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Ovarian Endometriomas: Sclerotherapy provides a Safe, Convenient, and highly effective Non-Surgical Alternative

by Dr. Geoffrey Sher on December 23, 2015

Women, who have advanced endometriosis, often have endometriotic ovarian cysts, known as endometriomas. These cysts contain decomposed menstrual blood that looks like melted chocolate…hence the name “chocolate cysts”. These space occupying lesions can cause chronic pelvic pain, pain with intercourse (dyspareunia) and painful menstrual periods, thus compromising quality of life. They can also activate ovarian connective tissue (stroma or theca) resulting in an overproduction of male hormones (especially testosterone). An excess of ovarian testosterone can severely compromise follicle and egg development in the affected ovary. Thus there are two reasons for treating endometriomas. The first is to alleviate symptoms and the second is to optimize egg and embryo quality.

Conventional treatment of endometriomas involves surgical drainage of the cyst contents with subsequent removal of the cyst wall (usually by laparoscopy).Unfortunately, with surgery normal ovarian tissue can be  inadvertently removed/damaged along with the cyst wall, thereby decreasing the number of available eggs for harvest. Since many women who have endometriomas also have advanced endometriosis and have had one or more previous surgeries, they often .have significant scarring and adhesions. This can compromise visualization of and access to anatomic structures during conventional laparoscopic surgical correction, increasing the risk of surgical complications.

Many patients with recurrent ovarian endometriomas are uncomfortable with the prospect of repeat surgery and its avoidance is often a factor in their decision to proceed with IVF. We recently reported on a new, effective and safe outpatient approach to treating endometriomas in women planning to undergo IVF. We termed the treatment ovarian Sclerotherapy.  The process involves; needle aspiration of the “chocolate colored liquid content of the endometriotic cyst, followed by the injection of 5% tetracycline hydrochloride into the cyst cavity. Such treatment will, more than 75% of the time result in disappearance of the lesion within 6-8 weeks. In some cases the injection of tetracycline into the endometrioma causes a reaction that results in clear or blood stained fluid collecting in the original cyst cavity where the endometrioma had been. Upon re-aspirating the fluid in the seroma, the lesion will usually disappears permanently most times. In a small number of cases, the endometrioma comes back and sclerotherapy must be repeated or surgical removal undertaken.

Ovarian sclerotherapy can be performed under local anesthesia or under conscious sedation. It has the advantage of being an ambulatory in-office procedure, low cost, and has a low incidence of significant post-procedural pain or complications and the avoidance of the need for laparoscopy or laparotomy.

Sclerotherapy is a safe and effective alternative to surgery for definitive treatment of recurrent ovarian endometriomas in a select group of patients planning to undergo IVF. Since the procedure is associated with a small, but yet realistic possibility of adhesion formation; its use should be confined to cases where IVF is the only treatment available to the patient. Women who intend to try and conceive through fertilization in their fallopian tubes (e.g; following natural conception or intrauterine insemination) are better off undergoing laparotomy or laparoscopy for the treatment of endometriomas.

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  • Saumya - August 31, 2016 reply

    I am 32 years old from India. Menstruating with pain since age 10.
    In May 2010, I was diagnosed with B/L Endometriotic Ovarian Cyst (Chocolate Cyst) in both of my ovaries. I was Married in November 2011.
    In March 2012, I had a Laparoscopy Ovarian Cystectomy and Adhesiolysis with D&C and was injected Lupron for six months to which I became highly allergic. As Lupron stopped, I started menstruating with heavy bleeding, severe abdominal pain and passage of clots, as always.
    In Oct 2014, I had Transvaginal Hysterosonosalpingogram, through which both of my tubes became patent, but I failed to conceive naturally.
    In May 2015, IVF ICSI was suggested. Before the procedure started my levels of TSH-2.41uIU/ml, AMH 1000-3.03ng/ml, FSH- 5.0 and LH- 2.6 IU/L at day 2 of my cycle). After stimulation of 14 days 3 follicles from right ovary and 4 follicles from left ovary were retrieved and fertilized out of which 2 embryos were transferred on day 4. The quality of the embryos were 7 cell and 8 cell on day 4 which was not impressive as told by the doctor. The result was negative. The doctor said that the egg quality was very weak due to which embryos did not mature. The doctor suggested donor egg to which we do not agree.
    In January 2016, my TVS showed Multiple Endometriomas in ovaries. The right ovary measures 72x44x78 mm across & 131.97ml in volume. The left ovary measures 57x37x57 mm across & 63.09ml in volume. The endometriomas measure 12-49 mm across.
    Intercourse has been extremely painful and hence I have abstained. Abdominal and lower back pain remains throughout the month and gets worse during menstruation. Menses last for 5 days in a cycle of 30 or 30+ days.
    Doctor suggests more cycles of IVF ICSI until positive result while other doctors suggest second Laparoscopy (with a risk of further damaging the ovarian reserve).
    We are a childless couple and wish to conceive as soon as possible. Please help.

