification systems are described, with no universal acceptance of any one system and no validation of
any of them. Hysteroscopy is the mainstay of both diagnosis and treatment, with medical treatments having no role in manage-
ment. There is a wide range of treatment techniques with no controlled comparative studies, and assessments are descriptive and
report fertility and menstrual outcomes, with more severe adhesions having the worst clinical outcomes. One of the most important
features of treatment is prevention of recurrence, with the best available evidence demonstrating that newly developed adhesion
barriers such as hyaluronic acid show promise for preventing new adhesions. Journal of Minimally Invasive Gynecology (2010)
17, 555–569 Crown Copyright Ó 2010 Published by Elsevier Inc. on behalf of the AAGL. All rights reserved.
Keywords: Asherman syndrome; Hysteroscopic treatment of adhesions; Hysteroscopic synechiolysis; Hysteroscopy; Intrauterine adhesions

Recognition that organic intrauterine adhesions can lead to
secondary amenorrhea has been demonstrated since the end of
the 19th century [1], although not until 1948, when Joseph
Asherman described the eponymous condition in 29 patients,
did the syndrome became popularized and treatment de-
scribed. Asherman’s original description related to postpreg-
nancy intrauterine adhesions in all cases, and such adhesions
remain the commonest cause of this syndrome. Asherman
expanded his original thoughts, and related endometrial
trauma and adhesion formation to menstrual disturbance,
cyclical pelvic pain, and subfertility including recurrent preg-
nancy loss [2]. Important in his description was that the adhe-
sions seemed to have an inherent effect on the endometrium,
The authors have no commercial, proprietary, or financial interest in the
products or companies described in this article.
Corresponding author: Jason Abbott, MB, BS, Royal Hospital for Women,
University of New South Wales, Barker St, Randwick, 2031 New South
Wales, Australia.
E-mail: j.abbott@unsw.edu.au
Submitted December 18, 2009. Accepted for publication April 30, 2010.
Available at www.sciencedirect.com and www.jmig.org
1553-4650/$ - see front matter Crown Copyright Ó 2010 Published by Elsevier Inc. on behalf of the AAGL. All rights reserved.
doi:10.1016/j.jmig.2010.04.016
causing it to be quiescent, rather than the adhesions causing
clinical effect merely by obstruction.
The terms ‘‘Asherman syndrome’’ and ‘‘intrauterine adhe-
sions’’ are often used interchangeably, although the syndrome
requires the constellation of signs and symptoms (e.g., pain
and menstrual disturbance) in the presence of intrauterine ad-
hesions. When the signs and symptoms are present in women
with intrauterine adhesions not caused by pregnancy, the term
‘‘Asherman syndrome’’ should be applied, despite this being
outside of the original description [3]. Given these conditions,
the diagnosis of Asherman syndrome can be made in women
with a uterus during their reproductive lifetime, whereas the
diagnosis of intrauterine adhesions can be made in women
with a uterus at any time during their life.
It is important to differentiate intentional intrauterine adhe-
sions such as those produced from endometrial ablation in any
of its various forms as treatment of dysfunctional uterine
bleeding to intrauterine adhesions that come to clinical atten-
tion because of symptoms. Intentionally induced intrauterine
adhesions and asymptomatic intrauterine adhesions do not
require any treatment and are not considered further in this
review except when comparative data may be necessary.
556
Data Sources
This review was produced by searching electronic resources
including Medline, PubMed, CINAHL, The Cochrane Library
(including the Cochrane Database of Systematic Reviews),
Current Contents, and EMBASE. The Medical Subject
Headings (MeSH) included all subheadings, and keywords
included ‘‘Asherman syndrome,’’ ‘‘Hysteroscopic lysis of
adhesions,’’ ‘‘Hysteroscopic synechiolysis,’’ ‘‘Hysteroscopy
and adhesions,’’ ‘‘Intrauterine adhesions,’’ ‘‘Intrauterine sep-
tum and synechiae,’’ and ‘‘Obstetric outcomes after intrauter-
ine surgery.’’
Epidemiology
The true incidence of intrauterine adhesions is unknown
because a large number of patients with intrauterine adhesions
have no symptoms [3]. The prevalence varies with geographic
location, the population being studied, and the availability of
investigations for diagnosis. Most early reports were summa-
rized in a 1982 review by Schenker and Margalioth [4], and
suggested geographic variations in intrauterine adhesions,
with increased awareness, differences in instrumentation
(sharp, blunt, or suction curettage), presence of genital tuber-
culosis, and availability of therapeutic termination of preg-
nancy cited as possible causes [3].
Such variations have not been reported in the last 20 years,
with prevalence varying between 0.3% as an incidental find-
ing in women undergoing intrauterine device placement with-
out gynecologic symptoms to 21.5% in women who have
undergone postpartum curettage [4]. It is possible that greater
recognition of the condition and the more widespread use of
hysteroscopy and noninvasive means of diagnosis such as
sonography have caused an increase in the diagnosis of intra-
uterine adhesions [5]. From 1894 to 1982, there were 1250
cases reported for treatment of intrauterine adhesions, and
from 1982 to 2008, more than 2500 cases have been reported
in the literature. Performance of both a greater number and
increasingly complex uterine surgical procedures in an
expanding world population may be contributing to a higher
number of reported cases, which may not necessarily repre-
sent a true increase in prevalence.
Histopathologic Features
Asherman syndrome causes endometrial fibrosis in which
the stroma is largely replaced with fibrous tissue and the glands
are replaced by inactive cubocolumnar endometrial epithe-
lium. The functional and basal layers are indistinguishable,
with the functional layer replaced by an epithelial monolayer
unresponsive to hormonal stimulation, and fibrotic synechiae
forming across the cavity [6]. The tissue is usually avascular,
although thin-walled telangiectatic vessels can be observed.
Calcification or ossification can occur in the stroma, and the
glands may be sparse and inactive or cystically dilated [6].
The resulting intrauterine adhesions may involve different
layers of the endometrium, myometrium, or connective tissue.
Journal of Minimally Invasive Gynecology, Vol 17, No 5, September/October 2010
When full thickness, adhesions may be composed of collagen
bundles, fibrous strips, or muscle with the same characteristics
as normal myometrium [6]. Biopsy specimens from patients
with intrauterine adhesions compared with patients without
intrauterine adhesions contain 50% to 80% of fibrous tissue
compared with 13% to 20% in the uterine wall [7].
Samples of endometrium from women with Asherman
syndrome are similar in appearance to those after induced
intrauterine adhesions, such as after transcervical resection
of the endometrium [8]. Histologically, the endometrium
appears atrophic with increased connective tissue despite
being in a nonaffected part of the uterus. This explains in
part the apparent lack of hematometra found clinically despite
the apparent blockage to the cervical os. These pathologic
findings are different from Asherman’s initial proposal of
a neurovascular reflex between the cervical os and the endo-
metrial lining leading to amenorrhea. However, Asherman
did recognize a relative lack of hematometra despite obstruc-
tion of the cervical os. The mechanism may be different, but
the result is the same: an atrophic and inert endometrial lining.
