In our last post, we described the condition called “Asherman’s syndrome” wherein scarring of the intrauterine cavity can cause aberrations of menstrual bleeding (in the most extreme cases very light or absent periods), infertility, recurrent pregnancy loss, and other pregnancy complications. The extent of the scarring is correlated with the risks for these problems; however, some women will have minimal scarring and little if any aberration of menses and still be at risk for one or more of these complications. In today’s post we will briefly address the diagnosis, treatment, and prevention of Asherman’s syndrome…
The first step to establishing the diagnosis is maintaining a high index of suspicion. It is surprising to me, for example, how often a woman will present with recurrent pregnancy loss, where she has never been asked about specific events surrounding her management and complications related to previous pregnancies and/or these previous losses (i.e., postpartum hemorrhage, D&C for retained products of conception and the timing of the same with regard to the length of time from the delivery, D&C’s for missed or incomplete miscarriages and elective abortions, prolonged bleeding, fever, infection or evidence of infection on the pathology report, length of time between the death of the baby and the actual miscarriage or medical/surgical evacuation of the uterus, complications related to the D&C’s themselves, such as hemorrhage or uterine perforation). Yet, we know that the risk of intrauterine scarring (synechiae) increases with the number of D&C’s, the duration between fetal loss and the procedure itself, and any of the other complications noted above.
Clearly, if a patient has complete absence of menstrual bleeding, a history of an intrauterine procedure and/or infection, and documented ovulation, the diagnosis is readily apparent. However, since not all Asherman’s patients will have the most extreme presentation of the condition, and since ultrasound alone is unlikely to help establish the diagnosis under these circumstances, it is probably under-diagnosed, or at best the diagnosis is delayed in many instances. Occasionally, the diagnosis can be made using sonohysterography in which fluid is used to distend the uterine cavity while performing an ultrasound, or by hysterosalpingogram in which a radio-opaque dye is instilled into the uterus to outline its contour, but by far the most efficient and reliable approach is to perform hysteroscopy in which the uterine cavity is directly visualized with the aid of a special instrument that provides light and magnification.
Interestingly, in one prospective study in which hysteroscopy was performed routinely following D&C’s for uterine evacuation of early pregnancy, intrauterine adhesions were found in 16% of women after one procedure and 32% after three or more (Friedler, et al., Hum Reprod 1993;8:442-44)! Similarly, Westendorp and colleagues (Hum Reprod 1998;13:3347-50) found that 40% of women who underwent a D&C for retained placenta longer than 24 hours after delivery, or who required a repeat D&C for incomplete abortions, had intrauterine adhesions present by hysteroscopy three months after the intervention and almost half of these had moderate to severe disease (Grade III and IV).
Although treatment for Asherman’s syndrome has had various approaches, successful treatment relies on the lysis (breakdown) of the adhesions and restoration of some degree (the more the better) of normal-appearing and functioning endometrium (the inner lining of the uterus). The gold standard at present involves surgical removal of adhesions under direct visualization using operative hysteroscopy. The success depends on the experience and skill of the surgeon and in the most severe cases (complete obliteration of the uterine cavity by scar tissue), the procedure can be quite difficult. Even in skilled hands, the risk of recurrence of scar tissue following the initial operation is very high and many surgeons try to minimize this risk by avoiding surgical techniques (such as electrocautery) that will further promote scarring. Following the procedure itself, patients are often placed on high doses of estrogen to stimulate the endometrium and in some cases, balloons, catheters, or other forms of stents are placed into the uterine cavity to help prevent adherence of the walls. Another option is to have repeated in-office hysteroscopic lysis of adhesions once the primary procedure has been performed.
Even with all these precautions, recurrence of adhesions is extremely common and success, measured in terms of restoration of fertility, is relatively low. In moderate to severe Asherman’s syndrome, recurrence rates range between 20-40% and 40-50%, respectively (Valle, et al., Am J Obstet Gynecol 1988;158:1459-70; Yu, et al., Fertil Steril 2008;89:715-22). Conception and pregnancy success depends on the success of the lysis of adhesions, the degree to which a normal endometrium can be restored, damage done to the uterus by the procedure itself and, eventually, the site of implantation of a subsequent pregnancy. As also reported in the article by Yu and colleagues noted above, “…the chances of conception in women who remained amenorrheic (2 out of 11); 18.2%) were significantly lower than in those who continued to have menses (37 out of74; 50%)…the conception rate in women who had reformation of intrauterine adhesions (2 out of 17; 11.8%) was significantly lower than that of women who had a normal cavity (26 out of 44; 59.1%)."
And, as we pointed out in our previous post, even if conception occurs, a good outcome is not guaranteed. Probably no more than one-third of women with moderate to severe adhesions will successfully carry a pregnancy and of those, there is increased risk for cervical incompetence, intrauterine growth restriction, fetal loss (early and late), placenta accreta or placenta previa, premature delivery, preeclampsia, cesarean delivery, uterine rupture, peripartum hemorrhage and hysterectomy.
In closing, let us just mention a few thoughts on prevention of Asherman’s syndrome. Based on several reports, the risk of Asherman’s could be reduced significantly if pregnancy-related D&C procedures could be minimized or done less traumatically. To that end, in recent years, the prostaglandin drug, misoprostol, has been used effectively even in first trimester uterine evacuations and compared to D&C is clearly associated with a reduction in risk for adhesions (Tam, et al., J Am Assoc Gynecol Laparoscop 2002;9:182-5). When given the option of instruments to use for D&C, a plastic suction curette is probably (but not completely) less traumatic than a sharp metal curette and efforts should be made to reduce the degree to which the endometrium is denuded by either. Prophylactic antibiotics, although rarely used when a D&C is performed, unless there is frank evidence of infection, might be considered in patients who opt to defer uterine evacuation following fetal loss in preference to awaiting spontaneous abortion. I think if I learned nothing else from this review myself, it was the fact that the risk of Asherman’s appears to go up dramatically with the length of time from fetal death to uterine evacuation although the factors that contribute to this risk are not entirely clear.