One century after its first description, treatment of Asherman’s syndrome (1) has not progressed enough to ensure that a high percentage of patients will regain fertility. I hope that one day it will be 100% treatable but it seems that this is a long way off and not a top priority for researchers or funding bodies. As important as treatment is for the women who have been diagnosed with Asherman’s syndrome, it is still difficult to justify why so little is being done to prevent it in the first place. Not all cases are preventable depending on the cause, but most are. Most cases (over 90% according to one study) (2) are caused by D&C and yet there are alternatives to D&C for every indication for which it is used. When D&C continues to be standard care for miscarriage management most cases of Asherman’s syndrome will continue to occur in women who have miscarried.
Asherman’s syndrome was first described in 1894 (1) and later further characterized in 1948(3). In those days there were no other options to D&C so naturally treatment (or more selective use of D&C) was the only solution to the problem. The situation today is very different with the discovery of drugs and hysteroscopy to replace D&C. These approaches would undoubtedly reduce the incidence of Asherman’s syndrome.
Unfortunately treatment is not a panacea. The outcomes of studies speak for themselves (see below). They range from 27% to 43% and include women of different classification severities (so presumably this rate is even less inspiring for women with more severe presentation). Note that all of these studies are recent. The most accurate way to present these results is to report number of live births per total patients treated because some women will either never conceive or give birth after treatment. Reporting live births per pregnancy is deceptive because the women who never got pregnant are discounted from the outcomes. It is very possible that some women never conceived because the endometrial damage they sustained and which led to Asherman’s syndrome was permanent and not able to be repaired by treatment enough to allow for successful implantation. Absence of adhesions does not imply that the endometrium is functioning properly- there could be fibrosis or very thin unresponsive endometrium. Unfortunately, to this date, there is no test which can ensure that the entire endometrium is functional. In the next part of this discussion about treatment (Part III), I will discuss in further detail the results from studies and difficulties in conducting studies on Asherman's syndrome.
Studies of modern success rates (#live births/#patients treated) after treatment of Asherman’s syndrome:
|1. Zikopoulos et al, 2004||(4)||20/46||43.5%|
|2. Fernandez et al, 2006||(5)||21/64||32.8%|
|3. Thomson et al, 2007||(6)||8/27||29.6%*|
|4. Yu et al, 2008||(7)||25/85||29%|
5. Robinson et al, 2008
|6. Pabuccu et al, 2008||(9)||22/71||31%|
* the paper itself quotes a 47% live birth rate but excludes 10 women ie. one third of the patient sample size from the calculation on the basis that they were not trying for pregnancy.
**the paper quotes a 46% (7/15) live birth rate, however 3 of those pregnancies were still ongoing at the time of publication.
The real outcomes, including the results of treatment by the best doctors in the field according to the Asherman's Syndrome International Support Group don’t look as inspirational in statistics as they do when presented as personal success stories.
Are these live birth rates high enough to justify treatment as the best solution to the problem of iatrogenic Asherman’s syndrome? Or that D&C should continue to be used routinely or as ‘standard care’?
I will not get into the serious obstetric complications sometimes encountered in future pregnancies (should patients be fortunate enough to be able to conceive and carry a pregnancy). I have saved this for another post as it is a whole other area that needs to be discussed in detail.
There is another very important reason for women to told the true success rates of treatment (and about future obstetric complications): awareness will undoubtedly create a push among patients and and more importantly women, in general, for prevention by using alternatives to D&C…
Continued in Part III
1. Fritsch, H. Ein Fall von volligem Schwaund der Gebormutterhohle nach Auskratzung Zentralbl Gynaekol 1894;18:1337-1342.
2. Schenker, JG and Margalioth, EJ. Intrauterine adhesions: an updated appraisal. Fertil Steril 1982;37(5):593-610.
3. Asherman, JG. Amenorrhea traumatica (atretica). J Obstet Gynaec Brit Emp 1948;55(23).
4. Zikopoulos, KA, Kolibianakis, EM, Platteau, P, de Munck, L, Tournaye, H, Devroey, P et al. Live delivery rates in subfertile women with Asherman's syndrome after hysteroscopic adhesiolysis using the resectoscope or the Versapoint system. Reprod Biomed Online 2004;8(6):720-5. Abstract
5. Fernandez, H, Al-Najjar, F, Chauveaud-Lambling, A, Frydman, R, and Gervaise, A. Fertility after treatment of Asherman's syndrome stage 3 and 4. J Minim Invasive Gynecol 2006;13(5):398-402. Abstract
6. Thomson Angus J M; Abbott Jason A; Kingston Ashley; Lenart Meegan; Vancaillie Thierry G. Fluoroscopically guided synechiolysis for patients with Asherman's syndrome: menstrual and fertility outcomes. Fertility and sterility 2007;87(2):405-10. Abstract
7. Robinson, JK, Colimon, LM, and Isaacson, KB. Postoperative adhesiolysis therapy for intrauterine adhesions (Asherman's syndrome). Fertil Steril 2008;90(2):409-14. Abstract
8. Yu, D, Li, TC, Xia, E, Huang, X, Liu, Y, and Peng, X. Factors affecting reproductive outcome of hysteroscopic adhesiolysis for Asherman's syndrome. Fertil Steril 2008;89(3):715-22. Abstract
9. Pabuccu Recai; Onalan Gogsen; Kaya Cemil; Selam Belgin; Ceyhan Temel; Ornek Turkan; Kuzudisli Ebru. Efficiency and pregnancy outcome of serial intrauterine device-guided hysteroscopic adhesiolysis of intrauterine synechiae. Fertility and sterility 2008;90(5):1973-7.