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.
My son and daughter in law are both fertile and had a 4 month pregnancy which was terminated due to her b in a pre mutated fragile X carrier and the fetus s has full blown fragile X. They went through two cycles of IVF but did not produce enough eggs. They bought donor eggs and implanted 2 but she miscarried. She had all of he genetic testing and a urging biopsy. Everything was normal for except for the clotting. So they put her on two shots a day for clotting. They did the implant with a frozen embryo and it failed. No pregnancy. They have three frozen left. Funds are very limited and the doctor has had no explanation for any of it. Any suggestions?
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 a decade 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
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.
•Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
•IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
•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
•Frozen Embryo Transfer (FET) versus “Fresh” ET: How to Make the Decision
•Frozen Embryo Transfer (FET): A Rational Approach to Hormonal Preparation and How new Methodology is Impacting IVF.
•Staggered IVF: An Excellent Option When. Advancing Age and Diminished Ovarian Reserve (DOR) Reduces IVF Success Rate
•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.
•The Role of Nutritional Supplements in Preparing for IVF
•IVF Egg Donation: A Comprehensive Overview
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Geoff Sher
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
My wife recently had laparoscopic surgery and was on birth control to control hormones. She had pretty much a full period a few days before she was coming off the pills. Will starting a FET cycle not at the exact time her cycle starts decrease her chance of success. Our doctor does not feel so.
1-3 days late wont matter.
Good luck!
Geoff Sher
Hi Dr Sher, I have a short luteal phase of only 11 days and a long & irregular follicular phase. My cycles are between 28 -45 days. Does this have any impact on infertility and what can I do about it?
Thanks so much in advance!
An 11 day luteal phase is quite adequate. However check your E2 and progesterone a week after “ovulation”.
Geoff Sher
Hi Dr. Sher, I had 2 failed iui this year. We were not able to get a biopsy of the first one but on our 2nd iui we sent the specimen and the result said it was a decidua. Does it mean i was pregnant but no implantation? I was wondering what causes failed implantation if there was a fertilization in the first place. My doctor diagnosed me with PCOS. And this cycle we’re not doing iui just timed intercourse.im taking letrozole 2.5mg twice a day from day 3-7. What are the blood tests i need to have prior trigger shot? You mentioned follicle size, estradiol level and number of days of ovarian stimulation are to be considered before the trigger. What day post LMP should i get tested for estradiol and what should the level be?How much dose of ovidrel is right to have a viable egg? Also, my doctor wants me to take duphaston and utrogestan supp for 25 days from day 16. When should i get my progesterone checked? I was reading your article about this and learned so much things about timing of trigger shot and dosage but somehow i need further explanation in accordance with my case. Thank you so much!
I really cannot inject myself into your treatment in progress. It does not feel right to do so. However, I can tell you that on Letrozole you are virtually on “automatic pilot”. It is virtually impossible to alter course once you have taken the medication. If Ovidrel is used in my opinion the dosage should be 500mcg. Notwithstanding, I think you should follow the advice given by your doctor and contact later, should you feel the desire to do so.
Intrauterine insemination (IUI), the injection of sperm into the uterus by means of a catheter directed through the cervix, has been practiced for many years. The premise of this procedure is that sperm can reach and fertilize the egg more easily if placed directly into the uterine cavity. IUI is a procedure that bypasses the cervix and places specially prepared sperm into a woman’s uterus around the time of natural or induced ovulation. The suggested advantage of IUI is that it shortens the path that sperm would normally take to a woman’s fallopian tubes.
In the early ‘60s, physicians were injecting small quantities of raw, untreated semen, (sperm plus the seminal plasma) directly into the uterus at the time of expected ovulation. However, when more than 0.2 ml of semen was injected in to the uterus, serious and sometimes life endangering shock-like reactions often occurred. It was subsequently identified that the reason for such reactions related to the presence of prostaglandins within the seminal plasma. This led to the practice of injecting small amounts (less than 0.2 ml) of raw semen. However, the pregnancy rates were dismal and side effects, such as severe cramping and infection were rampant.
