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.
Hi Dr. Sher!
I am almost 6 weeks pregnant and everything has been going well but today was a scare! I was feeling period like symptoms all morning and then saw my liner was full of bright red blood. My nurse at the clinic got me right in and for the first time I got to see a flickering heart beat on the ultrasound. No labs are back yet but she said bleeding is common in IVF pregnancies.
I am on Lovenox which is to be discontinued tonight (was started due to recurrent pregnancy losses, but no hypercoaguable disorders). My progesterone is PO and vaginal suppository.
She didn’t explain why bleeding is common so I would appreciate your knowledge and expertise on the matter please.
I hope to never see it again!
Could you explain why?
Dear Dr Sher,
I cannot thank you enough for your support and advice I found here – it is amazing what you do! Thinking of you often…especially when holding baby in my arms – thank you from the bottom of my heart!
I wanted to ask you few questions on behalf of my close friend who is on this bumpy road of transfers, chemical pregnancies and two miscarriages. The most devastating was emergency c section at 38 weeks due to undiagnozed velamentous cord insertion. She lost her daughter during this c-section …- it was13 months ago.
She found strength to try again but now has problems with endometrium thickness and quality. She had one chemical pregnancy with pgd tested embryo couple of month ago. Her doctor is worried that lining was completely damaged during this traumatic c section at the location where placenta was adhered…
Also, it appears that there is small pocket/niche in the scare and adenomioza caused by the section… Even though it seems that accumulation of fluid in the uterus subsided, she will have “rinsing ” treatments to heal the pocket.
Also, she is put on dipheraline for 3 months to see if it helps. And then she will transfer the last embryo.
1. Is this a good aproach with this dipheraline in your opinion?
And rinsing?
2. Is it possible that endometrium was damaged only locally and the rest remained functional?
And if so, is it possible for embryo to implant in this good portion of lining and develop not being affected by this potentially damaged part?
4. What would be the most reliable way to confirm the condition of endometrium and strengthen it?
5. She tried viagra couple years ago but different dosage/timing and it didnt seem to have any visual effect on her lining – but then her lining was still good enough to sustain pregnancy. Could viagra help now if it didnt work back then?
This will be her last attempt and any thoughts/ideas would be very, very appreciated!
Thank you,
Zuza
1. Is this a good aproach with this dipheraline in your opinion?
And rinsing?
A: I do not believe it will help
2. Is it possible that endometrium was damaged only locally and the rest remained functional?
And if so, is it possible for embryo to implant in this good portion of lining and develop not being affected by this potentially damaged part?
A: It all depends on the entire configuration of the uterine cavity and the amount of damage done.
4. What would be the most reliable way to confirm the condition of endometrium and strengthen it?
A: Hysteroscopic assessment, endometrial biopsy, US assessment of uterine blood flow and thickness of endometrium in response to estradiol administration
5. She tried viagra couple years ago but different dosage/timing and it didnt seem to have any visual effect on her lining – but then her lining was still good enough to sustain pregnancy. Could viagra help now if it didnt work back then?
A: This very much sounds like intractable damage to the basal (germinal) endometrium. If so, there is little chance that Viagra would work. If all else fails she would have to consider gestational surrogacy.
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 <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 <8mm is in most cases unlikely to yield a viable pregnancy.
A “poor” (<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.
The main causes of a “poor” uterine lining are:
1.Damage to the basal endometrium as a result of:
a.Inflammation of the endometrium (endometritis) most commonly resulting from infected products left over following abortion, miscarriage or birth
b.Surgical trauma due to traumatic uterine scraping, (i.e. due to an over-aggressive D & C)
2.Insensitivity of the basal endometrium to estrogen due to:
a.Prolonged , over-use/misuse of clomiphene citrate
b.Prenatal exposure to diethylstilbestrol (DES). This is a drug that was given to pregnant women in the 1960’s to help prevent miscarriage
3.Over-exposure of the uterine lining to ovarian male hormones (mainly testosterone): Older women, women with diminished ovarian reserve (poor responders) and women with polycystic ovarian syndrome -PCOS tend to have raised LH biological activity.. This causes the connective tissue in the ovary (stroma/theca) to overproduce testosterone. The effect can be further exaggerated when certain methods for ovarian stimulation such as agonist (Lupron/Buserelin) “flare” protocols and high dosages of menotropins such as Menopur are used in such cases.