Etiology
Any event that causes damage to the endometrium may
lead to development of intrauterine adhesions. There is often
a definable causative event on an unknown predisposing
background. The major cause of intrauterine adhesions is
damage to the basilar layer of the endometrium after curet-
tage. Pregnancy is certainly important; a review of 1856
women with intrauterine adhesions demonstrated that 67%
had undergone curettage because of induced or spontaneous
abortion, and 22% because of postpartum hemorrhage [4].
In the only class I study to examine the etiology of intrauterine
adhesions, 82 women were randomized to undergo either sur-
gical or nonsurgical management of incomplete miscarriage
[9]. At hysteroscopy 6 months after treatment, no intrauterine
adhesions were observed in women treated conservatively or
medically; however, 2 of 26 of women in the surgical group
(7.7%) had intrauterine adhesions. This is the first methodo-
logically sound evidence suggesting that uterine instrumenta-
tion is likely a predisposing factor in intrauterine adhesions.
While trauma to the nonpregnant uterus can also cause
intrauterine adhesions, the risk is lower, with rates of intra-
uterine adhesions estimated to be 1.6% after diagnostic curet-
tage, 1.3% after abdominal myomectomy, 0.5% after cervical
biopsy or polypectomy, and 0.2% after insertion of and intra-
uterine device (IUD) [4]. It is possible that newer endometrial
biopsy methods and hysteroscopic and laparoscopic
myomectomy may have reduced these rates further, although
data are not available.
Recurrent miscarriage is often associated with intrauterine
adhesions, with adhesions reported in 5% to 39% of women
with this problem [10–14]. It is uncertain whether these
intrauterine adhesions are a cause or consequence of the
recurrent abortions. Changes to the vascularization of
the endometrium have been demonstrated using pelvic
Deans and Abbott. Review of Intrauterine Adhesions
angiography, with a marked reduction in myometrial vascular
flow and even vascular occlusion in patients with
hypomenorrhea and amenorrhea [15]. Such changes may
have an effect on implantation, with a hypotrophic endome-
trium being unreceptive to an embryo, and the same conditions
may predispose to development of intrauterine adhesions.
Postpartum curettage resulted in the first reported case of
secondary amenorrhea due to intrauterine adhesions [1]. In-
strumental interventions performed between the 2nd and
4th postpartum weeks seem to result in more frequent and
severe intrauterine adhesions [4]. The risk of developing
intrauterine adhesions postpartum is high, affecting 21.5%
to 40.0% of women requiring uterine instrumentation
[4,16–18]. Curettage in the first 48 hours postpartum seems
to be less conducive to adhesion formation [19] suggesting
that endoganous estrogen levels have a major role. Postpar-
tum hemorrhage is a risk factor for intrauterine adhesions,
with an early report noting an incidence of intrauterine adhe-
sions of 9% [20]. Contributing factors include postpartum
uterine instrumentation or fibrosed retained products of con-
ception that may have caused the postpartum hemorrhage.
Surgical treatment of a silent miscarriage (missed abortion)
has been reported to lead to 31% of intrauterine adhesions
compared to an incomplete miscarriage, in which only about
6.4% of women are likely to develop intrauterine adhesions
[4]. This difference is likely due to the retained products in a si-
lent miscarriage causing greater fibroblastic effect before en-
dometrial regeneration can occur. Curettage after evacuation
of a hydatidiform mole is an uncommon cause of intrauterine
adhesions, with an incidence of 0.6% to 3% [4,21]. Possible
reasons for the lower rate may include underreporting,
molar tissue being less adhesiogenic or fibroblastic than
placental tissue, or the elevated estradiol or b-human
chorionic gonadotropin in molar pregnancy being protective
against the development of intrauterine adhesions.
Patients undergoing repeat curettage because of miscar-
riage have an increased incidence of intrauterine adhesions,
as high as 39% [10,13]. The number of procedures
performed seems proportional to the frequency and severity
of the intrauterine adhesions. In 1993, Friedler et al [22]
reported a 16% incidence of intrauterine adhesions found at
diagnostic hysteroscopy after curettage after a single miscar-
riage, with adhesions being thin and filmy and occupying less
than a third of the uterine cavity, whereas after 2 or 3 surgical
terminations of pregnancy, the incidence was 14% and 32%,
respectively, and the area of cavity affected increased to 58%.
A single class II study indicated that resective hystero-
scopic surgery predisposes to intrauterine adhesions. In that
study, the frequency of postsurgical intrauterine adhesions
was 6.7% after resection of uterine septa, 31.3% after resec-
tion of a single myoma, and 45.5% after resection of multiple
myomas [23]. Abdominal surgery involving the uterus has
also been implicated in the formation of intrauterine adhe-
sions. The risk of intrauterine adhesions after cesarean
delivery is estimated to be 2% [4], and after laparotomy
and full-thickness myomectomy is 1.3% [4].
557
Rare causes of intrauterine adhesions include genital
tuberculosis, with the condition first described in 1956 [24].
Tuberculous adhesions characteristically respond poorly to
intervention, with a poor prognosis for future fertility [3,4].
Pelvic irradiation is thought to be responsible for 0.05% of
cases in a large series [4]; however, this figure may be in-
creasing because of more widespread used of radiotherapy
to treat malignant disease of the pelvis. To date, there has
been only 1 reported case of Asherman syndrome after bilat-
eral uterine artery embolization [25], and another case has
been described after severe postpartum hemorrhage [26].
The contribution of infection to the development of
intrauterine adhesions is controversial [11,21]. Some
authors have stated that the findings of peritubal adhesions,
histologically evident endometritis, and bacterial isolation
in cases of Asherman syndrome support the role of
infection as a predisposing factor [12]. Opposing views
have suggested that bacterial pathogens are rarely isolated,
and the finding of inflammatory cells, degenerative products,
and tissue edema at histologic analysis of endometrial cells in
patients with intrauterine adhesions are not different com-
pared with patients without intrauterine adhesions [27]. Endo-
metritis after caesarean section is not reported to increase the
risk of intrauterine adhesions compared with cesarean deliv-
ery without infection [28], and the American Fertility Society
states that dilation and curettage in the setting of endometritis
has a nonsignificant effect on adhesion formation [29]. While
the evidence for infection contributing to the condition is lim-
ited, it seems reasonable that the postinfectious inflammatory
process could exacerbate traumatic endometrial damage
[30,31] and should be considered in the pathogenesis and
subsequent treatment of Asherman syndrome.
