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.
Dr Sher, I had a miscarriage last year in december in week 10. I did´nt bleed and everything looked perfect before the miscarriage according to the Dr and I even saw a little heartbeat. I got pregnant without any help. At the time I was 35 going on 36. I did not respond to Cytotec medicine Dr gave me the first time. I had only bad labor pains. So the Dr gave me another round of Cytotec. I started to bleed but not much. I went to the Dr once a week for 9 weeks and everytime they said that I had little blood left. The tenth week I woke up in my own blood bath and I was taken to the hospital and they operated me, and took out all the blood and everything that was left from the miscarriage (Medical scraping). My blood level was down to 82. When I got my menstruational period back I only had some spotting, dark spotting. Before I got pregnant I did´nt bleed so much during my menstruational period but I still felt that something was different. So i started seeking for fertility Dr and found out that my uterine lining is only 3 mm. I did a hysteroscopi and they did´nt find anything, only some smal bleeding. I started treatment two mounths ago to see if my uterine lining will respond to medicine and the Dr gave me 6 mg progynon day 1-12 (two oral and one vaginal), and Gonal-F (different dose) day 3-17. Everything looked good but not the uterine lining. It did´nt respond to the medicine and it is still 3 mm… My Dr thinks that I may have got pregnant with a thin uterine lining because I did´nt have strong menstruational period and if I have had the progesteron support it may have helped me. Or that the surgery went wrong. Only guesses. I also found out that I have heart shaped uterus. Maybee worth to mention, I also have Talassemia minor. I have never had any problems and I don´t need blood, but my blood levels have always been round 90. I write to you, in desperate need of help, because my Dr does not know what to do now. My plan was to do a insemination with donated sperms because I have no longer a partner but right now that is not an option with thin lining. What should I do? Should I try blood thinners? Can I fix my uterine lining with surgery or should I also try vaginal Viagra? The only problem is that we don´t have vaginal Viagra in Sweden. Is there anything else you think I should try? Menopur instead of Gonal-F? Thank you for taking your time to read my story.
Alas, the most likely scenario is that you had retained products of conception for quite a long time and this got infected leading to endometritis and damage to your uterine lining, that might not be reverable. How the D&C might have contributed to this is hard to say.
The considerable emotional, physical and financial burden associated with infertility treatment in general and with IVF in specific, demand that factors known to affect outcome be identified and regulated prior to initiating treatment.
Just as a successful garden needs a ”good” seed properly planted in fertile soil to produce healthy plants, successful embryo implantation requires a good seed (genetically “normal” embryo) and fertile soil (receptive uterine lining) to make a healthy baby. I have long used this “Seed/Soil Relationship” analogy to help clarify the critical nature of the interaction between embryo and endometrium in the successful propagation of pregnancy..
There have in the last decade been numerous reports suggesting that certain drugs/supplements (e.g. GCSF) and endometrial receptivity testing/preparation might dramatically improve implantation. As yet, none of these have been proven to be effective. This article addresses the influence of the most relevant and important factors that are known to affect .endometrial receptivity and discusses approaches to treatment:
1. Endometrial thickness
In 1989, I first demonstrated that in both normal and “hormonally stimulated” cycles, preovulatory endometrial thickness as assessed by ultrasound examination, is partially predictive of embryo implantation (pregnancy) potential following IVF. Ideally the endometrium should measure at least 8.0mm in thickness, (but preferably >9mm).
A “poor” endometrial lining is most commonly due to: 1) inflammation of the uterine lining (endometritis) that usually occurs as a result of endometritis (inflammation of the uterine lining that can follow a septic delivery, partial retention of the placenta following delivery, abortion or miscarriage, 2) severe adenomyosis (gross invasion of the uterine muscle by endometrial glandular tissue), 3) multiple fibroid tumors of the uterine wall) 4) prenatal exposure to the synthetic hormone, diethylstilbestrol (DES) and, 5) following >3, consecutive, back to back cycles of clomiphene citrate ovulation induction.
Treatment with vaginal Sildenafil (Viagra): Hitherto, attempts to augment endometrial growth in women with poor endometrial linings by bolstering circulating estrogen blood levels (through the administration of increased doses of fertility drugs, aspirin administration and with supplementary estrogen therapy) have yielded disappointing results.