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - August 31, 2016 reply

    Endometriosis with endometriomas can cause problems when it comes to stimulation. In such cases the space-occupying ovarian endometriomas alter the hormonal environment in the affected ovary(ies), compromising egg quality. They must be removed or treated with sclerotherapy in advance of IVF. Endometriosis also produces an immunologic implantation dysfunction in a third of cases (see below).

    Endometriosis is a complex condition where, the lack or relative absence of an overt anatomical barrier to fertility often belies the true extent of reproductive problem(s). All too often the view is expressed that the severity of related infertility is directly proportionate to the anatomical severity of the endometriosis itself, the implication being that the primary reason for endometriosis –related infertility is anatomical interference with egg transport to the Fallopian tube(s). This over-simplification and an erroneous view is often used to justify the performance of many unnecessary surgeries for the removal of small innocuous endometriotic lesions, on the basis of such “treatment” evoking an improvement in subsequent fertility.
    It is indeed indisputable that even the mildest form of endometriosis can compromise fertility. It is equally true that, mild to moderate endometriosis is by no means a cause of absolute “sterility”. Rather, when compared with normally ovulating women of a similar age who do not have endometriosis, women with mild to moderate endometriosis are about three to four times less likely to have a successful pregnancy. Two important reasons for such reduction in fertility potential are:
    a) Toxic Pelvic Environment: Endometriosis is associated with the presence of local pelvic toxins that significantly reduces the fertilization potential of eggs as they pass from the ovary to the fallopian tube via the pelvic cavity and,
    b) Immunologic Implantation Dysfunction (IID): Given that the pathogenesis of endometriosis almost certainly involves an abnormal immune response. In about one third of cases, activation of uterine natural killer cells (NKa) causes the uterus to reject the embryo (fertilized egg) as it attempts to gain attachment to the uterine lining (endometrium).
    The reported annual birth rate for normally ovulating women under 35 yrs who are free of endometriosis or any other pelvic disease, is about 70-80%. For women 35-40yrs of age, the comparable annual rate is about 40-50%, for women in their early 40’s, it is probably less than 20% and by the mid-forties, …around 10%. In contrast women in similar age categories who have even the mildest degree of endometriosis can expect a 3-4-fold reduction in the annual birth rate.
    Since, the reason for women with mild to moderate endometriosis having a much poorer reproductive performance has little to do with ovulation dysfunction or anatomical disease, it should come as no surprise that the use of fertility drugs, surgery to ablate small endometriotic deposits and minor adhesions, and/or intrauterine insemination is unlikely to any improvement in pregnancy rate over no treatment at all. Women under 35 years who fit this profile, and who conceive following fertility hormone therapy, intrauterine insemination (IUI) or surgery, should consider that they probably conceived in spite of (rather than due to), such treatment. Failure to recognize this reality carries with it the risk that when it comes to planning for another baby, the woman will erroneously belief that having conceived before means that there should be no difficulty in doing so again and be lulled into a false sense of complacency. In reality, the achievement of a viable pregnancy by a woman with mild/moderate endometriosis, whether it occurred spontaneously or following such treatment probably does not improve her subsequent ability to conceive.
    Younger women (under 30 yrs) with mild/moderate pelvic endometriosis (who have patent fallopian tubes, are ovulating normally and have fertile male partners), have about a 40% chance of having a baby within 3-4 years. Accordingly they justifiably can choose taking a “wait and see “approach, avoiding surgery, fertility drugs and intrauterine insemination (which in my opinion would be unlikely to improve the chance of a successful pregnancy over no treatment at all) and In Vitro Fertilization which by involving the direct extraction of eggs from the ovaries and initiating the fertilization process in the Petri dish/incubator, the IVF procedure facilitates fertilization, is much likely to be successful, but might have been avoided by a “wait and see approach”.
    Finally, I wish to point out that in addition to an inevitable toxic “peritoneal factor” present in all women with endometriosis, about 1/3 of women with endometriosis (regardless of its severity), also have an immunologic barrier to implantation involving NKa and possibly the action of antiphospholipid antibodies. This population of women are not likely to achieve a viable pregnancy conceive until/unless the IID is addressed through selective immunotherapy involving Intralipid, heparinoids (Lovenox/Clexane) and low dosage (short term) steroid therapy. It therefore behooves all women with endometriosis who are planning to have a family to be thoroughly tested which in my opinion should be performed in a reproductive immunology reference lab of which to my knowledge no more than a half dozen in the United States, capable of performing these tests with the required sensitivity. I preferentially use Reproductive Immunology Associates (RIA) in Van Nuys, CA.
    Given the effect of the accelerating biological clock, women over 35yrs who have endometriosis-related infertility, do not have time to waste and should, in my opinion do IVF as a first line approach, regardless of their immunologic status. In the absence of clear evidence of increased NK cell activity, I often recommend a conservative approach in women under 35years (who potentially can afford the time to wait). However, regardless of age, women who have increased NK cell activity, should in my opinion undergo IVF accompanied with immunotherapy with Intralipid (and sometimes heparin, Clexane or Lovenox) because without such treatment they are not likely to conceive regardless of the approach to treatment) undergo IVF.