Clinical Manifestations
Menstrual abnormalities are the most common symptom in
patients with Asherman syndrome. Of 2981 patients with in-
trauterine adhesions, 1102 (37%) reported amenorrhea, 924
(31%) reported hypomenorrhea, only 30 (1%) reported men-
orrhagia, and 179 (5%) reported normal menses [4]. The orig-
inal theory from Asherman for altered menses with cervical
adhesions was a neurovascular reflex that inhibited the
endometrium from normal hormonal response [2]. Subse-
quently, cases with cervical obstruction, hematometra, and
hematosalpinx were reported [24], and it is apparent that there
is a variance in manifestation of Asherman syndrome.
Hypomenorrhea is likely due to endometrial damage, with
the severity and location of adhesions correlated with the de-
gree of hypomenorrhea [13]. The residual endometrium may
become atrophic due to decreased uterine perfusion and
limited hormonal circulation locally [11], causing myome-
trial fibrosis, which is significantly increased in women
with intrauterine adhesions [7].
Pelvic pain from intrauterine adhesions is commonly cyclic
and associated with menstrual dysfunction. Pain is usually
associated with decreased or absent menstrual flow. The
558
mechanism may be due to outflow obstruction with backflow
into the fallopian tubes, creating hematosalpinx and retrograde
menstruation, or as a result of pockets of residual endometrium
responding to hormonal stimuli, with no route for egress [11].
Secondary infertility is a common initial symptom, with 1
large-scale review reporting this in 922 of 2151 patients with
intrauterine adhesions (43%) [4]. Subfertility may be due to
obstruction of sperm into the cervix or prevention of embryo
migration within the uterine cavity. Endometrial insuffi-
ciency may prevent implantation of the blastocyst [32]. As
with menstrual disturbance, the degree of symptoms does
not necessarily relate to the intrauterine disease, and it is
reported that women with eumenorrhea with subfertility are
more likely to have Asherman syndrome compared with their
fertile counterparts [33]. There is a high incidence of recur-
rent miscarriage, and its presence should alert the clinician
to consider the diagnosis of intrauterine adhesions. Defective
vascularization at the level of the denuded endometrium
inhibits effective implantation, leading to an occlusion of
blood supply to the uterus and early fetus [28].
Diagnosis
Because clinical examination usually fails to reveal abnor-
malities [20,24], other methods of investigation are necessary
for diagnosis. Sounding the uterus may reveal cervical
obstruction [24].
Hysteroscopy
Hysteroscopy is now established as the criterion standard
for diagnosis of intrauterine adhesions [34]. Compared with
radiologic investigations, hysteroscopy more accurately con-
firms the presence, extent, and degree of adhesions and the
quality of the endometrium. It provides a real-time view of
the cavity, enabling accurate description of the location and
degree of adhesions, classification, and concurrent treatment
of intrauterine adhesions [35]. At hysteroscopy, superficial ad-
hesions may have the same appearance as the adjacent endo-
metrium, fibrous or myometrial bands appear white and are
dense, and endometrial fibrosis appears as pale patches.
Fig. 1 shows the appearance of an intrauterine adhesion as
seen at hysteroscopy.
Office hysteroscopy is useful for both diagnosis and
second-look follow-up after treatment of intrauterine adhe-
sions. It is a well tolerated, less expensive, and convenient
alternative to inpatient hysteroscopy [36], although dense
adhesions may not be amenable to in-office treatment. Office
hysteroscopy and treatment of mild adhesions have been
reported to increase clinical pregnancy rates in women with
recurrent failure of in vitro fertilization [37].
Hysterosalpingography
Hysterosalpingography (HSG) is the historical method of
diagnosis of intrauterine adhesions [35]. It requires no
anesthesia, can be performed in an ambulatory setting, and
Journal of Minimally Invasive Gynecology, Vol 17, No 5, September/October 2010
Fig. 1. Note thick intrauterine adhesion (arrow) from front to back uterine
walls in the mid-cavity.
can enable diagnosis of tubal patency [3]. Filling defects
can be characterized by an irregular and angulated form
with sharp contours and homogeneous opacity, and are repro-
ducible [38]. In the case of severe and extensive lesions,
intravascular and intralymphatic extravasations may also be
observed. When complete occlusion occurs, HSG will fail
to show any contrast medium filling of the uterine cavity
[3]. Compared with hysteroscopy for diagnosis of intrauter-
ine adhesions, sensitivity of HSG is 75% to 81%; specificity,
80%; and positive predictive value, 50% [39,40]. The high
false-positive rate (%38%) [41] is a limiting factor.
Transvaginal Ultrasound
Transvaginal ultrasound (US) is inexpensive, noninvasive,
and a readily available procedure that can aid in the diagnosis
of intrauterine adhesions [42,43]. Hyperechoic areas within the
endometrium are characteristic. In widespread endometrial
destruction from intrauterine adhesions, the endometrial
echo may be difficult to visualize, with irregular thickness
or interruptions in the lining at the sites of fibrosis.
Echolucent areas with interruption of the endometrium (skip
lesions) may represent localized menstrual blood in areas in
which functional endometrium is preserved [3]. Overall, the
diagnostic ability of transvaginal US alone is poor, with sen-
sitivity of 52% and specificity of 11% compared with sono-
hystography and hysteroscopy [44]. The preoperative
endometrial thickness observed at transvaginal US may pro-
vide information for posttreatment prognosis. Patients with
thin preoperative endometrium are reported to have a poorer
response to surgical treatment than those with normal appear-
ing endometrium above an obstruction. This reflects severity
of intrauterine adhesions, and is in accord with surgical out-
comes [3,43]. Three-dimensional US may be more helpful
in evaluation of intrauterine adhesions, with sensitivity
Deans and Abbott. Review of Intrauterine Adhesions
reported to be 87%, and specificity of 45% compared with
3-dimensional sonohystography [45].
Sonohysterography or saline solution infusion sonohys-
terography (SHG/SIS) may be used to diagnose intrauterine
adhesions if there is at least 1 echogenic area between the an-
terior and posterior walls or if cavity distention is impeded
from tethering of the uterine walls by synechiae. This method
was as effective as HSG in a number of studies, with both
reported to have a sensitivity of 75%; positive predictive
value was 43% for SHG/SIS, and 50% for HSG, compared
with hysteroscopy [40,44]. Similar to HSG, SHG/SIS has
a high false-positive rate, and is best used as a screening
test for intrauterine adhesions, but can be used to assess
tubal patency. Three-dimensional sonohysterography has
the added advantage of estimating the volume of the endome-
trial cavity, which is decreased in the presence of intrauterine
adhesions [46,47].
