Tuesday, June 19, 2012

Insights from an Asherman's syndrome expert (Part II)

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.


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.


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.


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.

March C. Management of Asherman’s syndrome 2011 Jul;23(1):63-76.
Polishuk WZ, Anteby SO, Weinstein D. Puerperal endometritis and intrauterine adhesions. 1975 Aug;60(8):418-20.