In the mid-90’s I first reported on the finding that thee vaginal administration of Viagra for several days prior to the “hCG trigger “ or progesterone administration enhances uterine blood flow and estrogen delivery to the uterine lining and so improves endometrial thickening. Then In October 2002, I reported on the administration of vaginal Viagra to 105 women with repeated IVF failure due to persistently thin endometrial linings. All of the women had experienced at least two (2) prior IVF failures attributed to intractably thin uterine linings. About 70% of these women responded to treatment with Viagra suppositories with a marked improvement in endometrial thickness and 45% of these women achieved live IVF- births following a single cycle of treatment with Viagra. Nine percent (9%) miscarried. None of the women who had failed to achieve an improvement in endometrial thickness following Viagra therapy, subsequently and who underwent embryo transfers achieved viable pregnancies.
2.Uterine Pathology:
It has long been suspected that anatomical defects of the uterus might result in infertility.
While myomas (fibroids) embedded deep in the uterine wall, are unlikely to cause infertility, an association between their presence and infertility has been observed in cases where they distort the uterine cavity, or protrude as submucous polyps through the endometrial lining. It would appear that even small submucous myomas have the potential to prejudice implantation.
Far too many infertile women found to have a partial or complete septum in the uterus are subjected to surgical excision of the septum with a promise that this will enhance subsequent implantation. This is an erroneous belief. Contrary to popular belief, the presence of a septum that partially or completely partitions the uterine cavity, while being responsible (in some cases) for late miscarriages and premature onset of labor, does NOT cause failed implantation.
It is likely that most surface lesions in the uterine cavity, whether due to an endometrial, placental or fibroid polyp (no matter how small), or intrauterine adhesions, have the potential to interfere with implantation by producing a local “inflammatory”- type response, not too dissimilar in nature from that which is caused by a foreign body such as a intrauterine contraceptive device. Unfortunately, a dye X-Ray test (hysterosalpingogram/HSG) will often miss many smaller such lesions. The only reliable methods for diagnosing even the smallest of such lesions, is through the performance of a hysterosongram (HSN),a hysteroscopy or an MRI.
Hysterosonogram (syn. Saline ultrasound): This procedure involves the trans-cervical injection of a physiological saline solution via a catheter, into the uterine cavity. The fluid distended cavity is then examined by vaginal ultrasound for any irregularities that might point to surface lesions such as polyps, fibroid tumors, scarring, or a uterine septum. If performed correctly, the HSN is highly effective in recognizing even the smallest surface lesions that protrude into the uterine cavity. It is less expensive, less traumatic, and diagnostically, equally reliable as hysteroscopy. The only disadvantage lies in the fact that if a lesion is detected, it may require the subsequent performance of hysteroscopic surgical approach to treating the problem..
Hysteroscopy: Diagnostic hysteroscopy is an office procedure that is performed under intravenous sedation, general or local anesthesia, with minimal discomfort to the patient. The procedure involves the insertion of a thin, lighted, telescope like instrument known as a hysteroscope through the vagina and cervix into the uterus in order to fully examine the uterine cavity. The uterus is first distended with carbon dioxide gas, which is passed through a sleeve adjacent to the hysteroscope. As is the case with FUS, diagnostic hysteroscopy facilitates examination of the inside of the uterus under direct vision for defects that might interfere with implantation.
We have observed that approximately 8% of candidates for IVF have intrauterine lesions that require attention prior to undergoing IVF in order to optimize the chances of a successful outcome. We strongly recommend that all patients who have such lesions undergo surgery (D&C and/or hysteroscopic resection) to correct the pathology prior to undergoing IVF. Depending on the severity and nature of the pathology, therapeutic hysteroscopy may require general anesthesia. If so, it should be performed in an outpatient surgical facility or in a conventional operating room.
3. Immunologic factors
The implantation process begins six or seven days after fertilization of the egg. At this time, specialized embryonic cells (i.e., the trophoblast), which later becomes the placenta; begin growing into the uterine lining. When the trophoblast and the uterine lining meet, they, along with Immune cells in the lining, become involved in a “cross talk” through mutual exchange of hormone-like substances called cytokines. Because of this complex immunologic interplay, the uterus is able to foster the embryo’s successful growth. Thus, from the very earliest stage of implantation the trophoblast establishes a foundation for the future nutritional, hormonal and respiratory interchange between mother and baby. In this manner, the interactive process of implantation is not only central to survival in early pregnancy but also to the quality of life after birth.