Magnetic Resonance Imaging
Magnetic resonance imaging has been reported in the
diagnosis of intrauterine adhesions [48,49], although its
expense, limited availability, and unknown sensitivity as
a diagnostic method should necessarily limit its use to
research at this time. It may be useful in diagnosing
cervical adhesions causing obstruction when the upper
uterus, including endometrial remnants, can be assessed
[50]. At this time, intrauterine adhesion signal characteristics
have not been examined in detail, and it is anticipated that ad-
hesions would produce low signal intensity on T2-weighted
images [50].
Classification
Hysteroscopy is required for accurate classification of
Asherman syndrome [11]. Radiography and HSG have
been used to classify intrauterine adhesions [34], although
not considered standard practice. Classification of intrauter-
ine adhesions is useful because the prognosis is related to
the severity of disease [35]. The 7 reported systems proposed
for classification of Asherman syndrome are as follows.
1. March et al [34] were the first group to attempt to classify
intrauterine adhesions. Hysteroscopy was used to classify
intrauterine adhesions based on the degree of uterine cav-
ity involvement (Table 1).
2. Another system described adhesions in terms of their loca-
tion [51]. Adhesions were classified as isthmic, marginal,
central, and severe.
3. Valle and Sciarra [52] described a classification system to
incorporate type of adhesion (mild, moderate, or severe)
and the extent of occlusion (partial or total) (Table 2).
4. A European classification system was devised in 1984 and
refined 1989 as the European Society for Hysteroscopy
classification [53]. This system classifies intrauterine adhe-
sions as grade I through IV, and incorporates a combination
of hysteroscopic and HSG findings, as well as clinical
559
Table 1
Hysteroscopic classification of intrauterine adhesionsa
Classification Involvement
Minimal Less than one-fourth of uterine cavity; thin or filmy
adhesions; ostial areas, and upper fundus minimally
involved or clear
Moderate One-fourth to three-fourths of uterine cavity; no
agglutination of walls; ostial areas and upper fundus
only partially occluded
Severe More than three-fourths of uterine cavity; agglutination of
walls or thick bands; ostial area and upper cavity
occluded
a
Adapted with permission from [34].
symptoms (Table 3). Fig. 2 demonstrates an illustrated
guide to classification using this system. Although both
more precise and prognostic than earlier classification
systems, it is criticized for being difficult to use in clinical
practice [54], especially in differentiating grades III, IIIa,
and IIIb.
5. The American Fertility Society classification is based on
extent of endometrial obliteration, hysteroscopic appear-
ance of adhesions, and menstrual characteristics of the pa-
tient. Menstrual characteristics are also included because
of the perceived effect on fertility [29]. The classification
system can be undertaken with direct (hysteroscopy) or
indirect (HSG) assessment (Table 4). Stage of disease is
calculated from the Table 4, with stage 1 (mild) score
of 1d4, stage 2 (moderate) score of 5d8, and stage 3 (se-
vere) score of 9d12. The physician predicts prognosis as
excellent, good, fair, or poor based on stage, tubal
patency, and clinical judgment.
6. More recent classification systems have considered loca-
tion of intrauterine adhesions to be the most important
prognostic factor in determining postoperative pregnancy
rate [55]. In one of these classification systems, adhesions
are divided into degrees, with each degree containing 2
subtypes (Table 5). This system has been criticized be-
cause category IIIa (inability to perform HSG because
of obstruction of the cervical canal) generally has
a good prognosis for subsequent fertility after treatment,
Table 2
Intrauterine adhesions: hysteroscopic diagnosis, classification, treat-
ment, and reproductive outcomea
Classification Involvement/Extent
Mild adhesions Filmy adhesions composed of basal endometrium
producing partial or complete uterine cavity
occlusion
Moderate adhesions Fibromuscular adhesions that are
characteristically thick; still covered with
endometrium that may bleed when divided;
partial or total occlusion of the uterine cavity
Severe adhesions Composed of connective tissue; lacking any
endometrial lining, and likely to bleed when
divided; partial or total occlusion of the uterine
cavity
a
Adapted with permission from [52].
560 Journal of Minimally Invasive Gynecology, Vol 17, No 5, September/October 2010

Table 3
European Society for Hysteroscopy classification of intrauterine
adhesionsa
Grade Extent of intrauterine adhesions
I Thin or filmy adhesions easily ruptured by hysteroscope
sheath alone. Cornual areas normal.
II Singular filmy adhesions connecting separate parts of the
uterine cavity. Visualization of both tubal ostea possible.
Cannot be ruptured by hysteroscope sheath.
IIa Occluding adhesions only in the region of the internal
cervical os. Upper uterine cavity normal.
III Multiple firm adhesions connecting separate parts of the
uterine cavity. Unilateral obliteration of ostial areas of the
tubes.
IIIa Extensive scarring of the uterine cavity wall with amenorrhea
or hypomenorrhea
IIIb Combination of III and IIIa
IV Extensive firm adhesions with agglutination of uterine walls.
Both tubal ostial areas occluded.
a
From Wamsteker K. European Society for Hysteroscopy (ESH) classifi-
cation of IUA. 1989.

and this is reflected in most other classification systems, in

which these adhesions are given a relatively lower stage or
score.
7. The most recent classification system incorporates men-
strual and obstetric history, and intrauterine adhesion find-
ings (Table 6) [54]. In this classification system, a score of
0d4 (grade 1, mild) reflects a good prognosis, a score of
5d10 (grade 2, moderate) reflects a fair prognosis, and
a score of 11d22 (grade 3, severe) reflects a poor progno-
sis. This classification system has been compared with pre-
vious systems [34,53] assessing correlations with the result
that the new classification system correlated well with Fig. 2. Schematic representation of one type of classification system demon-
grades 1 and 3; however, there was much overlap in strating the variation in adhesion location and severity, and depicting one of
the problems with classification systems when cervical obstruction may pre-
grade II, which the investigators attribute to the
vent further evaluation of the uterine cavity.
differences in the inclusion of menstrual and reproductive
performance in assessment of these patients. The may have no symptoms. Treatment should, therefore, be
limitation of this new system is that it is not yet validated, reserved for patients with Asherman syndrome.
and it is based on a relatively small number of patients. There is almost universal support that surgical treatment is
the criterion standard in management of Asherman syndrome,
In summary, a number of reported classification systems
and there is no role for medical treatments. There is no consen-
have been published that can make comparison between
sus as to the optimal technique of division of adhesions.
studies difficult to interpret. Classification systems that
Equally, there is a lack of prospective randomized
incorporate clinical history may provide better prognostic
controlled trials on the treatment of Asherman syndrome.
information. However, to date, no classification or grading
The primary objective of intervention is to restore normal
system has been validated or received universal endorsement,
volume and shape of the uterine cavity. Secondary goals
which may reflect inherent deficiencies in all of these
include treating associated symptoms (including infertility)
proposed systems.
and preventing recurrence of adhesions.

