Ask Our Doctors – Archive
Our Medical Directors are outstanding physicians that you will find to be very personable and compassionate, who take care to ensure that you have the most cutting-edge fertility treatments at your disposal. This is your outlet to ask your questions to the doctors.
Hello Dr Sher,
I hope this email finds you well !
I’m 42, started fertility treatement at 40 and wasted precious time on IUI cycles. Unforunately, I was not up to speed on fertility related matters at that point. I have subsequently completed 2 rounds of IVF, first round produced 2 Euploid embryos (I have not attempted transfer yet), thought it sensible to try and obtain further Euploid embryos. The 2nd round produced no Euploid Embryos, only 1 mosaic. The same IVF protocol was undertaken both times, 150 IUI Menopur daily and I triggered with Burserelin.
I’ve joined another IVF clinic (in UK, alas USA is not a viable option), they have a different approach and their success levels are quite impressive, particulary for women over 40/more difficult cases.
I have completed a monitoring cycle with them, where they tested ovulation, horomone levels at various stages of the cycle etc. and various other things, everything seems to be working quite optimally.
However , I am concerned about my AMH level, it was 31 when I started the process at 40, now it 20.1 and I’m wondering if that now indicates poor ovarian reserve and whether it is worth spending vast sums of money to give IVF another go or is it the case that I’m very unlikely to produce another Euploid embryo given age and love AMH level. Just looking for some reassurance that it’s worth giving IVF another go.
My FSH level is very low for my age, if that makes any difference.
Many thanks for your time and help in advance!
Kindest regards,
Cassidy
Your AMH is fine (normal is >15pmol/L or >2ng/ml)
Geoff Sher
Dr. Sher,
Thanks so much for this great website and your guidance to many of us.
We had an IVF and now planning to transfer a Euploid embryo. (We have only 2 embryos). Wife is 38 years old. HSG shows:
– Right Fallopian tube is visualized. Free spillage of contrast seen.
– Left Fallopian tube is visualized, The caliber is dilated. There is no free spillage of contrast. Adhesions at the distal fimbrial end is a possibility. Mild Left hydrosalpingx with obliterated left fallopian tube.
However, on Abdominal or Vaginal Ultrasonography- there is no evidence of a dilated Fallopian tube.
Question: Do we need to get a salpingectomy or tube blockage procedure done before the FET? Could the hydrosalpinx noted on the HSG likely be just because of the dye pushed in ?
Thanks so much Dr. Sher
I would still go ahead and have the functionless tube removed or proximally ligated.
Tubal damage is one of the commonest causes of infertility. It is most often due to pelvic inflammatory disease (PID) caused by sexually transmitted bacterial infection with chlamydia trachomatis and Neisseria gonorrhea. Acute PID caused by such usually are associated with severe clinical manifestations such as rapid onset of fever, peritonitis and severe abdominal pain and as such cases are usually readily identified and treated. The problem is that the diagnosis is often missed because early symptoms mimic lesser clinical problems such as urinary, cervical and vaginal inflammation. As a result, (especially in 1st world countries) doctors often tend to “jump the gun” and initiate treatment with (often the wrong) antibacterial agents, without first conducting the appropriate urinary, cervical and vaginal cultures that are required to make a definitive diagnosis. This serves to explain why in countries such as the U.S.A, >70% of infertility caused tubal damage is unassociated with a history of a prior acute PID attack and goes undetected until irreparable damage has already been done and comes as a surprise.
It is essential to recognize that PID almost always affects both tubes and even when one tube appears to be open, both are likely to be damaged and functionally compromised. The reason that this is important to know is that patients are often erroneously led to believe that because one tube appears to be patent, they have a good chance of conceiving via that tube, even if the other tube is blocked.
In some cases, when inflammation results from retention of products of conception (following miscarriage or child birth), the uterine lining (endometrium) might become infected (endometritis), leading to scarring and sometimes permanent damage with resultant inability to thicken sufficiently (in response to estrogen), to support an implanting pregnancy. Other less frequent causes of tubal damage include, adhesions resulting from a ruptured or twisted ovarian cyst, pelvic surgery, peritonitis (due to conditions such as appendicitis, diverticulitis, Crohn’s disease, Ulcerative colitis ,trauma, etc.) or from endometriosis. Tubal damage through infection with tuberculosis is uncommon is a serious condition and irreparable. It is common in Asia (especially in India) but fortunately rarely encountered in the U.S.A. and other 1st world countries.
It is noteworthy, that a history of an ectopic pregnancy (pregnancy growing in the Fallopian tube) is highly suggestive of preceding tubal damage, usually due to PID. This is why once a woman has had an ectopic pregnancy, she has a reduced chance of conceiving again and if shg does, the chance of a second ectopic is about 20 times greater.
Tubal blockage can readily be diagnosed by a hysterosalpingogram (HSG) where a radio-opaque dye is injected through the cervix into the uterus. Successive x-rays are then taken in rapid succession to track passage of the dye into the uterus and then to determine whether it passes into the Fallopian tubes and then spills into the pelvic cavity. It is important to recognize that determination of the tubes being patent does not rule out tubal damage. All it tells you is that the petal-like fimbriated ends of the tubes have not fused and blocking their ends. It is especially important to take bear this fact in mind whenever the tubes are found to be open, in spite of there being a history of prior PID. The diagnosis can also be made by performing an out-patient surgical procedure known as laparoscopy where a thin telescope-like instrument introduced into the pelvic cavity allows visualization of pelvic organs and thus the failure of dye injected via the cervix into the uterus fails to pass via the tubes into the pelvic cavity.