4.Reduced blood flow to the basal endometrium:
Examples include;
a.Multiple uterine fibroids - especially when these are present under the endometrium (submucosal)
b.Uterine adenomyosis (excessive, abnormal invasion of the uterine muscle by endometrial glands).
“The Viagra Connection”
Eighteen years ago years ago, after reporting on the benefit of vaginal Sildenafil (Viagra) for to women who had implantation dysfunction due to thin endometrial linings I was proud to announce the birth of the world’s first “Viagra baby.” Since the introduction of this form of treatment, thousands of women with thin uterine linings have been reported treated and many have gone on to have babies after repeated prior IVF failure.
For those of you who aren’t familiar with the use of Viagra in IVF, allow me to provide some context. It was in the 90’s that Sildenafil (brand named Viagra) started gaining popularity as a treatment for erectile dysfunction. The mechanism by which it acted was through increasing penile blood flow through increasing nitric oxide activity. This prompted me to investigate whether Viagra administered vaginally, might similarly improve uterine blood flow and in the process cause more estrogen to be delivered to the basal endometrium and thereby increase endometrial thickening. We found that when Viagra was administered vaginally it did just that! However oral administration was without any significant benefit in this regard. We enlisted the services of a compound pharmacy to produce vaginal Viagra suppositories. Initially, four (4) women with chronic histories of poor endometrial development and failure to conceive following several advanced fertility treatments were evaluated for a period of 4-6 weeks and then underwent IVF with concomitant Viagra therapy. Viagra suppositories were administered four times daily for 8-11 days and were discontinued 5-7 days prior to embryo transfer in all cases.
Our findings clearly demonstrated that vaginal Viagra produced a rapid and profound improvement in uterine blood flow and that was followed by enhanced endometrial development in all four cases. Three (3) of the four women subsequently conceived. I expanded the trial in 2002 and became the first to report 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. Forty five percent (45%) achieved live births following a single cycle of IVF treatment with Viagra The miscarriage rate was 9%. None of the women who had failed to show an improvement in endometrial thickness following Viagra treatment achieved viable pregnancies.
Following vaginal administration, Viagra is rapidly absorbed and quickly reaches the uterine blood system in high concentrations. Thereupon it dilutes out as it is absorbed into the systemic circulation. This probably explains why treatment is virtually devoid of systemic side effects
It is important to recognize that Viagra will NOT be effective in improving endometrial thickness in all cases. In fact, about 30%-40% of women treated fail to show any improvement. This is because in certain cases of thin uterine linings, the basal endometrium will have been permanently damaged and left unresponsive to estrogen. This happens in cases of severe endometrial damage due mainly to post-pregnancy endometritis (inflammation), chronic granulomatous inflammation due to uterine tuberculosis (hardly ever seen in the United States) and following extensive surgical injury to the basal endometrium (as sometimes occurs following over-zealous D&C’s).
Combining vaginal Viagra Therapy with oral Terbutaline;
In my practice I sometimes recommend combining Viagra administration with 5mg of oral terbutaline. The Viagra relaxes the muscle walls of uterine spiral arteries that feed the basal (germinal) layer of the endometrium while Terbutaline, relaxes the uterine muscle through which these spiral arteries pass. The combination of these two medications interacts synergistically to maximally enhance blood flow through the uterus, thereby improving estrogen delivery to the endometrial lining. The only drawback in using Terbutaline is that some women experience agitation, tremors and palpitations. In such cases the terbutaline should be discontinued. Terbutaline should also not be used women who have cardiac disease or in those who have an irregular heartbeat.
About 75% of women with thin uterine linings see a positive response to treatment within 2-3 days. The ones that do not respond well to this treatment are those who have severely damaged inner (basal/germinal) endometrial linings, such that no improvement in uterine blood flow can coax an improved response. Such cases are most commonly the result of prior pregnancy-related endometrial inflammation (endometritis) that sometimes occurs post abortally or following infected vaginal and/or cesarean delivery.