    I strongly recommend that you visit http://www.DrGeoffreySherIVF.com. Then go to my Blog and access the “search bar”. Type in the titles of any/all of the articles listed below, one by one. “Click” and you will immediately be taken to those you select. Please also take the time to post any questions or comments with the full expectation that I will (as always) respond promptly.
    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
    • The Fundamental Requirements For Achieving Optimal IVF Success
    • Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
    • 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.
    • The “Biological Clock” and how it should Influence the Selection and Design of Ovarian Stimulation Protocols for IVF.
    • A Rational Basis for selecting Controlled Ovarian Stimulation (COS) protocols in women with Diminished Ovarian Reserve (DOR)
    • Diagnosing and Treating Infertility due to Diminished Ovarian Reserve (DOR)
    • Controlled Ovarian Stimulation (COS) in Older women and Women who have Diminished Ovarian Reserve (DOR): A Rational Basis for Selecting a Stimulation Protocol
    • Optimizing Response to Ovarian Stimulation in Women who Have Compromised Ovarian Response to Ovarian Stimulation in Women who Have Compromised Ovarian Reserve: A Personal Approach.
    • 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
    • Why did my IVF Fail
    • 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
    • Traveling for IVF from Out of State/Country–
    • 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
    • Endometriosis and Infertility: Why IVF Rather than IUI or Surgery Should be the Treatment of Choice.
    • Endometriosis and Infertility: The Influence of Age and Severity on Treatment Options
    • Treating Ovarian Endometriomas with Sclerotherapy.
    • IVF Egg Donation: A Comprehensive Overview

    Please call or email Julie Dahan, my patient concierge. She will guide you on how to set up an in-person or Skype consultation with me. You can reach Julie at on her cell phone or via email at any time:
    Julie Dahan
    • Email: Julied@sherivf.com
    • Phone: 702-533-2691
     800-780-7437