Considering its importance, it is not surprising that failure of proper function of this immunologic interaction during implantation has been implicated as a cause of recurrent miscarriage, late pregnancy fetal loss, IVF failure, and infertility. A partial list of immunologic factors that may be involved in these situations includes anti-phospholipid antibodies (APA), antithyroid antibodies (ATA), and most importantly activation of uterine natural killer cells (NKa). Presently, these immunologic markers in the blood can be only adequately measured by a handful of highly specialized reproductive immunology laboratories in the United States. I personally use Reproductive Immunology Associates in Van Nuys, CA or Reprosource in Boston, MA.
The Central role of Natural Killer cells: After ovulation and during early pregnancy, NK cells comprise more than 70% of the immune cell population of the uterine lining. NK cells produce a variety of local hormones known cytokines. Uncontrolled, excessive release of certain cytokines (i.e. TH-1 cytokines) is highly toxic to the trophoblast (“root system”) of the embryo” leading to their programmed death (apoptosis) and, subsequently to failed or compromised/dysfunctional implantation. In the following situations NK cells become activated, and start to produce an excess of TH-1 cytokines:
•Autoimmune Implantation Dysfunction: This is most commonly seen in association with a personal or family history of autoimmune diseases such as ith conditions such as Rheumatoid arthritis, hypothyroidism endometriosis and Lupus Erythematosus, Scleroderma, Dermatomyositis etc. It is also encountered in one third of women who have endometriosis (regardless of its severity), and in cases of “unexplained infertility” as well as with recurrent pregnancy loss (RPL).
•Alloimmune implantation dysfunction where the male and female partners share specific genetic (DQ-alpha and/or HLA) similarities This is commonly seen in cases of RPL and in cases of secondary infertility
Activated NK cells (NKa) can be detected through the K-562 target cell blood test and (more recently) through uterine biopsy for TH-1 cytokine activity. Treatment involves selective use of Intralipid (IL) or immunoglobulin (IVIG) therapy combined with oral steroids, initiated more 10-14 days prior to embryo transfer and in most cases of alloimmune implantation dysfunction, the transfer of a single blastocyst at a time.
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.
Hi Dr. Sher, this is your patient from the October FET cycle. I just got a positive home pregnancy test result, however there are few days left before the first beta (on the 9th of Nov). My nurse who can do Intralipid infusion here in Toronto is going to be away from the 8th to 15th of Nov. I wonder if i’d better do IL infusion now on the 7th of Nov, or is it safe to wait until the 16th ofNov (second beta is on 11th of Nov), or do i have to find another nurse to do it on the 12th of Nov if the second beta is OK (i.e. doubled).
Please advise.
Thank you!
CONGRATULATIONS!!!
I agree, do it now. Rather safe than sorry!
Geoff Sher
Hi,
Why cervical stitch important between 18-24 weeks even cervical length is 3.8cm. Is it necessary to have cerclage and after cerclage do we have pain afterward and any affect on baby.
With cervical Incompetence (CI) the cervix starts to shorten (efface) and dilate too early in the pregnancy giving rise to late (2nd trimester) miscarriage or premature birth. It can occur with first pregnancies (“Primary Cervical Incompetence”) or after a prior pregnancy (“Secondary Cervical Incompetence”). CI often occurs in women who give a history of cervical insufficiency in one or more prior pregnancies; late miscarriages or premature deliveries of unknown cause; cervical injury during a previous birth or dilation and curettage (D&C); congenital uterine abnormalities such as a partial/complete uterine septum / unicornuate uterus; prior conization or a LEEP procedure done for an early (pre)cancerous condition affecting the cervix or in women with a multiple pregnancies (twins or greater)
The diagnosis of CI is suspected when a woman in pregnancy that has advanced into the 2nd or early 3rd trimester presents with bleeding and low pain-grade contractions associated a bulging bag of membranes, frequently followed by a sudden gush of fluid per vagina and relatively rapid progression to complete expulsion of the fetus and placenta.
Threatened CI should be suspected by the detection of a partially dilated and shortened cervix with routine pelvic examination performed in the mid-trimester or early 3rd trimester.
