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.

19,771 Comments

  1. Hello Dr Sher, my period is always on time. Every 25th day
    My period is 3 days late so far, mild to mod cramping, white, milky discharge. I have been cramping since last week, 3/5. My period was supposed to start 3/15. I took a first response preg test(test 6 days before period)on Sunday and again today, both were negative. Should i wait a little longer before testing again or call my md

    • I would give it another week and if no period yet, then do an US to look for an ovarian cyst.

      An ovarian cyst is any collection of fluid, surrounded by a very thin wall, within an ovary. An ovarian follicle that is larger than 22mm is termed a functional follicular cyst. They are non-malignant (benign) and harmless and in most cases, don’t even cause symptoms, however, in some cases, rapid distention of the cyst , or rupture with bleeding , can lead to sudden and severe pain and in some cases, a disruption in hormone balance leads to vaginal bleeding.

      There are 2 varieties of “functional ovarian cysts:
      1.Follicle Cysts: In menstruating women, a follicle containing the unfertilized egg will rupture during ovulation. If this does not occur, a follicular cyst of more than 2.5 cm diameter may result. These cysts develop in response to stimulation with follicle stimulating hormone that is either self-produced (by the woman’s own pituitary gland (endogenous) or is induced by agonists (e.g. Lupron/Decapeptyl/Buserelin) that sometimes propagate increased and sustained pituitary FSH release.
      2.Corpus luteum cysts: These appear after ovulation or egg retrieval. The corpus luteum is the remnant of the follicle after the ovum has moved to the fallopian tubes. It usually degrades within 5-9 days. A corpus luteum of > 3 cm is regarded as being cystic.

      A:Follicular cysts: These lesions have special relevance in women about to undergo controlled ovarian stimulation (COS) with gonadotropins for IVF where they can literally, “throw a spanner in the works”, causing a delay, postponement and sometimes even cancellation of the cycle of treatment.

      Functional Ovarian cysts must be distinguished from “non-functional or cystic ovarian tumors”. By definition, “tumors are capable of independent growth. Thus “cystic ovarian tumors do not develop as a result of exposure to gonadotropin stimulation and it is this feature that distinguishes them from “functional” ovarian cysts.

      Aside from sometimes causing pain and dysfunctional uterine bleeding, unruptured follicular cysts are usually relatively non-problematic. As stated above, in some cases, functional “cysts” undergo rapid distention (often as a result of a minor degree of bleeding inside the cyst itself). In such cases the woman will often experience a sharp or aching pain on one or other side of her lower abdomen and/or deep seated pain during intercourse. The cysts may even rupture, causing sudden lower abdominal pain that exacerbates and may even simulate an attack of acute appendicitis or a ruptured ectopic (tubular) pregnancy. While very unpleasant, a ruptured “functional cyst” seldom produces a degree of internal bleeding that warrants surgical intervention. The pain, typically is made worse by movement. It stabilizes within a number of days but subsides progressively to disappear within about four to seven days.

      Whenever an ovarian cyst is detected (usually by ultrasound examination), the first consideration should be to determine whether it is a “functional cyst or a “cystic ovarian tumor”. The reason for this is that tumors are subject to a variety of complications such as twisting (torsion), hemorrhage, infection and even malignant change, all of which usually will require surgical intervention.

      Gonadotropin releasing hormone agonists (GnRHa) such as Lupron, Buserelin, Nafarelin and Synarel, administered daily, starting a few days prior to menstruation, all elicit an initial and rapid, out-pouring (“surge”) in pituitary LH and FSH release. This “surge” lasts for a day or two. Then as the pituitary reservoir of FSH and LH becomes depleted, the blood FSH and LH levels fall rapidly reaching near undetectable blood levels within a day or two. At the same time, the declining FSH result in a drop in blood E2 concentration leading to a withdrawal bleed (menstruation). The progressive exhaustion of Pituitary FSH/LH along with the decline in blood E2, is referred to as ” down-regulation” The continued daily administration of GnRHa or its replacement (supplanting) with a GnRH antagonist (e.g. Ganirelix, Cetrotide or Orgalutron) results in blood LH concentrations being sustained at a very low level throughout the ensuing cycle of controlled ovarian hyperstimulation (COH) with gonadotropins, thereby optimizing follicular maturation and promoting E2 induced endometrial proliferation.

      Functional follicular cysts resulting from controlled ovarian stimulation (COS), can occur regardless of whether down regulation with GnRHa (Lupron/Buserelin/Decapeptyl) is initiated in cases where the cycle of stimulation is launched with the woman coming off a BCP or when the agonist is initiated on day 20-23 (the mid luteal phase) of a natural cycle. When this happens it is due to the initial agonist-induced FSH “surge” sometimes so accelerating follicular growth that it leads to the development of one or more “functional follicular cysts”. These cysts release E2 and cause the blood E2 often to remain elevated (>70pg/ml). Depending on the extent of this effect, it sometimes leads to a delay in the onset of menstruation and thus also to deferment in the initiation of COS.

