Embryo Transfer: The “Holy Grail” of IVF.

Embryo transfer (ET) is undoubtedly a rate limiting factor in IVF. Unquestionably, the IVF doctor’s expertise in performing ET as one of the most important factors that will determine IVF outcome. It takes confidence, dexterity, skill, gentility and above all, experience to do a good transfer. This having been said, of all the procedures in IVF this is the most difficult to teach. It is a true “art” and there is little doubt that many women will fail to conceive following IVF simply because their doctor could not perform this procedure optimally.

Good quality embryos are those whose cells (blastomeres) continue to divide at a regular and predictable rate, such that  within 72 hours of fertilization they contain 5-9 cells and within 5-6 days, they will have developed into expanded blastocysts with >100 cells. Such embryos are the ones that are most likely to be “competent” (i.e., able to propagate a pregnancy upon being transferred to a receptive uterus). Conversely, embryos that fail to develop into expanded blastocysts within 5-6 days of being fertilized, are almost invariably chromosomally abnormal (aneuploid), “incompetent” and are unworthy of transfer.

The addition of preimplantation genetic screening (PGS) with full embryo karyotyping (which assesses all the embryo’s chromosomes), markedly improves the ability to select truly “competent” embryos for transfer. The select transfer of such PGS-normal blastocysts, vastly increases the baby rate per embryo transferred, markedly reduces the likelihood of miscarriage, and minimizes the occurrence of chromosomal birth defects such as Down’s Syndrome.

Shortly before performing ET, the embryos are put together in a single laboratory dish containing growth medium. The laboratory staff informs the clinic coordinator that the embryos are ready for transfer, and the coordinator prepares the patient and informs the physician that a transfer is imminent.

Ultrasound Guided Embryo Transfer: A Must!

Today all embryo transfers should, in my opinion, be performed under direct ultrasound guidance to ensure proper placement in the uterine cavity. All other factors being equal, such practice, properly conducted, will significantly enhanced embryo implantation and pregnancy rates.

Optimal Bladder filling to promote visualization:

I prefer to perform all embryo transfers with the patient having a full bladder. This tends to facilitate clear into visualization of the uterus by abdominal ultrasound and the bladder distention causes reflex nervous suppression of uterine contractility, reducing the chance of embryo expulsion. The patient is allowed to empty her bladder 10 minutes following the embryo transfer. In cases where at the time of ET, the bladder is found to be over-full or insufficiently distended this can be readily corrected. In cases of an over-full bladder the patient partially empty her bladder or it can be achieved through deliberate controlled catheterization and drainage. An under-filled bladder can be addressed by increasing fluid intake and monitoring bladder filling ultrasonographically or by catheterization followed by controlled bladder filling with sterile isotonic saline solution.

Adequate relaxation:

It is important that the woman be as relaxed as possible during the embryo transfer because many of the hormones that are released during times of stress, such as adrenalin, can cause the uterus to contract. Accordingly we offer our patients, an oral tranquilizer (usually 5mg of oral diazepam or Valium) taken about a half hour prior to the embryo transfer, to relax the woman and reduce apprehension.

Some IVF programs believe that imagery helps the woman relax and feel positive about the process and in the process reduce the stress level. In such a program, a counselor and/or clinical coordinator may help the woman focus on visual imagery for a few minutes immediately prior to embryo transfer so as to enhance her relaxation.

How Many Embryos should be transferred?

There is an overriding need to minimize the occurrence of multiple gestations, especially high order multiples (triplets or greater). This is because of the risk of prematurity-related complications increase proportionate to the number of babies in the uterus. Unfortunately there are several confounding considerations in determining how many embryos to transfer at a time:

  1. The stage of development that the embryos have reached by the time of the ET must also be taken into account in deciding how many to transfer. The reason for this is that blastocysts are far more likely to propagate pregnancies than are cleaved (day 2-3) embryos. So fewer blastocysts need be transferred at a time.
  2. The older the woman who produced the eggs, the greater the likelihood that upon being fertilized, the resulting embryo(s) would be “incompetent:”. It follows that the number of embryos that might safely be transferred per IVF procedure (without resulting in a high-order multiple) should be governed by the age of the egg provider. So, while it would be reasonable to restrict the number of “high grade” embryos transferred to a younger woman to one (1) or two (2), the same restriction would be inappropriate and unreasonable  in the case of  a  woman in her 40’s receiving embryos derived from the fertilization of their own eggs.
  3. Microscopic grade of the embryos. When a decision on how many embryos to transfer is often based upon the microscopic appearance of such embryos than their microscopic “grade” should be taken into consideration. Since it is less likely that a “lower grade” embryo would propagate a baby than would be the case for one that was of “high grade”, it follows that when it comes to older women, it would be both appropriate and acceptable to transfer more low-grade embryos at a time than were the embryos to be of “high grade”
  4. Embryo genetic “competency”. Since an embryo’s “competence” can largely be determined through PGS.). It is thus is feasible in the case of PGS-normal blastocysts to conduct single embryo transfers

As a rule of thumb however, I tend to transfer one (2) PGS-untested blastocysts to women under 40 years and, up to three (3) PGS-untested embryos to the uteri of women > 40 years I support a policy where single PGS-normal blastocysts are transferred to women of any age. 

