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, what is your opinion of antral follicle count of 10 (5 each ovary) on cycle day 6 for a 39 year old. I understand it is just part of the picture, but curious what your thoughts are. Many thanks in advance.
hat is not bad. However, it needs to be viewed against the back drop of your AMH to help in constructing an optimal protocol for ovarian stimulation.
Geoff Sher
HI Dr. Sher
I am 34 years old. I have a question about egg quality and pregnancy rate. I have (lean) PCOS and failed our first IVF cycle as all 9 of our embryos came back PGS normal : ( (I had 38 eggs retrieved and pretty bad OHSS). The second cycle, they decreased my meds and we were able to obtain 2 PGS normal embryos from that cycle but the andrology report mentions granular oocytes with vacuoles. I have read that this is due to hyper stimulation (I hyperstimmed again the second cycle again despite stopping all meds and coasting for 2 days). I have read that even with PGS normal embryos, if the oocytes are granular or have vacuoles, pregnancy likely won’t result. What are your thoughts on this? My transfer is scheduled for mid May and I want to be optimistic and go into it with a good mindset but after reading this, I am worried that it is hopeless : ( The embryos were graded as “good” quality. Thank you so much!
Polycystic ovary syndrome (PCOS) is a common hormonal system disorder among women affecting between 5% and 10% of women of reproductive age worldwide. Women with PCOS may have enlarged ovaries that contain multiple small collections of fluid (subcapsular microcysts) that are arranged like a “string of pearls” immediately below the ovarian surface (capsule).interspersed by an overgrowth of ovarian connective tissue (stroma). The condition is characterized by abnormal ovarian function (irregular or absent periods, abnormal or absent ovulation and infertility, androgenicity (increased body hair or hirsutism, acne) and increased body weight –body mass index or BMI.
Women with PCOS are at increased risk that ovarian stimulation with gonadotropins will result in the, of development of severe ovarian hyperstimulation syndrome (OHSS), a life-endangering condition that is often accompanied by a profound reduction in egg “competency” and on fertilization often yield an inordinately high percentage of “incompetent” embryos which have a reduced potential to propagate viable pregnancies.
Concern and even fear that their PCOS patients will develop of OHSS often leads the treating RE to take measures aimed at reducing the risk of this life-endangering condition. One such measures is to “trigger” egg maturation prematurely in the hope of arresting further follicular growth and the other, is to initiate the “trigger” with a reduced dosage of hCG (i.ed. 5,000U rather than the usual 10,000U of of Pregnyl/Profasi/Novarel, to use or 250mcg rather than 500mcg of Ovidrel or to supplant the hCG “trigger” with a Lupron “trigger” which causes a prompt LH surge from the woman’s pituitary gland to take place. While such measures do indeed reduce the risk of OHSS to the mother, this often comes at the expense of egg quantity and “competency”. Fewer than the anticipated number of eggs are harvested and those that are retrieved are far more likely to be “immature” and chromosomally abnormal (aneuploid”), or “immature” , thereby significantly compromising IVF outcome.