Soon after establishing the Northern Nevada Fertility Center in Reno in 1982 (the Nation’s first private in vitro fertilization (IVF program), we began to recognize the potential advantage of washing and centrifuging raw semen, so as to separate sperm from the seminal fluid, and thereby remove prostaglandins that cause most of the problems. We subsequently introduced and, thereupon, became the first to publish on intrauterine insemination (IUI) in the Journal, Fertility and Sterility (April 1984).
Indications for Intrauterine Insemination (IUI)
•Artificial insemination using frozen (donor) sperm: The recognition of HIV infection as a sexually transmitted disease, coupled with the fact that the virus is present in semen months before it can be detected in the blood, mandates that all donors have their semen cryopreserved (frozen) and stored for at least six months, whereupon, they be re-tested for HIV infection. Only upon confirmation of a negative test should the cryopreserved semen specimen be thawed and used for insemination. Since cryopreservation inevitably reduces sperm motility and function, it is not adequate to simply thaw the frozen specimen and then inseminate the raw semen into the vagina. Rather, the semen specimen should be processed for IUI. Provided that the recipient is ovulating normally, there is no need to administer fertility drugs, such as Clomiphene, Pergonal, etc.
•Artificial insemination with partner’s sperm: In cases of sexual dysfunction (impotence, retrograde ejaculation, etc.) or timing issues, partner’s sperm may need to be collected and processed in preparation of IUI.
•Cervical mucus hostility: Sometimes the cervical mucus acts as a barrier to the activation and passage of sperm as it passes through the cervical canal. Such hostility may be due to poor physical qualities of the mucus, cervical infection, or the presence of antisperm antibodies. In all but the latter situations, IUI can readily be performed during natural cycles, unless the woman has ovulation dysfunction. However, when infertility results from the presence of antibodies in the cervical mucus, IUI will likely be ineffectual and should be replaced by in vitro fertilization (IV).
•Absent or dysfunctional ovulation: In some cases where the woman requires the use of fertility drugs to induce normal ovulation, the concomitant performance of IUI might improve pregnancy rates.
Selecting the Fertility Drugs for Intrauterine Insemination (IUI)
Clomiphene citrate (Serophene, Clomid): Clomiphene citrate is taken orally for 5 days starting on day 2 to 5 of the menstrual cycle. Ovulation will usually occur 10 days later. In some cases, hCG is used to trigger the ovulation but this is often unnecessary. Clomiphene is a relatively inexpensive and safe method for inducing ovulation and this is why it is so commonly prescribed to women undergoing IUI. However, women receiving clomiphene have about a one third lower pregnancy rate per cycle than is the case using injectible fertility drugs. but it there are draw-backs. Here are a few reasons why this is so:
1)Clomiphene citrate is an anti-estrogen. .Ordinarily normally ovulating women (without exposure to clomiphene) produce a single dominant follicle which produces enough estrogen to promote optimal cervical mucous production and an adequate endometrial lining (>9mm) However, with clomiphene is used to induce ovulation, its anti-estrogenic effect blunts this response. In fact on clomiphene,it requires much more estrogen to override this effect such that unless at least 3 large follicles develop so as to allow the blood estradiol levels to rise above 400pg/ml, cervical mucus production and endometrial development will usually be insufficient to allow a healthy pregnancy to occur. Younger women with normal ovarian reserve (Day-3 FSH of <9miu/ml) will usually produce >3 follicles where as women over 40 years of age and those (regardless of age) with diminished ovarian reserve will rarely do so and thus are very unlikely to achieve viable pregnancies on clomiphene
2)Clomiphene induction of ovulation is associated with a 15-20% chance of a condition called luteinized unruptured follicle (LUF) syndrome where the hormonal changes that precede and accompany and follow ovulation (including a rise in blood progesterone level) occur but this happens without ovulation occurring .LUF syndrome thus leads to the erroneous conclusion that an egg has been released when, in fact, it remains “trapped” in the ovarian follicle.
