Asherman Syndrome - IVF - Dr. Geoffrey Sher

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Marissa (39y) and her husband, Pete (43y) presented with a history of having had 2 healthy children together. Marissa was a normally menstruating/ovulating lady with a fertile husband. The birth of her 2nd child was complicated by partial delivery of the placenta and was accompanied by a post-partum hemorrhage (bleeding). A manual removal of the retained piece of placenta was undertaken following which her uterus was deemed to be empty. After the birth of her baby, Marissa had a low-grade fever, lower abdominal pain, malaise and a malodorous lochia (post-delivery secretions) that persisted for greater than 2 weeks. At this point an ultrasound was done and it revealed that there was still some retained placental tissue in her uterus, and a D & C was performed. In the years that followed, Marissa noticed a marked reduction in menstrual flow. However, since she was still ovulating normally (based upon home ovulation testing, she thought nothing of it and tried in-vain to have a 3rd child.
When 3 years of trying to have another baby proved unsuccessful, the couple sought the services of a fertility specialist who performed a hysteroscopy to examine Marissa’s uterine cavity. This established that Marissa had significant intrauterine adhesions that were in-part obliterating her uterine cavity. The adhesions (synechiae) were transected and cleared and a balloon catheter was temporarily placed inside her uterine cavity to try and avert refusion of the inner opposing uterine surfaces. A follow-up hysteroscopy done 3 months later established that a regular contour of Marissa’s uterine cavity had been restored.
At this point, Marissa and Pete elected to do IVF. She responded well to a modest stimulation with gonadotropins (fertility hormones) and underwent an egg retrieval where 14 mature eggs were harvested from her ovaries. At the time of egg retrieval, her uterine lining measured 6.5mm (“inadequate”). Fertilization by intracytoplasmic sperm injection (ICSI) followed by culture, resulted in 5 blastocysts, four of which were determined by preimplantation genetic testing (PGT) to be chromosomally normal (euploid). These were frozen for subsequent transfer to the uterus at a later date.
About 4 months later an attempt was made to prepare Marissa’s uterus for frozen embryo transfer FET). However, the endometrial lining was refractive to hormone therapy with oral estrogen and aspirin therapy, failing to thicken beyond 7mm (very “inadequate”). The cycle was appropriately canceled.
Subsequently, when several attempts at stimulating endometrial growth with high dosage estrogen by oral/vaginal/ skin patch and intramuscular administration failed to improve matters, Marissa sought a consultation with me as a “last resort” before either abandoning further attempts at having a baby or resorting to Gestational Surrogacy.
It was clear to me that incomplete evacuation of Marissa’s uterus after the birth of her last baby had been at the root of her problem. This almost certainly had resulted in endometritis which severely damaged her basal (germinal”) endometrium and caused an inflammatory process that fused the inner surfaces of her uterine cavity. Because of this, implantation could not take place.
Endometrial Thickness and implantation potential:
It was as far back as 1989, when I first published a study that examined the correlation between the thickness of a woman’s uterine lining (the endometrium), and the subsequent successful implantation of embryos in IVF patients. This study revealed that when the uterine lining measured less than 8mm in thickness by the day of the “hCG trigger” (in fresh IVF cycles), or at the time of initiating progesterone therapy (in embryo recipient cycles, e.g. frozen embryo transfers-FET, egg donation-IVF etc.), pregnancy and birth rates were substantially improved. Currently, it is my opinion, that an ideal estrogen-promoted endometrial lining should ideally measure at least 9mm in thickness and that an endometrial lining measuring 8-9mm is “intermediate”. An estrogenic lining of less than 8mm is in most cases unlikely to yield a viable pregnancy.
A “poor” (less than 8mm) uterine lining is usually the result of the innermost layer of endometrium (the basal or germinal endometrium from which endometrium grows) ) not being able to respond to estrogen by propagating an outer, “functional” layer thick enough to support optimal embryo implantation and development of a healthy placenta (placentation). The “functional” layer ultimately comprises 2/3 of the full endometrial thickness and is the layer that sheds with menstruation in the event that no pregnancy occurs.
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[@unkim7085]

Hi doctor, what about the plasma inyection system nowadays?
I've been told they could work with thin endometriums