Apologies for the long delay... To
recap, in my last blog post I gave a brief background about Dr Charles March of
California Fertility Partners and his vast experience on Asherman’s syndrome (AS),
which he summarizes in his last review, Management of Asherman’s syndrome
(1). Dr March’s article emphasizes many important
issues that are often overlooked and reconsiders the validity of accepted
beliefs. It’s clear throughout that he has given a lot of critical as well as
practical thought to different aspects of Asherman’s syndrome. The review starts off with a background
including the epidemiology of AS, symptoms and diagnosis, then management,
which he summarizes by the acronym PRACTICE, for prevention, anticipation,
comprehensive therapy, timely surveillance of subsequent pregnancies, investigation (potential treatments
like anti-adhesive gels and vitamin supplementation to improve blood flow), and
continuing education (continuing medical education courses and literature).
I’ll focus on the parts of the review containing relevant
insights which I have not encountered in other reviews, or which are important
enough that repeating them is warranted.
General
1.
Asherman’s
syndrome is not rare. He points out that most physicians believe that AS
occurs rarely and fail to diagnose it
even when a patients exhibits obvious symptoms. Table 1. (page 64 of the
article) displays convincingly that AS is not rare by showing the prevalence of
AS in different populations of women undergoing hysteroscopy, and the incidence
of AS after various procedures
2.
The term
‘syndrome’ does not correctly describe the condition. This is because the
condition has varying symptoms and pathology, from endometrial sclerosis
without intrauterine adhesions (IUA), to IUA without endometrial sclerosis. However,
he points out that Asherman’s syndrome encompasses all of the different
possible manifestations of endometrial injury, from all possible causes and
varying symptoms. For this reason he continues using the term instead of IUA or
traumatic amenorrhea.
Etiology
3.
AS most
commonly occurs after dilation and curettage during or shortly after a
pregnancy. However, diagnostic curettage may also lead to AS. Ignorance
about this continues. I’ve heard several doctors who are not experts on AS and
probably haven’t read the literature on it claim that the condition only occurs
where there has been pregnancy and never in its absence. This old belief has
been proven to be untrue. Interestingly, Dr March mentions that curettage used
to be used during laparoscopy to investigate infertility, observing that this
probably caused more harm than good. It is very refreshing to hear doctors
reflect on their predecessors’ or colleagues’ mistakes and admitting that
sometimes what seems like a progressive approach turns out to be a step
backwards.
4.
There is
no evidence that uterine malformations such as Mullerian anomalies are more
prone to developing adhesions, even though there is very strong evidence
that the two are associated. He points out that the correlation can be
explained by the high miscarriage rate- and subsequent D&Cs- among this
group of women. Another reminder that correlation is not evidence of causation.
The bottom line is that injury from surgical trauma (or TB in some countries)
is what causes AS, and there is a tendency for some authors to mystify the
condition by neglecting the obvious associated risk factor i.e. women with
Mullerian anomalies tend to have more D&Cs which lead to AS.
5.
There is
no evidence that infection leads to AS. Dr March notes that infections
occurred in less than 1% of his patients. The Polishuk case series (2) showed that
among 171 women who underwent C-sections, of the 28 who had severe
endometritis, none developed de-novo adhesions (the one patient who did develop
cervical adhesions already had a previous history of AS from several
miscarriages treated by D&C (her AS was also ‘treated’ by D&C). Furthermore, there are no studies whatsoever that show any evidence that endometritis alone leads to AS.
6.
Endometriosis
may develop in AS with outflow obstruction and patent fallopian tube(s) if
treatment is delayed. This is an important point that isn’t mentioned
enough in my opinion. It’s also another good reason why AS should be prevented or if it's too late, treated to prevent further problems:
it can lead to 2 fertility problems for the price of one (a bargain nobody
wants).
7.
Inexperienced
operators can inadvertently cause uterine damage. New instrumentation and
technologies for intrauterine surgeries are proven to be safe by experts,
however they may not be so harmless if inexperienced operators use them.
Diagnosis
8.
Menstruation
and withdrawal bleeding cannot rule out AS. Some women with IUA have normal
periods (‘eumenorrhea’) and some women with amenorrhea have withdrawal bleeding
after hormone administration. Therefore hysteroscopy is the gold standard for
diagnosis. (HSG and SIS can lead to false positives). However, the opposite is
true: women with hypomenorrhea or amenorrhea after intrauterine surgery are
likely to have IUA.
9.
HSG and
SIS can rule out IUA, but cannot rule out endometrial sclerosis, which can
be diagnosed by hysteroscopy. On the other hand, one important advantage of HSG
is that it provides information on the patency of fallopian tubes, which
hysteroscopy does not. Single or bilateral tubal obstruction is in some cases
caused by AS if adhesions occlude the ostia/ostium, so it is important to
confirm after corrective surgery that the adhesions have not reformed. A
partial or complete obstruction of one or both ostium can lead to tubal
pregnancy or infertility.
Next time: Dr March’s advice about prevention, treatment and
monitoring of post-AS pregnancies.
References
March C. Management of Asherman’s syndrome Reprod Biomed Online. 2011 Jul;23(1):63-76.
Polishuk WZ, Anteby SO, Weinstein D. Puerperal endometritis and intrauterine adhesions. Int Surg. 1975 Aug;60(8):418-20.