3)More than 3 consecutive (back to back) of clomiphene will result in a very significant increase in the anti-estrogen effects (referred to in 1&2 above), such that unless a break of at least 1 full menstrual cycle is taken, the likelihood of a viable pregnancy declines to less than 10%, regardless of the woman’s age or her ovarian reserve.
4)Increased production of Luteinizing Hormone: Clomiphene causes the pituitary gland to produce increased amounts of FSH and LH. FSH promotes follicle growth development while excess LH causes the ovary to produce male hormones such as testosterone. While a little testosterone is indispensable to follicle and egg development, too much testosterone can have the reverse effect and harm egg development. This effect is even more deleterious in women with diminished ovarian reserve (elevated FSH levels) and those over 40 whose ovaries tend to produce more testosterone-like hormones.
The following additional factors must be considered when it comes to the use of Clomiphene:
1)It is best not being prescribed for more than three consecutive months in a row to anyone and certainly not without taking a full cycle break before restarting a fourth cycle of treatment. The reason is that after the 3-4 consecutive months of clomiphene therapy, the anti-estrogenic properties are compounded to the effect of virtually converting it to an anti-fertility drug. This explains why >80% of successful clomiphene pregnancies occur within the first 3 months of treatment, and why the vast majority of clomiphene pregnancies that occur after >3 consecutive (back-to-back) cycles of treatment are lost (usually due to early miscarriages).
2)Clomiphene should not be used in women that have diminished ovarian reserve (e.g. women with elevated FSH levels) or in women over 40 years of age.
The good news is that upon discontinuation of Clomiphene for 4-6 weeks, adverse effects disappear, leaving the slate clean.
The real benefit of clomiphene lies in its oral route of administration, low incidence of side effects, and its low cost. The birth rate per clomiphene IUI is about 7-10% per cycle of treatment (about 1/3 lower than when injectible fertility drugs are used.
Letrozole(Femara): Letrozole, like clomiphene is an oral agent induces ovulation that causes the pituitary gland to release large amounts of FSH as well as LH. The advantage that Letrozole has over clomiphene is that unlike the latter, it is NOT anti-estrogenic and thus does not compromise development of the uterine lining or adversely affect the production of cervical mucus. However as is the case with clomiphene, Letrozole causes increased LH release that can lead to overproduction of male hormones (e.g. testosterone) by the ovaries with potentially adverse effect on egg/embryo quality.
Thus while Letrozole does have potential advantages over clomiphene, the exaggerated LH-induced testosterone effect, especially in women over 40 years of age and/or those with evidence of diminished ovarian reserve limits its value.
Gonadotropins (Menopur, Gonal-f, Folistim and Puregon:) Women with absent or abnormal ovulation who require fertility drugs in preparation for IUI should receive gonadotropins. Granted, these agents are more expensive than clomiphene, but they have no anti-estrogenic properties.
The birth rate with gonadotropin IUI in women under 35 years of age (in the absence of male infertility, where it is much lower) is about 10-15%. However, success is affected by, and contingent upon, the procedure being performed (1) for the correct indications, (2) avoiding the performance of IUI when contraindications exist (see below) and, (3) where the woman is ovulating normally on her own. Success rates decrease as a woman’s age advances. In women 35-40 years of age the birth rate is 5-10% per cycle and for over 40 years, the birth rate per cycle is under 2%, declining to less than 1% after age 43.
Relative Contraindications to Intrauterine Insemination (IUI)
Advancing age: A woman’s natural ability to conceive declines with age starting after age 30. It falls more rapidly after age 35 and then, precipitously so after 40. The main reason for this is that the percentage of eggs that become chromosomally abnormal (aneuploid) through “wear and tear” increases as she gets older, such that by age 40 an ovulated egg is probably 3 times less likely to be able to propagate a viable pregnancy than at age 30. This explains the fact that under 35, the normally ovulating woman who receives injectible fertility drugs to induce ovulation has about a 10-12% chance of having a baby. In comparison, after age 40, the same woman would have about a 2% chance. For this reason alone, IUI is best suited to women under 35 and, in my opinion, should NOT be undertaken after age 40. Ages between 35 and 40 represent a “gray area.”