Viagra therapy has proven to be a god send to thousands of woman who because of a thin uterine lining would otherwise never have been able to successfully complete the journey “from infertility to family”.
ADDENDUM: PLEASE READ!!
INTRODUCING SHER FERTILITY SOLUTIONS (SFS)
Hitherto I have personally performed IVF- treatment and related procedures on patients who, elected to travel to Las Vegas to be managed by me. However, with the launching of Sher-Fertility Solutions (SFS) in April 2019, I have taken on a new and expanded role. Now, rather than having hands-on involvement I confine my services to providing hour-long online Skype consultations to an ever-growing number of patients (emanating from >40 countries), with complex Reproductive problems, who seek access to my input, advice and guidance. All Skype consultations are followed by a detailed written report that meticulously describes and explains my recommendations for treatment. All patients are encouraged to share this report with their personal treating doctor(s), with whom [subject to consent and a request from their doctor] I will, gladly discuss their case with the “treating Physician”.
Through SFS I am now able to conveniently provide those who because of geography, convenience and cost, prefer to be treated at home or elsewhere by their chosen Infertility Physician.
“I wish to emphasize to all patients with whom I consult, that in the final analyses, when it comes to management, strategy, protocol and implementation of treatment, my advice and recommendations are always superseded by that of the hands-on treating Physician”.
Anyone wishing to schedule a Skype consultation with me, can do so by: Calling my concierge (Patti Converse) at 1-800-780-7437 (in the U.S.A or Canada) or 702-533-2691, for an appointment. Patients can also enroll online on my website, http://www.SherIVF.com, or email Patti at concierge@SherIVF.com .
I was very recently greatly honored in receiving an award by the prestigious; International Association of Top Professionals (IAOTP). For more information, go to the press release on my website, http://www.sherIVF.com .
PLEASE HELP SPREAD THE WORD ABOUT SFS!
Geoff Sher
Dear Dr Sher,
I have recently just failed my 3rd ivf cycle. In my last cycle I retrieved 16 eggs, 14 fertilised, 6 made it to blastocyst and I had 1 top grade embryo transferred. My question is, I was only told to take 125mcg hcg-ovidrel as my trigger, do you think this could have affected the aneuploity of the eggs resulting in chromosomally abnormal embryos which were never going to implant? Even through the grade was top grade no embryos were PGS tested. I have read that egg meiosis might not haven place. Am I correct in thinking this?
Respectfully, quite frankly I do! In my opinion, that is too low a dosage to trigger optimal maturational division (meiosis)
Geoff Sher
I have previously had 1 full cycle of IVF which produced 3 blastocysts. was 32 years old when started IVF- Low AMH (4.3pmol./l) but told not happened naturally largely due to male factor infertility. The third transfer resulted in a pregnancy but had a missed miscarriage at 8 weeks.
Have recently started another fresh cycle- 4 eggs, all fertilised but only 3 developing normally. Had option to wait till 5 day but clinic recommended transfer on day 3. Had one transfer on day 3 just in case they dont reach blastocyst. I have had a single day 3 transfer and waiting a 2 week wait now. I am also on prednisolone and clexane. Are my chances alot lower as i had a day 3 tranfer?
Thanks.
If the embryo was chromosomally normal, it would no difference whether a day 2,3 or 5-6 day embryo were transfered. The issue is that the likelihood of it being chromosomally competent is far greater ifit made it to the blastocyst stage. There is NO advantage in transferring an embryo on day 3.
Geoff Sher
Dear Dr. Sher
I have high prolactin as I am on antipsychotics .Can I continue with my medication till egg retrieval stage of IVF with high prolactin. And stop medication after egg retrieval before FET. Will high prolactin effect the egg quality and its fertilization ?
You can continue the medications. However, a high prolactin can impact egg quality so I would discuss with your RE, the taking of meds to lower prolactin before ovarian stimulation.
Geoff Sher