Against this background, It is my considered opinion that when it comes to performing IVF in women with PCOS, the most important consideration must be the selection and proper implementation of an individualized or customized ovarian stimulation protocol. Thereupon, rather than prematurely initiating the “trigger” to arrest further follicle growth, administering a reduced dosage of hCG or “triggering with a GnRH agonist (e.g. Lupron/Buserelin) that can compromise egg “competency”….. use of one of the following techniques will often markedly reduce the risk of OHSS while at the same time protecting egg quality:
1. PROLONGED COASTING…my preferred approach: My preferred approach is to use a long pituitary down-regulation protocol coming off the BCP which during the last 3 days is overlapped with the agonist, Lupron/Buserelin/Superfact. The BCP is intended to lower LH and thereby reduce stromal activation (hyperthecosis) in the hope of controlling LH-induced ovarian androgen (predominantly, testosterone) production and release. I then stimulate my PCOS patients using a low dosage of recombinant FSH-(FSHr) such as Follistim/Gonal-F/Puregon. On the 3rd day of such stimulation a smidgeon of LH/hCG (Luveris/Menopur) is added. Thereupon, starting on day 7 of ovarian stimulation, I perform serial blood estradiol (E2) and ultrasound follicle assessments, watching for the number and size of the follicles and the blood estradiol concentration [E2]. I keep stimulating (regardless of the [E2] until 50% of all follicles reach 14mm. At this point, provided the [E2] reaches at least >2,500pg/ml, I stop the agonist as well as gonadotropin stimulation and track the blood E2 concentration daily. The [E2] will almost invariably increase for a few days. I closely monitor the [E2] as it rises, plateaus and then begins to decline. As soon as the [E2] drops below 2500pg/ml (and not before then), I administer a “trigger” shot of 10,000U Profasi/ Novarel/Pregnyl or 500mcg Ovidrel/Ovitrel. This is followed by an egg retrieval, performed 36 hours later. Fertilization is accomplished using intracytoplasmic sperm injection (ICSI) because “coasted” eggs usually have little or no cumulus oophoris enveloping them and eggs without a cumulus will not readily fertilize naturally. Moreover, they also tend to have a “hardened” envelopment (zona pellucida), making spontaneous fertilization problematic in many cases. All fertilized eggs are cultured to the blastocyst stage (up to day 5- 6 days) and thereupon are either vitrified and preserved for subsequent transfer in later hormone replacement cycles or (up to 2) blastocysts are transferred to the uterus, transvaginally under transabdominal ultrasound guidance. The success of this approach depends on precise timing of the initiation and conclusion of “prolonged coasting”. If started too early, follicle growth will arrest and the cycle will be lost. If commenced too late, too many follicles will be post-mature/cystic (>22mm) and as such will usually harbor abnormal or dysmature eggs. Use of “Coasting” almost always prevents the development of severe OHSS, optimizes egg/embryo quality and avoids unnecessary cycle cancellation. If correctly implemented, the worst you will encounter is moderate OHSS and this too is relatively uncommon.
2. EMBRYO FREEZING AND DEFERMENT OF EMBRYO TRANSFEDR (ET): OHSS is always a self-limiting condition. In the absence of continued exposure to hCG, symptoms and signs as well as the risk of severe complications will ultimately abate. Thus, in the absence of pregnancy, all symptoms, signs and risks associated with OHSS will disappear within about 10-14 days of the hCG trigger. Conversely, since early pregnancy is always accompanied by a rapid and progressive rise in hCG , the severity of OHSS will increase until about the 9th or tenth gestational week whereupon a transition from ovarian to placental hormonal dominance occurs, the severity of OHSS rapidly diminishes and the patient will be out of risk. Accordingly, in cases where in spite of best effort to prevent OHSS, the woman develops symptoms and signs of progressive overstimulation prior to planned ET, all the blastocysts should be vitrified and cryostored for FET in a subsequent hormone replacement cycle. In this way women with OHSS can be spared the risk of the condition spiraling out of control.
I strongly recommend that you visit http://www.DrGeoffreySherIVF.com . Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
·The IVF Journey: The importance of “Planning the Trip” Before Taking the Ride”
·Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
·IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
·The Fundamental Requirements For Achieving Optimal IVF Success
·Use of GnRH Antagonists (Ganirelix/Cetrotide/Orgalutron) in IVF-Ovarian Stimulation Protocols.
·Anti Mullerian Hormone (AMH) Measurement to Assess Ovarian Reserve and Design the Optimal Protocol for Controlled Ovarian Stimulation (COS) in IVF.
·Egg Maturation in IVF: How Egg “Immaturity”, “Post-maturity” and “Dysmaturity” Influence IVF Outcome:
·Commonly Asked Question in IVF: “Why Did so Few of my Eggs Fertilize and, so Many Fail to Reach Blastocyst?”
·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?
·Taking A Fresh Look at Ovarian Hyperstimulation Syndrome (OHSS), its Presentation, Prevention and Management
·Preventing Severe Ovarian Hyperstimulation Syndrome (OHSS) with “Prolonged Coasting”
·Understanding Polycystic Ovarian Syndrome (PCOS) and the Need to Customize Ovarian Stimulation Protocols.