    Geoff Sher

    I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

  • Nan - January 2, 2016 reply

    Hi Dr. Sher,

    I’m 36 years old and my husband is 39. Back in Jan 2014, I had myomectomy to remove a Big 15-cm fibroid located at the back of the uterus as well as 3-cm ovarian cyst on the left ovary and a chocolate cyst. We’ve protected intercourse for 7 months after the surgery. Then, June 2015, I’ve got pregnant but turned out it was ectopic and I had salpingectomy to remove my right Fallopian tube which appeared to be hydrosalpinx as well. Post op diagnosis also found that i have moderate to extensive adhesions along omental, bowel and pelvic side wall, stage 2 endometriosis and 2-cm uterine fibroid. (My left Fallopian tube appear grossly normal though.) Sep 2015, I had Hysterosonogram with saline and uterine cavity looks perfect. My ovarian reserve based on AMH level is 4.53. Husband’s semen analysis was very good. I had 2 failed FET transfer. I started stimulating cycle and be able to retrieve 23 eggs (mostly from my right ovary), 17 fertilized and 15 reached expanded blastocyst. We had NGS genetic testing on all 15 embryos and mere 5 embryos are normal. We transferred 2 normal embryos on each FET, but got negative on both rounds. First FET, Nov. 2015, Endo thickness was 6.16mm at 6 days before transfer. (Just right before 1st FET transfer, I had profuse discharge from cervical cyst. Its color look like chocolate lava. My RE said he’s never seen anything like this before. But he thought he shouldn’t affect embryo implantation as its not coming from the inside of uterus.) Second FET, Dec.2015, Endo thickness was 7.93mm at 6 days before transfer. I also did acupuncture before the 2nd FET. (My RE said that lining above 6 is considered good enough. He said he’s seen no difference in term of pregnancy rate between 6mm, 7mm, 8mm or higher at his clinic.) Both FET, I’m on 6mg estrace, 2 crinone, 1ml PIO and baby aspirin each day.

    I’ve read your blog discussing about natural killer cells I may have had based on my endometriosis diagnosis. However, since I was able to get pregnant by my own (even though it ended up with ectopic), will I be free from those killer cells. If such killer cell isn’t the issue here, what do you think would be my underlining problems of both failed transfers? What do you think we should do next? I’m looking forward to hearing your words.

    Thank you in advance for your time.
    Nan

    Dr. Geoffrey Sher

    Dr. Geoffrey Sher - January 2, 2016 reply

    Hi Nan,

    To have 5 blastocysts that were chromosomally normal is enviable and should have been sufficient to propagated a viable pregnancy. This strongly suggests an implantation dysfunction.

    By the way, in reality, 1/3 of women who have endometriosis (regardless of its severity) will have activated uterine NK cells. Not that these activated NK cells (NKa) are located in the uterus and NOT in the tubes. That is why even with NKa you can have an ectopic (tubal) pregnancy. I strongly suspect that you do have an immunologic implantation dysfunction (NKa) which if present and not addressed properly will thwart your achieving a viable intrauterine pregnancy.

    ADDITIONAL INFORMATION!
    Please go to the “home page” of this Blog, find the “search bar” and type in any of the articles below by title, “click” and you will immediately be taken to these.

    • Controlled Ovarian Stimulation (COS) for IVF: Selecting the ideal protocol
    • Ovarian Stimulation for IVF using GnRH Antagonists: Comparing the Agonist/Antagonist Conversion Protocol.(A/ACP) With the“Conventional” Antagonist Aproach
    • Ovarian Stimulation for IVF: Comparing “conventional” use of GnRH antagonists to the Agonist/Antagonist Conversion Protocol (A/ACP)
    • IVF: Factors Affecting Egg/Embryo “competency” during Controlled Ovarian Stimulation(COS)
    • The BCP: Does Launching a Cycle of Controlled Ovarian Stimulation (COS). Coming off the BCP Compromise Response?
    • Measuring and Interpreting Blood hCG to Assess Pregnancy Viability Following ART Treatments.
    • IVF Failure and Implantation Dysfunction: The Role of Endometrial Thickness, Uterine Pathology and Immunologic Factors
    • 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
    • Immunologic Implantation Dysfunction: Importance of Meticulous Evaluation and Strategic Management:(Case Report)
    • Traveling for IVF from Out of State/Country–
    • A personalized, stepwise approach to IVF at SIRM”; Parts 1 & 2 (posted March, 2012)
    • The Role of Nutritional Supplements in Preparing for IVF
    • Frozen Embryo Transfer (FET): What Does it Involve?
    • Endometriosis and Infertily
    • Treating Ovarian Endometriomas with Sclerotherapy.

    I invite you to call 702-699-7437 or 800-780-7437 and set up a one hour Skype consultation with me to discuss your case in detail.

    I also suggest that you access the 4th edition of my book ,”In Vitro Fertilization, the ART of Making Babies”. It is available as a down-load through http://www.Amazon.com or from most bookstores and public libraries.

    Geoff Sher

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