The Embryo Transfer Process:

When the woman is in the proper position, and her bladder is adequately filled, the physician first inserts a speculum into the vagina to expose and rigorously clean the outer cervix with a sterile, isotonic saline solution to remove any mucus or other secretions, followed by a gentle lavage of the outer cervical canal with Human Tubal Fluid (HTF)  An abdominal ultrasound transducer is placed suprapubically on the lower abdomen to allow clear visualization of the uterus is clearly visualized. Thereupon, using sterile technique, I introduce a sonically activated embryo transfer cannula (with an empty internal catheter through the entire length of the cervical canal until the sonically activated tip reaches the junction of the cervical canal and uterine cavity. The laboratory is then notified to load a catheter with the embryo (s) to be transferred and deliver them to me in the procedure room. At this point the empty catheter is removed from the positioned cannula and the embryo-loaded catheter is passed via the perfectly positioned cannula, to within approximately one (1) centimeter of the top of the uterine cavity, whereupon the embryologist is directed to slowly inject the embryo(s) into the uterus. The passage of the embryos into the uterine cavity can be tracked by ultrasound visualization. A period of about 30 seconds is allowed to elapse, whereupon the catheter and cannula are simultaneously withdrawn slowly. Thereupon, the catheter is immediately returned to the laboratory where it is examined under the microscope to make sure that all the embryos have been released. Any residual embryos would be promptly re-transferred using the same technique.

Frozen Embryo Transfers:

Available evidence suggests that FET (of previously cryopreserved embryos) is at least as successful as is the transfer of “fresh” embryos and might even have the edge. The probably explanation is certainly unlikely to have anything to do with the freezing process itself. The reason likely has to do with being able to better able to prepare the uterus optimally for embryo implantation by using targeted hormone replacement therapy that when a “fresh” transfer is performed immediately following ovarian stimulation with fertility drugs.

I prefer for my patients to initiate FET cycles with oral contraceptive (OC) starting within 5-6 days of the start of menses to the recipient. This is later overlapped with an “agonist such as Lupron  daily for 5-6 days. The OC is then withdrawn, but the daily Lupron injections are continued until the onset of menstruation. Next, the Lupron dosage is reduced and intramuscular (IM) estradiol valuate (Delestrogen) is administered every 3 days. The objective of the estradiol is to achieve and sustain an optimal plasma E2 concentration of 500pg/ml-1,000pg/ml and a 9mm endometrial lining as assessed by ultrasound examination. Intramuscular (preferably)  and/or intravaginal progesterone is administered daily starting about 6 days prior to the FET and continued along with twice weekly IM Delestrogen until the 10th week of pregnancy or until it has been confirmed that the patient is not pregnant. Daily oral dexamethasone commences with the Lupron start and continues until a negative pregnancy test or until the completion of the 8th week of pregnancy. Then it is tapered down and discontinued. The recipient also receives prophylactic oral antibiotics starting with the initiation of Progesterone therapy, until the day after ET. Usually we would thaw vitrified blastocysts with the objective of having 1, 2 or 3 for transfer; depending on a couple’s stated preference. Commencing on the day following the ET, the patient inserts a vaginal progesterone suppository daily and this is continued until the completion of the 8th week of pregnancy or until a negative pregnancy test. An alternative regimen for women who cannot tolerate intramuscular Progesterone (PIO), is to supplant this with daily vaginal Crinone 8% or Endometria inserts. Blood hCG pregnancy blood pregnancy tests are performed 13 days and 15 days after the first progesterone administration is commenced.

 

The male partner or another companion is expected to remain with the patient for emotional support and otherwise tending to her needs for the one hour she remains recumbent. Immediately prior to being discharged following the embryo transfer procedure, an exit interview is conducted whereby the patient/couple is/are given directions.

8 Comments

Jenna

Hi Dr. Sher,

I am in the middle of frozen embryo transfer cycle. My cycle day 2 ultrasound was normal but my lining check ultrasounds(cycle days 13 and 16) showed 4mm of free fluid in the distal part of my uterus near my cervix. This is my first ever frozen cycle, although I did 6 fresh cycles 5 years ago and never had this issue then. I do not have blocked tubes or a hydrosalpinx. I have a history of endometriosis and a previous c-section for my twin pregnancy 5 years ago. I am waiting to hear back from my Doctor to find out if cycle will be cancelled or not. My questions are what would cause this fluid? How do you usually manage a case like mine? And is this likely to happen again in my next cycle if this cycle is cancelled? Thanks for any information you can provide.

reply
Dr. Geoffrey Sher

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

reply
Nancy

Hi Dr. Sher,

My uterine lining is thin and ranges between 5-6mm. Have you seen patients lining grow to 8mm with delestrogen injections prepping for FET transfer?

Thanks!

reply
Dr. Geoffrey Sher

I doubt this alone will work.

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

reply
Tara

If embryos are making it to day 5 But am early blasts and arresting on day 6, would you recommend transfer on day 3 to a 40yr old (me) or to continue to try for blasts?

reply
Dr. Geoffrey Sher

No!! I would do a day 6 blastocyst transfer because embryos that do not make blastocyst by then are almost invariably incompetent anyway and are not would not have resulted in a viable pregnancy anyway…had they been transferred earlier on.

Geoff Sher

reply

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