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Abnormalities in Uterine Circulation
By Eric Daiter, M.D.


The size of the uterine cavity and its circulation is critically important for pregnancy. Uterine circulation can be altered by the presence of fibroids, endometrial polyps or scar tissue (Ashermann's syndrome).

Uterine fibroids, known as leiomyoma uteri, are tumors of the smooth muscle cells in the wall of the uterus. The uterine wall is primarily composed of smooth muscle cells (the myometrium). A uterine fibroid is thought to originate as a mutation within one of these myometrial (smooth muscle) cells that leads to the progressive loss of it own growth regulation. Each fibroid tumor grows from a single progenitor cell (each tumor arises from one single cell) and all the cells within a particular fibroid contain the same abnormal DNA that favors growth. Different fibroid tumor originate from different muscle cells, each with their own genetic (DNA) abnormality so that each tumor may grow at its own rate (some faster and some slower). Fibroid tumors are not malignant (cancer) yet there is an uncommon cancer called "leiomyosarcoma" that is composed of malignant smooth muscle cells. It is not clear whether these cancers develop from benign fibroids or whether they arise independently. Fibroid tumors of the uterus are common. About 75% (3 of 4) of uterine specimens removed during abdominal hysterectomy contain fibroids (many are quite small) and about 15-20% of hysterectomies performed in the USA are for problems involving fibroids.

The role of uterine fibroids in reproduction is usually not clear. If the fibroid is presenting (bulging) into the uterine cavity (submucosal) then it may obstruct one of the fallopian tube entrances or it may present a mechanical or other barrier to implantation. If the fibroid replaces an entire wall of the uterus, then it might interfere with the blood supply to the uterine structures around it or an embryo implanting near it. If the fibroid is predominantly on the outside of the uterus with projection into the pelvis and abdomen then it may outgrow its own blood supply and become degenerate or infected. Degenerating or infected fibroids may result in pain and irritability (contractions) of the uterus that can be associated with complications of pregnancy (preterm labor, severe pain).

Most fibroids do not seem to interfere with fertility and should not be removed unless (a) a reproductive problem is identified and (b) all other treatable causes for the reproductive problem have been evaluated and excluded. An exception is the presence of a large intrauterine filling defect seen on HSG, which should be removed. Another exception is a fibroid compressing the fallopian tubes or creating a tremendous distortion of the uterine cavity.

Endometrial polyps appear to be organized overgrowths of the uterine endometrium, although the precise mechanisms leading to their development are not clearly defined. The endometrial lining of the uterine cavity grows in response to estrogen and is architecturally restructured in response to progesterone. If the response to estrogen is excessive, either in the presence of unopposed estrogen (such as during periods of anovulation) or whenever the bioactivity of the circulating estrogen is increased (such as with increased numbers of estrogen receptors or with decreased metabolism of estrogen) overgrowth of the endometrium may occur. If these overgrowths organize and develop their own blood supply then they become polyps.

The mere presence of polypoid overgrowths in the uterine cavity may (at least theoretically) interfere with implantation and fertility. I have envisioned polyps as acting sort of like IUDs in the cavity, creating a hostile environment for embryo implantation. I remove endometrial polyps in women with reproductive problems and these women (anecdotally) seem to do remarkably well in subsequent fertility efforts. A well designed research project describing fertility outcome after treatment for different types of endometrial polyps would be valuable.

Endometrial polyps are not always benign. I removed one normal appearing endometrial polyp hysteroscopically and this was found to contain an endometrial adenocarcinoma (cancer) on pathology report. Therefore, in the presence of any atypical overgrowth of tissue it is always important to think about the possibility of cancer.