When during the non-pregnant state there is suspicion of CI, this should be investigated through the performance of one or more of the following:
1.A hysterosalpingogram (HSG-dye x-ray test) to evaluate for a well demarcated anatomical transition from endocervical canal to the uterine cavity (without evidence of “funneling”) and to detect a deformity (congenital or acquired) of the uterus, that can also lead to mid- trimester miscarriage and premature birth.
2.A vaginal ultrasound examination to measure the length of the cervical canal (it should measure more than 2.5 cm) and to exclude pathology of uterine wall(e.g.; fibroids)
3.A diagnostic hysteroscopy to carefully evaluate uterine scarring, fibroid tumors protruding into or distorting the uterine cavity and for the congenital deformities such as a uterine septum.
Treatment:
Cervical incompetence is routinely treated by the placement of a temporary circumferential non-absorbable tape or suture around the neck of the cervix at the 12th-14th week of pregnancy per vagina (“McDonald cerclage”. The advantage of this approach is that the cerclage can readily be removed a week or two before delivery, thereby allowing a subsequent spontaneous vaginal birth to take place The disadvantage of placing a McDonald cerclage” is the ever present risk of puncturing the fetal membranes while inserting the stitch. This sometimes prompts the overcautious OB/GYN to place the stitch well below the cervical-uterine junction, thereby increasing the likelihood that it will slip or tear and thus fail to prevent cervical shortening and dilatation.
After undergoing a preliminary assessment to confirm the diagnosis of cervical incompetence, non-pregnant women in whom a McDonald cerclage has failed, should be considered for the elective placement of a permanent, non-absorbable cerclage “Shirodkar suture”(, prior to undertaking another pregnancy. In fact I believe that this should be considered as the primary (initial) approach. The reason is that in the absence of a pregnancy, it is possible, through careful surgical dissection, to ensure the correct placement of the suture (usually a double strand of #2 nylon is used), and in so doing, maximize its effectiveness. The one relative disadvantage to this approach is that the completely buried Shirodkar suture, is sometimes not amenable to removable before delivery. Accordingly, such women would require delivery by Cesarean section. Notwithstanding this, we hold that a Cesarean delivery, is a relatively small price for a woman who has usually experienced recurrent pregnancy loss, and/or repeated premature deliveries, to pay to have a healthy baby.
Hope this enlightens and helps you.
Geoff Sher
Hi Dr Sher,
I’m hoping for some advice. I am 40 years old and have done 6 rounds of IVF. We are currently struggling to produce blastocysts following previous success.
Would it be possible for you to let me know your thoughts on the following:
– agonist, antagonist or flare cycle
– introduce the pill prior to commencing for 2 weeks?
– not include an LH due to my age and potentially compromising egg quality (i.e. menopur)
Cycle 1 – Antagonist (0.25 Orgalutran, 225 Puregon). 3 eggs collected, 1 blastocyst (down syndrome).
Cycle 2 – Flare (Synarel, 300 Puregon, 150 Menopur). 12 eggs collected, 4 blastocyst, 2 PGS normal.
Cycle 3 – Flare (Synarel, 300 Puregon, 150 Menopur). 9 eggs collected, 2 blastocyst, 1 PGS normal.
Cycle 4 – Long down reg (Synarel, testosterone patches, 300 Puregon, 150 Menopur), 15 eggs collected, 0 blastocyst (potentially due to a testicular aspiration)
Cycle 5 – Long down reg (Synarel, testosterone patches, 300 Puregon, 150 Menopur), developed cyst and after draining cycle cancelled as not many follicles
Cycle 6 – Long down reg (Pill, Synarel, testosterone patches, 300 Puregon, 150 Menopur), 20 eggs collected, 0 blastocysts.
really really really appreciate your help… thank you, Emily.
Respectfully, I do not agree with the use of testosterone patches or “Flare protocols (see below). Also, failure to conceive in spite of transferring PGS-normal blastocysts suggests an implantation dysfunction.
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
•Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the “Conventional” Antagonist Approach
•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 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
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.
Hi DR Sher. I did a fresh IVF cycle with a 5 day transfer where 2 embryos were transferred. My hcg levels were 64 on my first blood test. 167 2 days later then dropped to 154 4 days later. Now today 2 days later it is 205. They told me to stop all medication and expect bleeding and I have to go back next week. Just wondering what your opinion is. They said it is a “dysfunctional” pregnancy
I am afraid it does not look promising. However, I would repeat the test in 2 days, just to be sure.
Geoff Sher