PREVENTION OF CERVICAL DYSPLASIA BY VACCINATION
The quadrivalent HPV recombinant vaccine (Gardasil) is recommended for all females 8–26 years of age, with a target age of 11–12.
• The vaccine uses noninfectious particles to protect against the 4 HPV types (6, 11, 16, 18) that cause 70% of cervical cancer and 90% of genital warts.
• Three doses are given: initial, then 2 months later, then 6 months later, for an approxi-mate cost of $300.
Recommendations
• Administer to all females age 8–26, with a target age of 11–12. Efficacy is highest before the patient’s immune system has been presented with HPV.
• Testing for HPV is not recommended before vaccination. No easy method of identifying all HPV types is currently available.
• Continue regular Pap smears according to current guidelines because the vaccine does not prevent against all HPV types that can cause genital warts or cervical cancer.
• Sexually active women can receive the vaccine. Women with previous abnormal cervi-cal cytology or genital warts also can receive the vaccine, but it may be less effective. It can be given to patients with previous CIN, but benefits may be limited.
• The vaccine is not recommended for pregnant, lactating, or immunosuppressed women.
MU¨LLERIAN ANOMALIES
Uterine anomalies have been divided into 7 types by the American Fertility Society (1988). This classification is based on the developmental problem responsible for the irregular shape. Uterine anomalies may result from 3 mechanisms: stage 1) failure of one or both of the 2 müllerian ducts to form, stage 2) failure of the 2 ducts to fuse completely, or stage 3) failure of the 2 fused mullerian ducts to dissolve the septum that results from fusion.
Failure to Form
Hypoplasia/Agenesis
• A woman may lack a vagina, a cervix (the bottom one-third of the uterus that opens into the vagina), the fallopian tubes, or the entire vagina and body of the uterus (except for the fundus). This occurs from a developmental problem with a section of both of the müllerian ducts.
• These anomalies are commonly associated with urinary tract anomalies because the structures that give rise to the urinary tract lie close to the müllerian ducts and are affected by the same injurious insult.
Unicornuate Uterus
• When one of the müllerian ducts fails to form, a single-horn (banana-shaped) uterus develops from the healthy müllerian duct. This single-horn uterus may stand alone. However, in 65% of women with a unicornuate uterus, the remaining müllerian duct may form an incomplete (rudimentary) horn.
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• There may be no cavity in this rudimentary horn, or it may have a small space within it, but there is no opening that communicates with the unicornuate uterus and vagina.
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• In the latter case, a girl may have monthly pain during adolescence because there is no outlet for the menses from this rudimentary horn. This pain would lead to identifica-tion of this problem. In some cases, the rudimentary horn contains a cavity that is continuous with the healthy single-horn uterus, but is much smaller than the cavity within the healthy uterus.
• There is a risk that a pregnancy will implant in this rudimentary horn, but because of space limitations, 90% of such pregnancies rupture.
Failure to Fuse
Didelphys Uterus
• A double uterus results from the complete failure of the 2 Müllerian ducts to fuse together (stage 1 of development). So each duct develops into a separate uterus, each of which is narrower than a normal uterus and has only a single horn.
• These 2 uteri may each have a cervix or they may share a cervix. In 67% of cases, a didelphys uterus is associated with 2 vaginas separated by a thin wall. Preterm delivery is common if pregnancy occurs in these patients.
Bicornuate Uterus
• This is the most common congenital uterine anomaly (45%). It results from failure of fusion between the müllerian ducts at the “top.” This failure may be “complete,” which results in 2 separate single-horn uterine bodies sharing one cervix.
• Alternatively, in a “partial” bicornuate uterus, fusion between the müllerian ducts had occurred at the “bottom” but not the “top.” Thus, there is a single uterine cavity at the bottom with a single cervix, but it branches into 2 distinct horns at the top. Because the ducts never fused at the top, these 2 horns are separate structures when seen from the outside of the uterus.
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• Preterm delivery and malpresentation are common with pregnancy.
Failure to Dissolve Septum
Septate Uterus
• A septate uterus results from a problem in stage 2 or 3 of uterine development. The two müllerian ducts fused normally; however, there was a failure in degeneration of the median septum.
• If this failure was “complete,” a median septum persists in the entire uterus, separating the uterine cavity into two single-horned uteri that share one cervix.
• If this failure was “partial,” resorption of the lower part of the median septum occurred in stage 2 but the top of the septum failed to dissolve in stage 3. Thus, there is a single cervix and uterine cavity at the bottom, but at the top that cavity divides into two distinct horns.
• Because this uterine anomaly occurs later in uterine development, after complete duct fusion, the external shape of the uterus is a normal-appearing single unit. This is dis-tinct from the bicornuate uterus, which can be seen branching into two distinct horns when viewed from the outside.
• Preterm delivery and malpresentation are common with pregnancy.