Significant Male Infertility: Contrary to popular belief, the performance of IUI in cases of male infertility does not improve success rates over regular and well-timed intercourse alone. In vitro fertilization with intracytoplasmic sperm injection (IVF/ICSI) is the only method to optimize pregnancy rates in association with male refractory infertility.
Tubal damage
1.Post-Pelvic Inflammatory Disease (PID): It is very important to understand that Fallopian tubes are not mere “pipes” through which sperm, egg and embryo must pass to achieve an intrauterine pregnancy. They are vital and sophisticated organs that serve intricate functions in the reproductive process. They transport sperm in the direction of the ovary, while at the same time, the fimbriae (petal-like extrusions at the end of the tube) apply themselves to the area of the ovary from which the egg is ovulating in order to pick up the extruding egg, and carry it back down the tube towards the uterus. About one third of the way back, the egg encounters the sperm and fertilization occurs. Thereupon, the resulting embryo is transported to the uterine cavity where it hopefully will implant.
PID, the commonest cause of damaged Fallopian tubes will, unless it is diagnosed and effectively treated very early on, inevitably and permanently disrupt the sophisticated function and continuity of the inner lining of both Fallopian tubes. In more severe cases, the intricate muscular arrangement of the tubal wall is also damaged, compromising the time-sensitive and programmed migration of sperm, egg and embryo. In advanced cases of PID, the fimbria fuse, thus compromising egg pick-up, and ultimately blocking the tube(s) completely.
PID almost always affects both Fallopian tubes. Indeed, one tube might be more damaged than the other, but both will be affected to a greater or lesser degree. That is why, even if one tube remains or is surgically rendered patent, the problem of markedly reduced fertility and the increased risk of a subsequent tubal pregnancy remains an ever present risk and reality. Thus, the use of fertility drugs to induce ovulation, or the use of microsurgery to open Fallopian tubes and free surrounding adhesions are often not curative of infertility. Furthermore, in cases where a pregnancy follows, the result is often a tubal (ectopic) gestation. This also serves to explain the fact that the intrauterine pregnancy rate following ovulation induction (with or without concomitant IUI) is likely to be to be at least 10 times lower in women with PID, and why, when a pregnancy does ensue, it is 10 times more likely to be a tubal (ectopic).
Thus, in women who have had PID, IVF is the only way to safely bypass the “damaged plumbing” and initiate a viable intrauterine pregnancy.
2.Post-Tubal Ligation. In large part, the same holds true following successful reconnection of previously ligated (tied) Fallopian tubes. The reason is that even with successful surgical reestablishment of tubal patency, there is always a degree of shortening of the tube(s) or a degree of damage due to surgical scarring of the inner lining of the tube(s). Even when tubes are normal, the birth rate per IUI cycle is about 10%, and following any form of tubal damage (PID or surgically-induced) the success is 5-10 times lower per IUI cycle (i.e. 1%-2%). Hence, IUI can hardly be justified in such cases, and IVF becomes the only effective and viable option.
Endometriosis:
While the exact cause of endometriosis remains an enigma, it is now apparent that immunologic dysfunction is a significant feature of this disease, and that a toxic environment exists in the pelvis (surrounding the tubes and ovaries) in patients with this condition. As a consequence, ovulation – whether spontaneous or induced by fertility drugs – commits the egg to pass through a toxic pelvic environment in order to reach the sperm waiting in the fallopian tube. This significantly reduces the egg’s fertilization potential. Furthermore, once the fertilized egg reaches the uterus, immunologic factors associated with endometriosis increase the risk of the embryo being rejected before pregnancy can be diagnosed. Such women may experience repeated “mini-miscarriages.”
