A normal uterine cavity and endometrial lining are essential in order to conceive and maintain a pregnancy. Scar tissue in the uterine cavity (Asherman’s syndrome) can interfere with conception, or increase the risk of miscarriage. The condition is often so severe that it destroys most of the basal (germinal) layer of the endometrium from which the uterine lining (endometrium) develops each month. When most of the basal endometrium is incapacitated, no regeneration of the endometrium can take place and amenorrhea (cessation of menstruation) or infertility can follow. The condition often results in fusion/adhesion of the opposing endometrial surfaces, but can also simply destroy the basal layer of endometrium without resulting in adhesions (non-adhesive Asherman’s).

Asherman’s syndrome most commonly results from post-partum or post-abortal inflammation involving the uterine lining (endometritis), but it can also occur (although infrequently) following uterine surgery such as removal of fibroid tumors (myomectomy) that encroach upon (or penetrate into) the uterine cavity.

The treatment of adhesive Asherman’s syndrome is resection of scar tissue by hysteroscopy. A hysteroscope is a telescope-like instrument that is introduced via the vagina and cervix into the uterine cavity allowing visualization of and access to the entire uterine cavity, enabling surgical resection of scar tissue. The objective is to remove as much scar tissue as possible and to free adhesions that fuse the walls of the uterine cavity together, so as to enable viable basal endometrium to resume growth and progressively cover as much of the surface of the uterine cavity as possible. Post-operatively, a small balloon is often placed in the uterine cavity for a day or two, to keep the opposing surfaces separated in the hope of preventing recurrence of adhesion formation. The woman usually receives supplemental estrogen to encourage endometrial growth.

Endometritis of a severity sufficient to produce Asherman’s Syndrome often scars and blocks the uterine entrances into the Fallopian tubes. However it is not always the case. The lining can be damaged while the tubes remain open. In such cases, if the uterine lining cannot support proper embryo implantation, a pregnancy could still implant in a Fallopian tube leading to an ectopic (tubal) pregnancy. Unless it is diagnosed early (by blood testing in combination with ultrasound examination) and treated medically or surgically, the ectopic pregnancy will rupture with serious and potentially life endangering consequences.

About 8 years ago, we reported on the use of Viagra vaginal suppositories to improve blood flow and hence enhanced delivery of estrogen to the endometrium. In this manner, we have been able to improve endometrial development in about 75% of women who otherwise were unable to develop an “adequate” uterine lining. Most of these women had undergone several failed IVF attempts. Many of the women who were successfully treated with Viagra subsequently conceived following IVF and went on to deliver healthy babies. One such case immediately comes to mind. It involved a woman who was from Singapore and who following 15 failed IVF attempts due to poor endometrial development conceived on her first IVF-Viagra attempt with us following Viagra therapy.

But Viagra is often ineffective in thickening the uterine lining in women with Asherman’s syndrome. The reason is that with Asherman’s there is often such widespread destruction of the basal endometrium (from which fresh endometrial cells must be generated), that regardless of the improvement in uterine blood flow and improved estrogen delivery, the endometrium just can’t respond. In such cases, the woman should consider using a gestational surrogate or pursuing adoption.