Ashermann's syndrome is the occlusion or obliteration of the uterine cavity due to damage to the lining of the cavity (endometrium). This is not common but is important to recognize it if indeed present. When the endometrium is destroyed beyond a certain depth (believed to be the basalis level which is the level that promotes subsequent growth) in the context of hypoestrogenism (a low circulating estrogen concentration) then permanent scar tissue can easily form within the cavity. Clinical situations that increase the chance of Ashermann's Syndrome include :

  • overzealous dilatation and curettage (especially for a missed abortion, postpartum bleeding, or septic abortion),

  • intrauterine surgery to remove fibroid tumors, uterine structural defects (septum, bicornuate uterus, large polyps), or at cesarean section

  • infections related to IUD use (or the placement of any foreign object within the uterine cavity),

  • some uncommon infections of the uterus (such as intrauterine tuberculosis or Schistosomiasis)

  • radium insertion into the uterus for the treatment of gynecologic cancers

The finding for Ashermann's Syndrome on hysterosalpingogram (HSG) exam is intrauterine filling defects These are irregular areas within the normally triangular shaped cavity where the distending media is excluded due to the presence of the adhesions. Thin adhesions may be primarily composed of fibroconnective tissue with little blood supply. The thicker the adhesions, the greater the likelihood that they are vascular and possibly also partially muscular. Vascular and muscular adhesions are much more difficult to repair and seemingly pose a greater problem for fertility.

Repair of intrauterine adhesions is most easily and safely performed by hysteroscopy. Operating scissors can be used through some hysteroscopes but tend to be a bit flimsy for any but very thin filmy adhesions. A type of operating hysteroscope called a resectoscope allows the surgeon to apply electrical current through a monopolar cutting instrument attached as the operating element of the hysteroscope and lysis (cutting) of the adhesions can then be performed. In more complex cases of adhesions, repeated procedures may be required to accomplish complete lysis of the adhesions. After each hysteroscopic repair in which cautery is used or extensive lysis of adhesions is accomplished, the patient is typically placed on higher dose estrogen replacement (say, Premarin 1.25 or 2.5 mg by mouth each day for 30-60 days, with a Provera withdrawal flow brought on at the end of this time) to promote the regrowth of endometrium (lining) over the repaired sites. Occasionally, a stent (such as an IUD or pediatric foley balloon) is also placed within the cavity to keep the sides of the uterus apart during the repair period.

For mild to moderate adhesions, you might expect a 60-80% chance of successful pregnancy after repair. For more extensive adhesions the chance of a successful pregnancy is lower. If a pregnancy does occur after repair of Ashermann's Syndrome there is a greater chance of preterm labor and delivery (delivery of a premature baby), placenta accreta (where the placenta invades the uterine wall into the muscular component of the wall and becomes difficult to impossible to remove) and postpartum hemorrhage (heavy bleeding after the delivery of a baby).

Dr. Eric Daiter graduated from the University of Pennsylvania, where he was awarded an academic scholarship and was enlisted into the University Scholar's Program and the Benjamin Franklin Scholar's Program.

Dr. Daiter graduated medical school at Temple University Medical School in Philadelphia and completed the Obstetrics and Gynecology residency program at Albert Einstein College of Medicine in New York. He completed his Reproductive Endocrinology and Infertility fellowship at the Hospital of the University of Pennsylvania. He has considered a career as a physician scientist in research medicine and has published several articles on molecular events that occur during the human embryo's implantation into the uterus. Dr. Daiter entered private practice in 1994, where he joined a successful referral based infertility practice and further developed his clinical skills. Dr. Daiter emphasizes the basic principles of infertility patient care, including the importance of highly personalized, cost considerate, state of the art, one on one care for his patients. He specializes in all aspects of In Vitro Fertilization, with a patient success rate among the highest in the state. He has performed several hundred advanced operative laparoscopic and hysteroscopic surgeries, utilizing the most modern laser techniques.

Dr. Daiter opened his Edison, NJ office in 1997. The office continues to support the highest level of professional care for infertile couples. Extended office hours are available for patient convenience.

Eric Daiter, M.D.
34-36 Progress Street
Suite B-4
Edison, New Jersey, 08820

Web Site URL: http://www.drdaiter.com/index.html
E-Mail: info@drdaiter.com
Phone: (908) 226-0250
Fax: (908) 226-0830



The information presented in these articles are offered for informational purposes only. These pages have been written by Dr. Eric Daiter, yet are not intended to replace the medical advise offered by your personal physicians or healthcare professionals.

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