·“Triggering” Egg Maturation in IVF: Comparing urine-derived hCG, Recombinant DNA-hCG and GnRH-agonist:
·The “Lupron Trigger” to Prevent Severe OHSS: What are the Pro’s and Con’s?
•.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.
•Implications of “Empty Follicle Syndrome and “Premature Luteinization”
•Premature Luteinization (“the premature LH surge): Why it happens and how it can be prevented.
•Preventing Severe Ovarian Hyperstimulation Syndrome (OHSS) with “Prolonged Coasting”
If you are interested in seeking my advice or services, I urge you to contact my concierge, Julie Dahan ASAP to set up a Skype or an in-person consultation with me. You can also contact Julie by phone or via email at 702-533-2691/ Julied@sherivf.com You can also apply online at http://www.SherIVF.com .
*FYI
The 4th edition of my newest book ,”In Vitro Fertilization, the ART of Making Babies” is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.
Geoffrey Sher MD
Hi Dr.Sher,
My question is specifically about the trilaminar appearance. Is it recommended to transfer 2 embryos with a lining of 10.6 but that is NOT trilaminar? Or should I cancel and try again next cycle?
Thank you,
Natalee Ware
Thew trilaminar appearance is in my opinion no longer relevant. It is the thickness that counts and 10.6 mm is good!
Geoff Sher
Hi
My infertility is due to a prolactinoma. My prolactin has been normal since 2012 on bromocryptine and the tumor is as small as a pea now but I still don’t ovulate. Amh 3.97. I’ve had two egg retrievals and retrieved 50 eggs between both cycles. Round one 21 eggs>13 fertilized>2 blasts (1 abnormal, 1 untested. Round two 29 eggs>15 fertilized>4 blasts (2 abnormal, 1 normal, 1 mosaic). We transferred my only normal March 1 and it failed. Lining was 8.9 and all hormone levels normal. My husband had normal semen analysis and dna fragmentation. I’ve had further endocrine bloodwork with only one level not normal. Vitamin d at 27 so I’ve started d3. My dr says I am highly atypical of the results they’ve seen particularly when I’m only 30 and all tests have been normal. Hsg and shg normal as well. He says I’m getting high eggs good fertilization but they seem to drop off after day 2 or 3 and he can’t give me an explanation why this is happening or why my transfer failed. I’ve asked for an autoimmune test, mthfr test, hgh in my cycle, era test, embryo glue, killer cells tests all of which my dr says are unnecessary expenses. He did order a karotype test on me which I’m currently waiting for. Basically I’m just looking for advice as I’m getting frustrated that he doesn’t seem to want to look further into why I’m getting low blastocysts numbers and have failed transfer with a pgs normal hatching embryo.
Dear doctor Sher,
I hope that you will help me with a question regarding fibroids. I recently had a missed miscarige week 10. The examination after the miscarige showed an intramural/submucous fibrom 10 x 10 mm posterior in corpus uteri clouse to fundus and with ca. 50 % distrubing the uterine cavity. Also 3-4 fibroids of few mm scatterd in the myometrium. It is also described that in the cesarian scar the myometrium is thin and replaced by the fibrous tissue. I am not sure wheater the fibroid which disturb the cavity should be remouved before trying to get pregnant again? Is it normal for a scar after cesarian to look like that with thin myometrium? Thank you in advance for your answer. Best regards.
If the fibroid id protruding into the uterine cavity it could be the cause and it should be removed, probably hysteroscopically.
Fibroids or leiomyomas are non-malignant muscle tumors that grow in the uterine wall. They can be found in about one out of every five (1:5) women >30Y of age. Fibroids are far more prevalent in African Americans and women and less frequent in other ethnic groups (i.e. Caucasians and Asians).