      Failure of menstruation to commence within 4-7 days of initiating treatment with GnRHa suggestive of an underlying “functional ovarian cyst” and calls for an ultrasound examination to make the diagnosis. Once diagnosed, depending upon the number and size of cysts detected. There are two therapeutic options:
      1)Wait for the cyst to absorb spontaneously and for menstruation to ensue: While it at first might seem that this approach of continuing GnRHa therapy in order to cause absorption of the cyst(s) within a week or two might be a good approach , it often has unintended consequences. First there is the real possibility that prolonged uninterrupted GnRHa therapy might blunt subsequent ovarian follicular response to gonadotropin therapy and second, if menstruation does not follow within 10-14 days, the cycle will usually need to be cancelled.
      2)Immediate needle aspiration of the cyst(s) under local anesthesia. I personally favor needle aspiration, sooner rather than later in such cases. Menstruation will usually follow a successful aspiration within 2-4 days. Upon menstruation a blood E2 level is measured and as soon as it drops below 70pg/ml COS can be initiated.

      B. Corpus Luteum cysts: As with follicular cysts, so at times do Corpus Luteum cysts also bleed, distend and cause fain. They often delay onset of spontaneous menstruation by a week or longer (Halban syndrome”.). In isolated cases, internal bleeding within the cyst substance causes pain, rapid enlargement of the lesion and by ultrasound examination reveals local areas of absorption causing it to appear as a “complex” cystic lesion that simulates a tumor, prompting surgical intervention. Sadly, there are countless cases where women have had an entire ovary removed due to this happening.

      “Functional ovarian cysts” rarely present as a serious health hazard. In the vast majority of cases they spontaneously resolve within 2-4 weeks while “cystic tumors” will not. Accordingly, the persistence of any ovarian cyst that persists for longer than 4 weeks should raise suspicion of it being a tumor rather than with a “functional cyst”. Since ovarian tumors can be (or become) malignant, all ovarian cysts that persist for longer than 6 weeks (whether occurring in non-pregnant or pregnant women), should be considered for surgical removal and this should be followed by pathological analysis.
      Good luck!

      Geoff Sher

  2. Hello, I just had a clear HSG. Tubes were not blocked and uterus looked good. Two days ago, I had an SIS and trial transfer. They saw some adhesions. I have normal periods and have never had a d & c, c section. I do have endometriosis confirmed by laparoscopy at 13. I had a healthy pregnancy five years ago from an IVF cycle. We want another, and I am nervous about doing a hysteroscopy to have adhesions cut. Will this cause more adhesions? Do you recommend hysteroscopy to confirm adhesions and then have those removed? I have heard I need to see a specialist for this. Do you agree it should be a specialist or can most doctors perform this?
    Thank you!

    • I absolutely recommend a hysteroscopy to free intrauterine adhesions by an expert..

      Geoff Sher

  3. Hey Dr. Sher, I think I recall you saying you defrost frozen embryos the morning of an FET. Our clinic does the same. I’m just curious— what’s the rationale behind doing it morning of vs day before?

    Reason I ask is I was reading an interesting study which suggested that an embryo’s hatching status (or lack thereof) is perhaps a good prediction of whether or not it will implant (and a clinical pregnancy achieved). But the study seemed to suggest defrosting the day before was ideal.

    That said, clearly just one study but it got me thinking about the reasoning for defrosting day of transfer. I imagine there’s a good reason for it, just curious what it was.

    Thank you in advance!

    • Defrosting the day before is OK too. But by defrosting the morning of allows the opportunity should one or both not survive (fornutely uncommon) to then be able to thaw another on the spot and transfer later in the same day.

      Geoff Sher

  4. Hello, we are about at the end of the road for trying to conceive (40s), and have tried 17 cycles of assisted repro. And have had 4 blighted ovums of 6 m/c. From ours and donor cycles. Recently we saw the hla dq matching article here, nk cells discussion, and wondered if this was something we should look into? .We have frozen donor embryos and wondered if we should even try, or maybe this testing could give some answers In regard to repeated blighted ovums? Thanks

    • Respectfully, I would not go again until: 1) the chromosomal status of your embryos is known; b) A thorough reassessment of the reason for repeated failure has been determined and addressed (likely an implantation dysfunction…anatomical or immunologic):