Management Table 4
American Fertility Society classificationa
After diagnosis of intrauterine adhesions, treatment is
Extent of cavity involved ,1/3 1/3-1/2 .2/3
considered when there are symptoms of pain or menstrual Score 1 2 4
dysfunction that are unacceptable to the patient, or more com- Type of adhesions Filmy Filmy and dense Dense
monly when there is a history of infertility or recurrent preg- Score 1 2 4
nancy loss and the patient wishes to conceive [35]. It is Menstrual pattern Normal Hypomenorrhea Amenorrhea
important to remember that intrauterine adhesions (and Score 0 2 4
a
Asherman syndrome) are not life-threatening, and patients Adapted with permission from [29].
Deans and Abbott. Review of Intrauterine Adhesions 561

Table 5 Although Asherman described a return to menstruation in

Degree and location of intrauterine adhesionsa all 29 patients within 1 month after treatment, our current
Degree Location understanding of the pathophysiologic findings makes it
I Central adhesions (bridgelike adhesions) likely that many of these women had minimal intrauterine
IIa Thin or filmy adhesions (endometrial adhesions) adhesions with localized obstruction. This technique cur-
IIb Myofibrous or connective adhesions rently has a limited role, and uterine perforation could still
II Marginal adhesions (always myofibrous or connective) be an outcome of blind cervical probing.
IIa Ledgelike projections
IIb Obliteration of 1 horn
III Uterine cavity ‘‘absent’’ at hysterosalpingography
IIIa Occlusion of internal os (upper cavity normal) Dilation and Curettage
(pseudo–Asherman syndrome)
IIIb Extensive coaptation of uterine walls (absence of uterine Before hysteroscopy, blind dilation and curettage followed
cavity) (true Asherman syndrome) by oral estrogen therapy and placement of an IUD was advo-
a cated for treatment of Asherman syndrome [4]. In a review of
Adapted with permission from [55].
women treated in this manner, 1049 of 1250 (84%) reported
Expectant Management return of normal menses, 540 of 1052 (51%) conceived,
142 of 559 (25%) miscarried, and 306 of 559 (55%) delivered
There is a role for expectant management, with an early
at term. Fifty of 559 (9%) delivered prematurely, and in 42 of
report of 23 women with amenorrhea with Asherman
559 (9%), pregnancy was complicated by placenta accreta.
syndrome observed expectantly. Of these, 18 (78%) began
Because hysteroscopy was not in widespread use, many pa-
having regular menses after 1 to 7 years [4]. Fertility is also
tients in this review had mild adhesions, and more severe
reported to have returned in 133 of 292 women (45.5%)
cases were treated using open hysterotomy and lysis. Inas-
observed expectantly who desired fertility, who conceived
much as blind dilation and curettage is associated with
within the same follow-up period [4]. These 25-year-old
a high risk of uterine perforation and a low success rate [3],
data are not classified by any of the 7 systems described.
it should now be considered obsolete.
Although based on descriptions alone, many of these women
had cervical obstruction only and, therefore, intrauterine
adhesions would be considered minimal, with an expected Hysteroscopy
good obstetric outcome.
Hysteroscopic treatment enables lysis of intrauterine ad-
Cervical Probing hesions under direct vision and with magnification. Uterine
distention has the dual role of providing visualization and
This is the original surgical intervention described for separating the uterine walls, providing direct breakdown of
Asherman syndrome in women with cervical stenosis with- adhesions and acting to increase tension at the point of adhe-
out damage to the uterine cavity or endometrium [56]. sion, making division easier. Mild adhesions may simply be
Table 6
divided using fluid distention of the cavity or blunt dissection
Clinicohysteroscopic scoring system of intrauterine adhesionsa with the tip of the hysteroscope [57]. Fig. 3 shows mild adhe-
sions before and after fluid distention.
Hysteroscopic findings Score
Division of moderate to severe adhesions is more techni-
Isthmic adhesions 2 cally challenging and requires greater surgical skill and more
Filmy adhesions
advanced instrumentation. In general, adhesiolysis begins
Few 1
Excessive (.50% of cavity) 2 caudally, with filmy or central adhesions divided first to in-
Dense adhesions crease cavity size, and then advanced cephalad until the uter-
Single band 2 ine architecture has been restored. Lateral or dense adhesions
Multiple bands (.50% of cavity) 4 should be divided last because they are associated with
Tubal ostia
a higher risk of uterine perforation [3].
Both visualized 0
Only 1 visualized 2
Neither visualized 4 Instruments for Adhesiolysis
Tubular cavity (sounds ,6) 10 Mechanical instruments such as semirigid 5F to 7F scissors
Menstrual pattern through a 6.5-mm operating hysteroscope [11] can be used to
Normal 0
divide adhesions under direct vision [34,52]. Sharp dissection
Hypomenorrhea 4
Amenorrhea 8 may, in theory, minimize destruction of the endometrium [3].
Reproduction An 18-gauge, 80-mm Tuohy needle may also be used as a sharp
Good obstetric history 0 instrument alongside a 2.5-mm hysteroscope [58,59].
Recurrent pregnancy loss 2 Advantages include low cost and, should perforation occur,
Infertility 4
decreased risk of visceral injury (compared with use of
a
Adapted with permission from [54]. energy sources), and a disadvantage is that they are less
562
Fig. 3. A, Hysteroscopic view of minor adhesion is seen in the central portion of the cavity (arrow). B, With hydrostatic pressure alone, the adhesion is divided.
hemostatic. Fig. 4 shows adhesions being lysed using hystero-
scopic scissors.
Monopolar electrosurgery with a knife electrode has been
described as an adhesiloytic instrument [52,60–63].
Advantages include precise hemostatic cutting, although
there is an increased risk of visceral damage if uterine
perforation occurs [35], and additional endometrial damage
may predispose to recurrence of intrauterine adhesions
[64,65]. Bipolar vaporization using the Versaport instrument
(Versapoint Electro-Surgical System, Gynecare, Inc., Menlo
Park, CA) to divide intrauterine adhesions has been
described [66,67], and uses saline solution as a distention
medium, decreasing the risk of electrolyte disturbance
compared with glycine. Use of the Nd-YAG laser has also
been reported [52,62,68], although with all energy
modalities, there is risk of significant visceral injury should
perforation occur [11].
Techniques for Intrauterine Adhesiolysis
Insertion of a Laminara tent (Shivata Medical Products
Co., Nagoya, Japan) into the cervix preoperatively may assist
in placement of the hysteroscope and aid in the dissection of
Fig. 4. Hysteroscopic scissors are used to mechanically divide dense adhe-
sions in the uterus.
Journal of Minimally Invasive Gynecology, Vol 17, No 5, September/October 2010
difficult dense cervical adhesions [69]. Pressure lavage under
US guidance is based on sonohysterography, in which a con-
tinuous infusion of saline solution leads to mechanical disrup-
tion of intrauterine adhesions. This technique is likely to be
successful only in patients with mild adhesions [70].