Fibroids, enlarge and/or distort uterine configuration. They can produce symptoms such as heavy, painful and prolonged menstrual periods. Other symptoms include pain with intercourse, backache, severe abdominal pain when large fibroids run out of blood supply or when superficial fibroids on a stem (pedunculated) undergo twisting (torsion). Sometimes fibroids will protrude into the uterine cavity, cause severe cramping and bleeding and so irritate the uterine lining as to compromise embryo attachment (anatomical implantation dysfunction). Women with fibroids are also at greater risk of miscarriage, premature delivery, malposition of the baby (mandating cesarean delivery) and an increased risk of bleeding after birth (post-partum hemorrhage)
Diagnosis can be made by one or more of the following symptoms/presentations: Symptomatology, pelvic examination pelvic ultrasound, hysterosalpingogram (HSG), sonohysterogram (HSN), CT-scan or MRI..
Fibroids are classified as:
•Submucosal: Here the fibroid grows just under the lining of the uterine cavity (mucosa) or protrudes into the uterine cavity. They might mold into the underlying uterine muscle (sessile) or be on a stalk (pedunculated). Submucosal fibroids can change the shape of the uterine cavity, irritate the lining and prevent implantation, cause miscarriage. These lesions must be removed in their entirety prior to undertaking embryo transfer, usually hysteroscopically. (see below)
•Subserosal: – Here the tumors grow under the outer layer (serosa) of the uterus. These fibroids will not compromise implantation, but if they are large, causing severe pain, and especially if they are multiple, pedunculated and thus at risk of undergoing torsion (twisting) the3y should be removed, usually laparoscopically. (See below).
•Intramural: – when the fibroids develop within the muscular wall of the uterus. This is the commonest presentation. Unless they are large and multiple and do not encroach on the uterine cavity, they can be left alone Surgical removal is usually by laparoscopy or laparotomy/abdominal open incision (See below)
The uterus is composed of a thick layer of smooth muscle (myometrium) surrounding the endometrial lining into which the embryo implants and which serves to protect and nourish a growing pregnancy. These tumors are rarely malignant (see below). Fibroid tumors, even large ones, can occur without producing any symptoms at all.
For the most part, only those fibroids that impinge upon the uterine (endometrial) cavity (submucosal) affect fertility. Exceptions include large fibroids in the muscle wall of the uterus (intramural) that can block the openings of the fallopian tubes as they enter the uterus, and where multiple fibroids cause abnormal uterine contraction patterns.
In some cases multiple uterine fibroids may so deprive the uterine lining (endometrium) of blood flow, that the delivery of estrogen to the endometrium is curtailed to the point that the lining cannot thicken sufficient to support a pregnancy. This can result in early 1st trimester (prior to the 13th week of pregnancy) miscarriages. Large or multiple fibroids, by curtailing the ability of the uterus to stretch in order to accommodate the spatial needs of a rapidly growing pregnancy, may precipitate 2nd trimester (beyond the 13th week) miscarriages and/or trigger the onset of premature labor.
Sizable fibroid tumors are usually easily identified by simple vaginal examination. However, even the smallest fibroid can be identified by transvaginal ultrasound. Sometimes it is difficult to tell if the fibroid is impinging on the uterine cavity. In such cases, a hysteroscopy (where a telescope like instrument, inserted via the vagina into the uterine cavity) or a sonohysterogram where injected fluid, distends the uterine cavity allowing for examination of its inner configuration can help distinguish between intramural and submucosal fibroids. CT scan and MRI can also be used to distinguish between fibroid tumors and another condition that also involves affects the uterine muscular wall, known as adenomyosis. This condition is characterized by endometrial tissue growing deeply into the uterine wall.. Given the often-diffuse nature of adenomyosis, it can be very difficult to remove surgically. This contrasts with fibroid tumors, which are well defined and are usually easily removed.
Surgical Treatment: The mainstay for the treatment of fibroid tumors is surgical removal (myomectomy). Small, asymptomatic fibroids that do not impinge upon the endometrial cavity will usually not require treatment other than observation and vigilance. Large fibroids and submucosal fibroids should be removed prior to starting fertility treatments such as In Vitro Fertilization (IVF) in order to decrease the chance of implantation failure, miscarriage, pregnancy complications and premature labor. Intramural and subserosal fibroids are readily removable by laparoscopic resection or via an abdominal incision. The former allows for a more rapid convalescence and is ideal for the removal of small and accessible superficial fibroid tumors, while the latter approach is preferred for treating larger and less accessible fibroids.