      Whenever a patient fails to achieve a viable pregnancy following embryo transfer (ET), the first question asked is why! Was it simply due to, bad luck?, How likely is the failure to recur in future attempts and what can be done differently, to avoid it happening next time?.
      It is an indisputable fact that any IVF procedure is at least as likely to fail as it is to succeed. Thus when it comes to outcome, luck is an undeniable factor. Notwithstanding, it is incumbent upon the treating physician to carefully consider and address the causes of IVF failure before proceeding to another attempt:
      1.Age: The chance of a woman under 35Y of age having a baby per embryo transfer is about 35-40%. From there it declines progressively to under 5% by the time she reaches her mid-forties. This is largely due to declining chromosomal integrity of the eggs with advancing age…”a wear and tear effect” on eggs that are in the ovaries from birth.
      2.Embryo Quality/”competency (capable of propagating a viable pregnancy)”. As stated, the woman’s age plays a big role in determining egg/embryo quality/”competency”. This having been said, aside from age the protocol used for controlled ovarian stimulation (COS) is the next most important factor. It is especially important when it comes to older women, and women with diminished ovarian reserve (DOR) where it becomes essential to be aggressive, and to customize and individualize the ovarian stimulation protocol.
      We used to believe that the uterine environment is more beneficial to embryo development than is the incubator/petri dish and that accordingly, the earlier on in development that embryos are transferred to the uterus, the better. To achieve this goal, we used to select embryos for transfer based upon their day two or microscopic appearance (“grade”). But we have since learned that the further an embryo has advanced in its development, the more likely it is to be “competent” and that embryos failing to reach the expanded blastocyst stage within 5-6 days of being fertilized are almost invariably “incompetent” and are unworthy of being transferred. Moreover, the introduction into clinical practice about a decade ago, (by Levent Keskintepe PhD and myself) of Preimplantation Genetic Sampling (PGS), which assesses for the presence of all the embryos chromosomes (complete chromosomal karyotyping), provides another tool by which to select the most “competent” embryos for transfer. This methodology has selective benefit when it comes to older women, women with DOR, cases of unexplained repeated IVF failure and women who experience recurrent pregnancy loss (RPL).
      3.The number of the embryos transferred: Most patients believe that the more embryos transferred the greater the chance of success. To some extent this might be true, but if the problem lies with the use of a suboptimal COS protocol, transferring more embryos at a time won’t improve the chance of success. Nor will the transfer of a greater number of embryos solve an underlying embryo implantation dysfunction (anatomical molecular or immunologic).Moreover, the transfer of multiple embryos, should they implant, can and all too often does result in triplets or greater (high order multiples) which increases the incidence of maternal pregnancy-induced complications and of premature delivery with its serious risks to the newborn. It is for this reason that I rarely recommend the transfer of more than 2 embryos at a time and am moving in the direction of advising single embryo transfers …especially when it comes to transferring embryos derived through the fertilization of eggs from young women.
      4.Implantation Dysfunction (ID): Implantation dysfunction is a very common (often overlooked) cause of “unexplained” IVF failure. This is especially the case in young ovulating women who have normal ovarian reserve and have fertile partners. Failure to identify, typify, and address such issues is, in my opinion, an unfortunate and relatively common cause of repeated IVF failure in such women. Common sense dictates that if ultrasound guided embryo transfer is performed competently and yet repeated IVF attempts fail to propagate a viable pregnancy, implantation dysfunction must be seriously considered. Yet ID is probably the most overlooked factor. The most common causes of implantation dysfunction are:
      a.A“ thin uterine lining”
      b.A uterus with surface lesions in the cavity (polyps, fibroids, scar tissue)
      c.Immunologic implantation dysfunction (IID)
      d.Endocrine/molecular endometrial receptivity issues
      Certain causes of infertility are repetitive and thus cannot readily be reversed. Examples include advanced age of the woman; severe male infertility; immunologic infertility associated with alloimmune implantation dysfunction (especially if it is a “complete DQ alpha genetic match between partners plus uterine natural killer cell activation (NKa).
      I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.

      •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.
      •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: How Many Attempts should be considered before Stopping?
      •“Unexplained” Infertility: Often a matter of the Diagnosis Being Overlooked!
      •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

      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

  5. Dear Dr. Sher,
    i am 36 and had 2 failed FET; during the first one i had major pain, as the uterus is quite twisted and has a scar which i have from my previous c-section 12 years ago; for that reason the second FET we did using sedation. The doctor performed Cervical Dilation during the FET, but the implantation failed again.

    now we plan the next FET; the doctor suggest to do Cervical Dilation BEFORE the FET, the question i have are:

    1) would you recommend to do the Cervical Dilation the same cycle as the FET ?
    2) do you generally recommend a rest cycle (or more) between 2 FET for increased probability of implantation ?

    kind regards
    Diana

    • 1) would you recommend to do the Cervical Dilation the same cycle as the FET ?

      A: Preferably not

      2) do you generally recommend a rest cycle (or more) between 2 FET for increased probability of implantation ?

      Yes!

      Geoff Sher