Hysteroscopy and Associated Techniques
Instillation of methylene blue dye to stain the endometrium
and guide the hysteroscopist to pockets of normal endome-
trium is described as helpful because the endometrium stains
well but connective tissue and myometrium do not [52]. This
technique is not helpful in instances of complete uterine oblit-
eration, and is best suited to treatment of mild and marginal
adhesions.
An entirely different technique of dissection, myometrial
scoring, has been described [71], in which six to eight
4-mm deep incisions are created in the myometrium using
a resectoscope and Collins knife electrode from the fundus
to the cervix. These incisions enable widening of the uterine
cavity. In a similar technique, a transverse incision is added at
the uterine fundus [61]. These techniques create a cavity, and
it is hypothesised that the endometrium may regenerate over
this new exposed surface area. All treated women had severe
intrauterine adhesions, and results of these techniques
demonstrated restoration of the cavity in 71.0% [71] and
51.6% [61], respectively. Pregnancy was achieved in 3 of 7
women (2.9%) [71] and 12 of 31 (38.7%) women [61].
Use of physical landmarks is described in cases of an
obliterated endometrial cavity in which the dense adhesions
are treated as a uterine septum. A cervical dilator is directed
from the cervical canal toward the 2 ostia, which creates 2 lat-
eral landmarks, leaving a fibrous septum, which is divided
transcervically under laparoscopic guidance. This technique
is not without risk: 2 of 6 women in the only reported series
experienced uterine perforation, and 1 had substantial hemor-
rhage [72]. The clinical results were encouraging, with cavity
restoration in all cases, and 5 pregnancies achieved in 4
women, resulting in 4 live births. The 50% major complica-
tion rate is of substantial concern, and the technique should
be performed only by expert hysteroscopists.
Deans and Abbott. Review of Intrauterine Adhesions
Fig. 5. Left, Using an image intensifier, an obliterated cavity demonstrates an intravascular flow pattern (arrow), indicating incorrect placement of the needle into
the myometrium. Right, After sharp dissection using this technique, the cavity is seen to be reconstructed (arrow), with flow demonstrated in the right tube.
Fluoroscopic guidance enables a radiologic view of
pockets of endometrium behind an otherwise blind-ending
hysteroscopic view. Using a Tuohy needle as an instrument
in parallel with a small-diameter hysteroscope, radiopaque
dye (Ultravist 76.9%; Iopromide; Scherring AG, Pharmaceu-
tical Division, Berlin Germany) can be injected into an area of
dense adhesions at the point of obliteration of the cavity. Un-
der image intensifier control, views can be obtained of normal
areas of endometrium and direct sharp synechiolysis under
hysteroscopic vision [58]. Fig. 5 demonstrates the radiologic
findings before and after this technique was performed. This
technique requires a substantial amount of equipment, ex-
poses the patient (and staff) to ionizing radiation, and is tech-
nically challenging. Fluoroscopic guidance to divide
intrauterine adhesions has also been described in an outpatient
setting using a specialized balloon-tipped catheter inserted
through the cervix [73]. This treatment seems to be limited
to patients with mild adhesions only, and there are no long-
term data for this technique.
Transabdominal US has been advocated as a technique to
guide hysteroscopic division of intrauterine adhesions
[3,65,71,74,75], with a reported reduced risk of uterine
perforation [75]. Ultrasound is readily available and familiar
to gynecologists; however, total reported numbers in these
studies are small, and success and perforation prevention is
both surgeon- and sonographer-dependent. Perforations in
as many as 5% of cases have been reported with use of this
technique [67,71,72]. More recently, the use of transrectal
US has been used to guide hysteroscopic synechiolysis,
with reported success in 1 patient [76]. There is also a single
case report of intracorporeal US control to guide adhesiolysis
[77] that requires 3 modalities: hysteroscopy, laparoscopy,
and US. Its use cannot be recommended without further
research.
The use of laparoscopic guidance is controversial because,
although advocates suggest its use in division of severe intra-
uterine adhesions [67,71,72], perforations have been reported,
and perhaps its primary use is best considered for immediate
recognition and treatment with minimal extrauterine trauma
[3,67,71,72].
563
Laparotomy, hysterotomy, and blunt dissection through
adhesions using a finger or curette are the traditional treat-
ment for severe intrauterine adhesions [2,24,78]. A review
of 31 cases in which this approach was used revealed that
16 of 31 women (52%) achieved conception, with 11
(38%) live births and 8 (26%) term deliveries. Five of 16
pregnancies (31%) were complicated by placenta accreta
[4]. In contemporary practice, this technique is rarely used,
and is reserved only for severe cases in which other tech-
niques are not practical or possible [21].
Risks and Complications of Hysteroscopic Synechiolysis
Perforation of the uterus is more likely with severe adhe-
sions, and is technique-dependent, generally ranging from
2% to 5% [3]. Hemorrhage can occur in 6% to 27% of cases
[3]. Injury to myometrial blood vessels may obstruct the
surgeon’s view and enable rapid absorption of distention
medium, which can lead to significant electrolyte distur-
bances including hyponatremia. Repeated cervical dilation
increases the risk of cervical incompetence and complica-
tions such as mid-trimester loss [61]. Because of the high
risk of recurrence of adhesions, patients should be counselled
about repeat surgery [3], particularly in severe cases [52].
Genital Tuberculosis
Genital tuberculosis is described here separately because
there are few reported cases of lysis of intrauterine adhesions
due to this infection, although outcomes are particularly poor,
with recurrence reported in all patients in 3 separate studies
[63,78–80].
Ancillary Treatments
Physical Barriers
Insertion of an IUD provides a physical barrier between
the uterine walls, separating the endometrial layers after lysis
of intrauterine adhesions [4,34,81]. The Dalcon shield was
the first described IUD to be used, in 1966, with moderate
success but significant associated problems. Since then, it
564 Journal of Minimally Invasive Gynecology, Vol 17, No 5, September/October 2010
has been reported as an adjunctive treatment in many studies
[14,34,51,52,57,60,62,67,75,82–85]. The type of IUD is
reported to be important. Copper-containing IUDs provoke
an inflammatory reaction [86], and T shaped IUDs are
thought to have too small a surface area to be truly effective
in providing a physical barrier [87]. The loop IUD (e.g.,
Lippes loop) is considered the IUD of choice when treating
intrauterine adhesions [3], although it is no longer available
in many geographic areas. In a small nonrandomized study,
postoperative IUD plus hormone therapy was compared
with hormone therapy alone, and no significant difference
was found in the re-formation of adhesions [88]. Because
of the suppressive effect on the endometrium, progesterone
loaded IUDs should not be used postoperatively.