Myomectomy can affect fertility in several ways. If the endometrial cavity is entered during the surgery, there is a possibility of post adhesions forming within the uterine cavity. This should always be checked by the performance of a hysteroscopy or through a sonohysterogram, prior to beginning fertility treatment. Because myomectomy can be bloody, there is a high likelihood of post-operative abdominal adhesion formation, which could bind down or encase the ovaries, preventing the release of the eggs, or block the ends of the fallopian tubes. For this reason, it is important that myomectomies be formed only by accomplished surgeons, who are familiar with techniques to limit blood loss and prevent adhesion formation.
Regardless of whether the laparoscopic or abdominal approach is employed, adequate closure of the uterine wall is essential in order to reduce the subsequent risk of uterine rupture during pregnancy or labor. This is one of the main arguments used against the use of laparoscopic removal of large, multiple or remotely situated fibroids. While laparoscopic myomectomy requires but a few days (at most) for post-operative convalescence, abdominal myomectomy usually requires 6-8 weeks of recovery time. When myomectomy necessitates or results in the uterine cavity being entered (purposefully or inadvertently), it should always be followed up with a “2nd look” hysteroscopy to rule out scar tissue formation, which occurs frequently in the presence of submucosal fibroids.
Uterine polyps (and in some cases, also submucosal fibroids), can usually be removed hysteroscopically (through the vagina). This eliminates the need for abdominal surgery and greatly reduces the recovery time. Hysteroscopic surgery is only useful if the majority of the fibroid protrudes into the endometrial cavity, ensuring that the tumor defect will not be too large. This surgery is often done under laparoscopic guidance, to reduce the risk of uterine perforation. After hysteroscopic surgery it is often advisable to prescribe cyclical hormonal therapy for a few months to encourage regeneration of the endometrial lining over the area of tumor defect and healing of the uterine muscle. A 2nd look hysteroscopy should be performed a few months later in all cases, to rule out scar tissue formation even if it means delaying or deferring the initiation of definitive fertility treatment.
Medical Treatment: The growth of fibroid tumors is estrogen-dependent. Thus when a woman enters menopause and stops making female hormones, fibroids tend to shrink in size on their own. Conditions that mimic menopause can also reduce the size of fibroid tumors. The most common of theses treatment is with a medication such as leuprolide acetate (Lupron), which shuts off the communication of the brain with the ovaries, preventing hormone production. However, this type of medication can only be taken for a limited period (usually 6 months) and once the medication is stopped the fibroids will usually regain their original size within a few months. The medication is therefore only a “temporary fix,” used mostly to decrease the size of large fibroids in order to make their ultimate surgical removal easier, or to help a woman bridge the gap until spontaneous menopause sets in. For the majority of women there is no major benefit from Lupron therapy prior to surgery.
Embolization of Fibroid Tumors: Myomectomy always carries the small (although infrequent) risk that severe, uncontrollable intra-operative bleeding could require the performance of a hysterectomy (complete removal of the uterus) as a life saving measure. Moreover, some women are poor candidates for surgery. This is where a new procedure known as embolization comes in. Embolization is a procedure in which small particles are injected into the arteries of the uterus under radiological guidance to shut off the blood supply to the fibroids, in the hope that they will “shrink” and perhaps, even disappear.
Embolization is relatively new to the field of gynecology and little is known about its potential effects on future fertility. We are concerned that in the process of shutting off the blood supply to the uterus, it will permanently so reduce endometrial blood flow, as to compromise embryo implantation. For this reason, I do not currently recommend this therapy for women who still wish to conceive and carry a baby in their uterus. At present, it seems best suited for symptomatic women who are finished with their childbearing or who are planning to use a gestational surrogate.
Malignant Change in Fibroid Tumors: Fibroids rarely undergo malignant change. The reported incidence is less than 1 in 2000 cases. Fibroids usually grow very slowly (over a number of years). However, when growth occurs rapidly over a month or two, especially in older women who have large fibroids, it should raise the suspicion of this very rare but extremely serious complication.
Hope this helps !
Geoff Sher