Tubal blockage can occur anywhere along the course of the fallopian tube(s). It sometimes occurs in the part of the Fallopian tube that passes through the wall of the uterus (this is often due to post-pregnancy endometritis) It can also occur in the mid-section of the tube. Most commonly however, it occludes the far end of the tubes.
In some cases Fallopian tubes damaged by PID will become distended with trapped tubal secretions that often contain toxins that are capable of killing eggs, sperm and embryos. Such distended Fallopian tubes (hydrosalpinges) can leak fluid back into the uterine cavity where the can destroy transferred embryos upon contact. This is why patients who have hydrosalpinges and are considering undergoing IVF, should first have hydrosalpinges surgically removed or (at the very least) have the affected tube(s) surgically clipped or tied as they emerge through the uterine wall. This will avoid subsequent back flow when IVF is performed. Understandably, it is often hard for patients to come to terms with the fact that following such surgery they no longer have any possibility of having functional Fallopian Tubes. Such women should be counseled that hydrosalpinges are functionless tubes anyway and that any attempt to open such tubes surgically in an attempt to restore fertility would be an exercise in futility, anyway.
In a nutshell: Infertility associated with tubal blockage, especially if due to PID, is an absolute indication for IVF. I would go even further in stating that any tubal damage due to PID, whether or not it is associated with blockage is an indication for IVF, especially when detected in older women and those who because of age or diminished ovarian reserve (DOR) have no time to waste on other less successful treatments.
Finally, tubal surgery is a very poor alternative to IVF. Besides, with more than 10% of pregnancies that occur following surgery to correct on PID-related damage ending up as ectopic pregnancies (a potentially life-threatening situation). Why take such a risk anyway?
Good luck!
Geoff Sher
Does sex before FET help the embryo stick?
Good question. It is possible that there are substances in the ejaculate that signal the uterus that the embryo is soon to arrive in the uterus and to prepare for this. That is definitely the case in some mammals and might also be so in humans. So, yes! It certainly will do no harm. I would suggest the night vprior to FET.
Good luck!
Geoff Sher
Good day,
I am 35 years old and have been through 4 failed IUI and 2 IVF Cycles. Good quality embryos were collected, however, on both occasions, no implantation occurred. We have recently done our Chicago Blood Tests and have been told that we have Homozygous Mutated 4G/4G Genotype. As a result, it has been suggested that we take Clexane and ASS from day 1 of our next stimulation. Can you explain what is this condition and could it be the reason of recurrent implantation failure? Is this something that merits concern?
Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
1.Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
2.Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about 15y ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
3.The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
4.Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
a.A“ thin uterine lining”
b.A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
c.Immunologic implantation dysfunction (IID)
d.Endocrine/molecular endometrial receptivity issues
e.Ureaplasma Urealyticum (UU) Infection of cervical mucous and the endometrial lining of the uterus, can sometimes present as unexplained early pregnancy loss or unexplained failure following intrauterine insemination or IVF. The infection can also occur in the man, (prostatitis) and thus can go back and forth between partners, with sexual intercourse. This is the reason why both partners must be tested and if positive, should be treated contemporaneously.
Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
•The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation (COS)
•The Fundamental Requirements for Achieving Optimal IVF Success
•Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
•Ovarian Stimulation in Women Who have Diminished Ovarian Reserve (DOR): Introducing the Agonist/Antagonist Conversion protocol
•Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
•Human Growth Hormone Administration in IVF: Does it Enhances Egg/Embryo Quality and Outcome?
•The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
•Blastocyst Embryo Transfers should be the Standard of Care in IVF
•IVF: How Many Attempts should be considered before Stopping?
•“Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
•IVF Failure and Implantation Dysfunction:
•The Role of Immunologic Implantation Dysfunction (IID) & Infertility (IID): PART 1-Background
•Immunologic Implantation Dysfunction (IID) & Infertility (IID): PART 2- Making a Diagnosis
•Immunologic Dysfunction (IID) & Infertility (IID): PART 3-Treatment
•Thyroid autoantibodies and Immunologic Implantation Dysfunction (IID)
•Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management 🙁 Case Report)
•Intralipid and IVIG therapy: Understanding the Basis for its use in the Treatment of Immunologic Implantation Dysfunction (IID)
•Intralipid (IL) Administration in IVF: It’s Composition; how it Works; Administration; Side-effects; Reactions and Precautions
•Natural Killer Cell Activation (NKa) and Immunologic Implantation Dysfunction in IVF: The Controversy!
•Endometrial Thickness, Uterine Pathology and Immunologic Factors
•Vaginally Administered Viagra is Often a Highly Effective Treatment to Help Thicken a Thin Uterine Lining
•Treating Out-of-State and Out-of-Country Patients at Sher-IVF in Las Vegas:
•A personalized, stepwise approach to IVF
•How Many Embryos should be transferred: A Critical Decision in IVF?
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ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
Founded in April 2019, Sher Fertility Solutions (SFS) offers online (Skype/FaceTime) consultations to patients from > 40 different countries. All consultations are followed by a detailed written report presenting my personal recommendations for treatment of what often constitute complex Reproductive Issues.
If you wish to schedule an online consultation with me, please contact my assistant (Patti Converse) by phone (800-780-7437/702-533-2691), email (concierge@SherIVF.com) or, enroll online on then home-page of my website (www.SherIVF.com).
PLEASE SPREAD THE WORD ABOUT SFS!
Geoff Sher
What do you do to prevent the rubber core from getting into the progesterone in oil and contaminating the medicine. I only got one dose from the progesterone vial and rubber is in it. From my understanding, you cannot use the medicine if something gets in it. I thing the 18 gauge needles are dull and so big that they push the rubber into the medicine.
This is very rare. Frankly however, I doubt the rubber core would contaminate the progesterone!
Geoff Sher