To date, there have been no class I studies investigating
the use of IUDs after hysteroscopic lysis of intrauterine adhe-
sions. There is a risk of infection when an IUD is introduced
into the uterus immediately after adhesiolysis, quantified as
8% in 1 series [85], and perforation of the uterus during
IUD insertion is a further risk.
Use of a Foley catheter for 3 to 10 days is similarly re-
ported to act as a physical intrauterine barrier after surgical
lysis of intrauterine adhesions [2,34,73,79,84,85,89,90]. In
a nonrandomized study, a pediatric Foley catheter was
inflated and placed in the uterus for 10 days in 59 patients
postoperatively in a 4-year study and compared with use of
an IUD postoperatively for 3 months in 51 women treated
in the next 4 years. Most striking was that amenorrhea
continued in 19% of the Foley group and 38% of the IUD
group, with poor fertility rates in the IUD group (20 of 59
[34%]) and Foley group (14 of 51 [28%]). There were
fewer infections in the Foley group, and a lower recurrence
rate of intrauterine adhesions as assessed at HSG [85].
Use of a fresh amnion graft over an inflated Foley catheter
to prevent recurrence of intrauterine adhesions after hystero-
scopic lysis in 25 women with moderate to severe Asherman
syndrome has been reported, demonstrating minimal adhe-
sion reformation in 48% of patients with severe adhesions
[90]. However, no fertility data for this technique have
been reported.
Newer adhesion barriers include modified hyaluronic acid,
and have been reported to be successful after treatment of in-
trauterine adhesions [91–93]. Hyaluronic acid has been used
as a barrier agent to prevent adhesion formation after
abdominal or pelvic surgery [94], with the antiadhesive ef-
fects depending on the preparation’s molecular weight and
concentration [95]. In a prospective, single-blind, random-
ized, controlled study of 150 women undergoing suction cu-
rettage after incomplete, missed, or recurrent miscarriage, 50
were randomized to receive Seprafilm (Genzyme Corp., Cam-
bridge, Massachusetts), and 100 patients served as a control
group [92]. There was stratification depending on the perfor-
mance of previous curettage. In 32 women who received
Seprafilm who had not undergone a previous curettage proce-
dure, all became pregnant in the 8 months after the procedure.
In the control group, 34 of 56 patients (54%) who had never
undergone a previous curettage procedure conceived. If pa-
tients had not become pregnant 8 months after the interven-
tion, HSG was performed to review the endometrial cavity.
In the treatment group (women who had previously under-
gone at least 1 curettage procedure), adhesion formation reoc-
curred in 1 of 10 patients (10%); however, intrauterine
adhesions were observed in 7 of 14 (50%) of the untreated
group. There were no reported adverse reactions using Sepra-
film in the endometrial cavity, and US examination did not
demonstrate any abnormal echoes at follow-up of the patients
receiving treatment.
Auto-cross-linked hyaluronic acid gel may be more suit-
able for preventing intrauterine adhesions because of higher
sensitivity and prolonged residency time on the injured sur-
face compared with unmodified hyaluronic acid [96]. In
a prospective randomized controlled trial of 84 women,
auto-cross-linked hyaluronic acid gel (Hyalobarrier gel;
Baxter International Inc., Deerfield, IL) was compared with
no therapy after surgical treatment of Asherman syndrome.
Postoperative US studies showed that the walls of the uterine
cavity remained separated for at least 72 hours. At second-
look hysteroscopy 3 months after the procedure, intrauterine
adhesions were significantly reduced in patients receiving the
adhesion barrier (6 of 43 [14%]) compared with the control
group (13 of 41 [32%]) (p ,.05) [91].
These newer adhesion barrier studies provide encouraging
results with more methodologically sound studies than tradi-
tional barriers such as IUDs or Foley catheters. Further studies
are essential before these barriers are used in routine practice.
Hormone Therapy
In 1964, Wood and Pena [97] described estrogen therapy to
stimulate regeneration of the endometrium and promote reepi-
thelization of the endometrium after surgical treatment of in-
trauterine adhesions. Various regimens have been described
for postoperative treatment with estrogens (e.g., a daily dose
of 2.5 mg of conjugated equine estrogen) with or without op-
posing progesterone for 2 to 3 cycles [11,21,58,59]. No
comparative studies have been performed on dosage,
administration, or combination of hormones. In a related
study, 60 women undergoing dilation and curettage during
the first trimester of pregnancy were randomized to receive
estrogen and progestin or no treatment [98]. Women in the
combined hormone group had a significantly thicker endome-
trium (0.84 cm vs 0.67 cm) and endometrial volume (3.85 cm2
vs 1.97 cm2) compared with the control group [99]. This sug-
gests that there may be a benefit to postoperative treatment of
intrauterine adhesions; however, no data are available at this
time on pregnancy or intrauterine adhesion recurrence.
Adverse effects of estrogen or estrogen plus progesterone
must be evaluated in the absence of evidence, with nausea,
headache, and the risk of thromboembolic disease considered
if using this treatment. Preoperative estrogen therapy has also
been suggested to be of potential benefit in increasing endo-
metrial thickness before any surgical intervention, although
data are limited [35].
Deans and Abbott. Review of Intrauterine Adhesions 565

Table 7
Major obstetric complications after hysteroscopic treatment of intrauterine adhesionsa
Source Pregnancy, % Miscarriage, % Live birth, % Obstetric complications
Friedman et al [125] 24/30 (80) 1/24 (4) 23/24 (96) Placenta increta (n 5 1), exuterine sacculation (n 5 1),
paper-thin uterine fundus (n 5 1)
Valle and Sciarra [52] 143/187 (76) 26/143 (18) 114/143 (80) Placenta accreta requiring hysterectomy (n 5 1), ectopic
pregnancy, 2%
Deaton et al [112] 1/1 (100) 0/1 (0) 1/1 (100) Spontaneous uterine rupture at 25 weeks, cesarean
hysterectomy because of uncontrolled bleeding
Hulka [113] 1/1 (100) 0/1 (0) 1/1 (100) Uterine rupture in pregnancy
Roge et al [119] 28/52 (54) 10/28 (36) 18/28 (64) Partial placenta accreta (n 5 2)
Katz et al [117] 66/72 (92) 15/66 (23) 46/72 (64) Perinatal death (baby) after premature delivery
McComb and Wagner [72] 5/6 (83) 1/5 (20) 4/5 (80) Placenta previa (n 5 1)
Protopapas et al [71] 3/7 (43) 1/3 (33) 2/3 (67) Hysterectomy because of placenta accreta
Capella-Allouc et al [61] 12/28 (43) 5/15 (33) 9/15 (60) Abnormal placenta (n 5 2)
Feng et al [108] 156/186 (84) 11/156 (7) 145/156 (92.9) Abnormal placenta (n 5 4)
Zikopolous [67] 20/46 (43) NA 20/20 (100) Hysterectomy because of placenta accreta (n 5 2)
Shiau et al [122] 1/1 (100) 0/1 (0) 1/1 (100) Uterine rupture in subsequent pregnancy
Yu et al [124] 39/85 (46) 5/39 (13) 27/39 (69) Cesarean hysterectomy because of placenta accreta
(n 5 2), manual removal (n 5 3)
Thompson et al [59] 9/17 (53) 1/9 (11) 8/9 (89) Bleeding requiring cesarean hysterectomy (n 5 1)
NA 5 data not available.
a
Data are given as No. (%).