In spite of these anti-fertility influences, many women with mild endometriosis do in fact conceive on their own, or following ovarian stimulation with fertility drugs. However, for reasons already referred to, the chances of conception are significantly reduced. And if they are ovulating normally on their own, the addition of fertility drugs will afford no additional benefit. Simply put, women in their late 20’s to early 30’s who have the time can anticipate about a 40% chance of conceiving on their own within two or three years (contingent upon their ovulating normally and having a fertile male partner). The occurrence of pregnancy in the latter cases occurs in spite of, rather than due to, such treatment. Such women may consider deferring any invasive treatments in favor of a “wait-and-see” approach. Conversely, women over the age of 35 whose egg quality is inevitably on the decline, IVF offers the only rational approach.
Fertility Drugs and Multiple Births
Normally ovulating women usually develop a number of follicles (fluid filled spaces within the ovary (ies) that contain eggs and produce estrogen) during the first week of the menstrual cycle. All but one (and sometimes two) of the follicles fail to develop to the point of being eligible for ovulation. The process is known as Selection. It is important to recognize that in all normally ovulating women, the one or two follicles selected to ovulate will inevitably be larger than the remaining follicles, regardless of whether the woman is receiving fertility agents such as Clomiphene or Pergonal, etc. Simply put, one or two follicles will always show enhanced development over the others, and as soon as these selected follicles ovulate, all the remaining follicles are rendered incapable of following suit. As a result, normally ovulating women no not have a greater incidence of high order multiple pregnancies. In contrast, women who do not ovulate at all, and those who ovulate irregularly or dysfunctional do not have the ability to select one or two dominant follicles for ovulation. As such, following the administration of fertility drugs for ovarian stimulation, numerous follicles may develop at the same rate, and several eggs can be ovulated simultaneously. This translates into a greater chance of pregnancy, but also a greater chance of multiple pregnancies. It is interesting that almost all reported cases of high order multiple pregnancies (greater than twins) following the use of fertility drugs have occurred in women who do not ovulate normally on their own.
It follows that only those women with absent or abnormal ovulation are at-risk for high order multiple pregnancies. They, therefore, need to be counseled regarding the consequences of premature birth and the availability of selective pregnancy reduction towards the end of the third month of pregnancy. Another alternative is to avoid the issue completely by choosing in vitro fertilization (IVF), where the number of potential babies can be limited by the number of embryos transferred to the uterus.
It is indeed unfortunate that fertility treatment has become so regimented that most patients find themselves being ushered through a scripted treatment process. As an example, clomiphene, though favored for its convenience and low cost, does NOT yield the same success as IUI with gonadotropin stimulation. In fact the per-cycle success rate of IUI using clomiphene is about 30% less. Also, women with endometriosis (regardless of severity) have much lower success with IUI (see above). Women over age 40 have such a low success with IUI that they cannot afford the time wasted in the process. Such women need IVF.
For the majority of couples who require an individualized strategic plan of action at an early stage, such an approach is emotionally, physically, and financially draining, leaving them both suspicious and critical of the intent of the medical profession.
The introduction of inexpensive Micro-IVF changes the landscape. In fact, the success rate is three times higher than with IUI. This plus the low the relatively low cost of Micro-IVF (as compared with conventional IVF) is a major advantage of the approach.
Good luck!
Geoff Sher
Dr Sher
I am 43 and had a failed donor egg transfer and 1 failed FET. with great quality embryos. I had 4 hysteroscopic myomectomies but had a lining thickness of 11mm during my last transfer. Can you tell me what my real chances are for a successful FET. Should there be other tests done before my next FET? I have 2 embryos left to transfer.
Thank you
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 a decade 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
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).
My answer to patients who ask me when is the time to stop undergoing IVF is ….Aside from the weight of the financial burden, the time to stop is when in spite of thorough and comprehensive evaluation, there is no remediable and treatable explanation for repeated failure.
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.
•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
•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
•Traveling for IVF from Out of State/Country–
•A personalized, stepwise approach to IVF
•How Many Embryos should be transferred: A Critical Decision in IVF.
•The Role of Nutritional Supplements in Preparing for IVF
Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
Julie Dahan
•Email: Julied@sherivf.com
•Phone: 702-533-2691
?800-780-7437
Geoff Sher
I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.