Pelvic Factor

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Pelvic Factor Detection

Pelvic Abnormalities
  • Abnormal Male Outflow
  • Vaginal Problems
  • Cervical Problems
  • Uterine Problems
  • Proximal Tubal Disease
  • Bilateral Tubal Ligation
  • Distal Tubal Disease
  • Pelvic Adhesions
  • Endometriosis

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Embryo implantation into a receptive uterine environment is necessary for the development of a successful pregnancy. Barriers to implantation (within the uterus) can exist for the preimplantation embryo (fertilized egg) that enters the uterine cavity.

During In Vitro Fertilization, 4 or 5 good quality embryos are often placed into the uterine cavity 2-3 days after retrieval and there is usually a dramatic reduction in the number of embryos that actually will implant and develop into a pregnancy.

Research on natural conception suggests that a large percentage of fertilized eggs are lost both prior to implantation and also following implantation prior to the clinical detection of pregnancy. The reason for such a high loss rate remains unclear. Most researchers are just now beginning to study the molecular events that occur at the time of embryo implantation. There is an enormous complexity to these molecular interactions.

Research results on cell adhesion molecules (CAMs, sometimes referred to as “molecular glue” that allows the embryo to adhere to the uterine wall) that may be involved in the process of human embryo implantation include the “beta 3 integrin subunit” and “osteopontin.” This research has been publicized, is fascinating, and yet none of the results have a widely accepted clinical role. Therefore, this testing is experimental.

Molecular events associated with embryo implantation are discussed in greater detail in the implantation sections for In Vitro Fertilization (contained in Common Infertility Procedures).

Clinical attention has been predominantly directed at detection and correction of anatomic abnormalities associated with unsuccessful implantation.

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“Congenital abnormalities of the Mullerian ducts” are a relatively common group of uterine defects associated with reproductive difficulty. These abnormalities result from problems in development in female offspring that occur at an embryonic stage. Normally two “tubes” known as Mullerian ducts fuse at about 8 weeks of gestation (when the mother is in the 8th week of pregnancy) in embryos that are destined to become girls, and these fused ducts then go through changes that result in the formation of the uterus and fallopian tubes. This process is complete by about the 20th week of pregnancy. When there is a problem in the normal development of the uterus and tubes then anatomic abnormalities with reproductive impact can occur. DRAWING AVAILABLE

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Mullerian duct abnormalities include

(1) septate uterus:

This is a partial lack of resorption of the poorly vascularized tissue within the uterine cavity. The remaining tissue creates a wedge shaped septum in the fundus (top) of the uterine cavity.

Implantation of an embryo onto this septum, and within a septate uterus, has a markedly greater chance of spontaneous abortion (miscarriage) compared with a normally developed uterus. There is also an increase in preterm labor and delivery as well as abnormal fetal lie or presentation (such as breech).

Fortunately, the repair of the septate uterus is fairly straightforward and usually very effective, requiring only an outpatient surgical procedure. Reportedly, repair of a septate uterus will improve the miscarriage rate from about 90% if untreated to about 10-15% if treated.

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(2) unicornuate uterus:

This is the failure in development of 1 of the Mullerian ducts, most likely due to a failure in migration (movement) of the duct to its proper location resulting in its total loss. The resulting unicornuate or half uterus has connection to only 1 fallopian tube since the other tube was to be formed from the “lost” Mullerian duct.

The caliber (size) of the cavity in the unicornuate uterus is very important in determining the likelihood of reproductive success. Unfortunately there is no accepted benefit for the treatment of these uterine defects.

The unicornuate uterus is associated with renal abnormalities (renal agenesis or lack of a kidney on the side of the missing Mullerian structures) and reproductive problems (abnormal lie or presentation, intrauterine growth retardation, preterm labor and delivery, incompetent cervix).

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(3) bicornuate uterus:

Occurs with a partial lack of fusion of the Mullerian ducts, resulting in a single cervix and two uterine cavities in a heart shaped partially unified uterus. Reproductive outcome may be normal so no treatment is indicated unless reproductive problems are identified.

Reports suggest an increase in spontaneous abortion (miscarriage), preterm labor and delivery, and abnormal presentation (breech). The patient with recurrent pregnancy loss, a bicornuate uterus, and treatment for all other identified causes for the losses may reasonably consider repair of the uterus.

The treatment is surgical repair requiring a laparotomy with unification of the uterine cavities. The laparotomy requires a lengthy postoperative recovery period.

Success with this surgery is generally quite good, improving the miscarriage rate from about 90-95% if untreated (and the cause for the recurrent losses) to about 25-30% if treated.

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(4) didelphic uterus:

This results from a complete lack in fusion of the Mullerian ducts with duplication of the uterus and cervix so that the patient has 2 cervices and two uteruses (each smaller than normal). This is commonly also associated with a vaginal septum so that there are 2 vaginal canals at the top of the vaginal vault.

Occasionally, one of the sides will become obstructed and result in pain as blood accumulates in the obstructed region.

These are associated with abnormal lie or presentation as well as preterm labor and delivery.

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(5) rare abnormalities:

There are an entire host of intermediate or somewhat unique problems associated with abnormal development of the Mullerian structures. Isolated endometrial (lining of the uterus) or cervical (mouth of the uterus) agenesis (lack of development) are rare. Communicating and noncommunicating uterine horns that failed to fuse and canulate properly are possible.

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Asherman’s syndrome is the occlusion or obliteration of the uterine cavity due to damage to the endometrium (lining of the cavity). This is not common but is important to recognize if 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 form within the cavity. Clinical situations that increase the chance of Asherman’s Syndrome include

  • overzealous dilatation and curettage (especially for a missed abortion, postpartum bleeding, or septic abortion),
  • intrauterine surgery to remove fibroid tumors or uterine structural defects (septum, bicornuate uterus, large polyps),
  • infections related to IUD use (or the placement of any foreign object within the uterine cavity),
  • some uncommon infections in the uterus (Tuberculosis, Schistosomiasis), or
  • radium insertion into the uterus for the treatment of a gynecologic cancer
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The finding on hysterosalpingogram (HSG) exam for Asherman’s Syndrome 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 (scar tissue). 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 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. 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 Asherman’s Syndrome there is a greater chance of preterm labor and delivery (delivery of a premature baby), placenta previa (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).

Uterine fibroids, known as leiomyoma uteri, are tumors of the smooth muscle of the uterus. Fibroid tumors of the uterus are common, with about 75% (3 of 4) of uterine specimens removed at the time of abdominal hysterectomy having fibroids (many are quite small) and about 15-20% of hysterectomies are performed for problems involving fibroids.

The uterine wall is primarily composed of smooth muscle (the myometrium). A uterine fibroid is thought to originate as a gene mutation within one of these myometrial (smooth muscle) cells that leads to the progressive loss of its 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 tumors 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.

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 is throughout 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 degenerate or become infected, resulting 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. Fibroids should not be removed unless a reproductive problem is identified and all other treatable causes for the problem have been evaluated and either treated or excluded. One 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.

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