Techniques for Increasing Vascular Flow to Endometrium
Various case reports have described increasing vascular
perfusion to the endometrium using medication such as aspi-
rin, nitroglycerin, and sildenafil citrate [99–102]. Despite
reported pregnancies after using these medications [103], fur-
ther research is required to evaluate their efficacy and possi-
ble adverse effects given this off-label use. At this time, they
cannot be recommended as an ancillary treatment after lysis
of intrauterine adhesions.
Antibiotic Therapy
There are no data to support the use of antibiotics before,
during, or after surgical treatment of Asherman syndrome.
The American College of Obstetricians and Gynecologists
guidelines for antibiotic use in gynecologic procedures do
not recommend their use in diagnostic or therapeutic hystero-
scopy [104]. There is, however, a theoretic risk of secondary
infection, and it has been proposed that infection may be
a primary cause of intrauterine adhesions. This has led many
surgeons to treat patients undergoing surgical lysis of Asher-
man syndrome with preoperative or intraoperative antibiotics,
and some continue with postoperative antibiotic therapy.
Postoperative Assessment
Because of the high rate of recurrent intrauterine adhe-
sions after treatment, with any surgical intervention used, as-
sessment of the uterine cavity is worthwhile, usually after 2 to
3 cycles after treatment, with the recurrence rate for intrauter-
ine adhesions in as many as one-third of patients with mild to
moderate intrauterine adhesions [52,79,105] and as many as
two-thirds of patients with severe intrauterine adhesions [61].
Ambulatory methods include office hysteroscopy and HSG,
with recurrence of more than mild intrauterine adhesions
likely requiring anesthesia and division as described.
Outcomes after Hysteroscopic Treatment
Most patients with amenorrhea seem to achieve menstrua-
tion after hysteroscopic treatment of intrauterine adhesions,
with studies reporting the return to normal menses between
92% and 96% in most groups [59,67,84,106,107]. The
severity of intrauterine adhesions is related to the odds of
resumption of normal menses, with more severe adhesions
associated with poorer prognosis [21,81,108].
It is more difficult to obtain accurate data on fertility and
pregnancy outcome from recent studies because of the variable
duration of follow-up and the retrospective nature of most
studies in this area. Of 36 articles that reported fertility and ob-
stetric outcomes after hysteroscopic management, the preg-
nancy rate was approximately 63% (968 of 1542 patients),
and of women who conceived, the live birth rate was 75%
(696 of 930) [3,18,21,51,52,59,61,62,63,65,67,71,74,75,80,
81,84,87,106,107–122].
Various pregnancy complications have been described
after hysteroscopic treatment of Asherman syndrome; major
obstetric complications are given in Table 7. In 696 births
reported after hysteroscopic treatment of intrauterine
adhesions, 17 pregnancies were complicated by placental
abnormalities including placenta accreta and increta
[52,65,67,71,72,121,123]. The risk of premature delivery
was also increased in patients with intrauterine adhesions,
with reported rates of 40% to 50% after synechiolysis
[61,67,71,72]. Uterine rupture has been described after
hysteroscopic surgery to treat Asherman syndrome, and it
is thought that the mechanism for this is a weakened and
scarred myometrium, in particular if perforation occurs
during the index procedure. Seven peripartum hysterectomies
have been performed in women who had previously
undergone treatment of intrauterine adhesions [52,59,67,71,
111,122], and 1 neonatal death was reported [116].
566
The primary issue with the determination of pregnancy-
related complications of treatment of Asherman syndrome
arises from poor data collection, with most studies being ret-
rospective and cases reported individually without a denomi-
nator for a particular method of treatment or for individual
pregnancy complications. These data suggest that factors
that may lead to Asherman syndrome as an index problem
may be subsequently linked to obstetric problems, and pa-
tients who are considering pregnancy should be counselled
about the higher than usual rate of obstetric complications
and be managed in a high risk setting, with premature deliv-
ery and potential placental attachment problems considered
as possible outcomes.
Prevention
Development of intrauterine adhesions seems to be largely
idiosyncratic in any woman. However, there are simple prin-
ciples that may help prevent development of intrauterine
adhesions:
1. Reduce the need for instrumentation of the pregnant
uterus via use of contraceptives and possibly medical
management of miscarriage [3,9,123].
2. Use additional US techniques to differentiate blood clots
from retained products of conception, in particular when
the uterus has undergone instrumentation already. Use
of saline infusion sonohysterography has been reported
to be useful [124], as has color velocity imaging and
pulsed Doppler US [125]. Such techniques may promote
conservative management appropriately and decrease
uterine instrumentation.
3. Perform hysteroscopically guided removal of retained
products of conception compared with nonselective blind
curettage [60].
4. When hysteroscopically guided removal of products is not
possible, use a suction catheter or blunt curette rather than
a sharp instrument [3].
Conclusion
In the recently published guidelines for management of in-
trauterine adhesions [126], the quality of the data is poor. The
sporadic nature of this condition and the multitude of classi-
fication systems, management approaches, and varying
methods for measuring outcomes (e.g., menstrual function,
pain, and infertility) result in this condition likely continuing
to have poor evidence. From both the guidelines and this re-
view, there is clearly a need for a unified approach to a clas-
sification system and validation of such a system. The use of
perioperative adjunctive treatments including antibiotic
therapy, adhesion barriers, and the type and dose of hormone
therapy requires international collaboration and study. Such
agreement would result at worst in a prospective database
of outcomes for various approaches, and at best could form
the foundation for randomized comparative trials.
Journal of Minimally Invasive Gynecology, Vol 17, No 5, September/October 2010
It is clear that intrauterine adhesions can lead to menstrual
dysfunction and infertility. The diagnosis of intrauterine ad-
hesions is best achieved using hysteroscopy, with saline so-
lution infusion sonohysterography and HSG offering
reasonable alternatives. However, their limitations must be
recognized. Treatment is best performed surgically, and treat-
ments improve both menstrual function and fertility out-
comes, although there is no evidence for an optimal
technique. The more severe the adhesions, the worse the clin-
ical outcome. No one method of treatment can be recommen-
ded over any other, and adhesion recurrence is unpredictable.
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