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Arcuate Uterus
This type of uterus is essentially normal in shape with a small midline indentation in the uter-ine fundus, which results from failure to dissolve the median septum completely.
• It is given a distinct classification because it does not seem to have any negative effects on pregnancy in regard to preterm labor or malpresentation.
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DES Uterus
The daughters of mothers exposed to diethylstilbestrol (DES) during pregnancy are predis-posed to uterine abnormalities and clear cell carcinoma of the vagina.
• Two-thirds have abnormalities, including a small, incompletely formed uterus (“hypoplastic”) and/or a T-shaped cavity; and 50% have cervical defects, for example, an incompletely formed cervix that predisposes to cervical insufficiency. The mecha-nism by which DES disrupts normal uterine development is not known.
ENLARGED UTERUS
Leiomyoma Uteri
Location. It is a benign smooth muscle growth of the myometrium. It is the most common benign uterine tumor. It is 5 times more common in black women than white women. It can develop in a number of anatomic locations.
• Intramural. The most common location of a leiomyoma is within the wall of theuterus. When small it is usually asymptomatic and cannot be felt on examination unless it enlarges to where the normal uterine external contour is altered.
• Submucosal. These myomas are located beneath the endometrium and can distort theuterine cavity. The distorted overlying endometrium may not respond appropriately to the normal hormonal fluctuations, resulting in unpredictable, often intermenstrual, bleeding. Abnormal vaginal bleeding is the most common symptom of a submuco-sal myoma and can result in anemia. Menorrhagia is defined as heavy menses and metrorrhagia is defined as irregular bleeding in between menses. Menometrorrhagia consists of both heavy menses and bleeding in between the menses.
• Subserosal. These are located beneath the uterine serosa. As they grow they distortthe external contour of the uterus causing the firm, nontender asymmetry. Depending on their location they can put pressure on the bladder, rectum or ureters. If they are pedunculated, attached to the uterus by a stalk, they can become parasitic fibroids. They break away from the uterus and receive their blood supply from another abdom-inal organ (such as the omentum or the mesentery of the intestine).
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With permission Lyndon M. Hill, M.D., Magee Women’s Hospital, iame.com
Figure II-4-11. Submucosal Leiomyoma
Natural History. Changes in size are dependent on the reproductive life stage of the woman.
• Slow growth. Most leiomyomas are small, grow slowly, and cause no symptoms. Onlywhen massive in size do they cause pelvic pressure symptoms.
• Rapid growth. Estrogen receptors are increased in leiomyomas resulting in rapidenlargement during times of high estrogen levels, such as pregnancy.
• Degeneration. During times of rapid growth, myomas may outgrow their blood sup-ply, resulting in ischemic degeneration of a fibroid. Common degenerations that are seen include hyaline, calcific, and red degeneration. The latter, also known as carneous degeneration, can cause such extreme, acute pain that the patient requires hospitaliza-tion and narcotics. This is most common during pregnancy.
• Shrinkage. When estrogen levels fall, with estrogen receptors no longer stimulated,leiomyomas will typically decrease in size. This predictably occurs after menopause but can also occur when estrogen levels are medically reduced through gonadotropin
releasing hormone (GnRH) agonist suppression of follicle-stimulating hormone (FSH).
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Diagnosis
• Pelvic examination. In most cases the diagnosis is made clinically by identifying anenlarged, asymmetric, nontender uterus in the absence of pregnancy. The size of the fibroid is compared with the size of a pregnant uterus. A pregnant uterus that reaches the umbilicus is approximately 20 weeks in gestation; if the pregnant uterus reaches the symphysis pubis, it is approximately 12 weeks in gestation.
• Sonography. Traditional abdominal or vaginal ultrasound can image large intramuralor subserosal myomas. Saline infusion sonography is helpful for identifying submu-cosal myomas by instilling 5–10 mL of saline into the uterine cavity before visualizing the uterine cavity with an endovaginal sonogram probe.
With permission Lyndon M. Hill, M.D., Magee Women’s Hospital, iame.com
Figure II-4-12. Saline Ultrasonography Demonstrating an Intracavitary Leiomyoma
• Hysteroscopy. Submucosal myomas may be identified by visualizing them directlywith hysteroscopy.
• Histology. The only definitive diagnosis is by surgical confirmation of excised tissue.
Management
• Observation. Most leiomyomas can be managed conservatively and followed expec-tantly with regular pelvic examinations.
• Presurgical shrinkage. After 3–6 months of GnRH analog therapy, with resultant hypoes-trogenic state, a 60–70% reduction in size of the fibroids can be expected. However, once the leuprolide (Lupron) is terminated, there will be a regrowth of the fibroid within 6 months. Thus, GnRH analogs cannot be used for definitive cure, but they can be used in the adjuvant setting with surgical therapy. If a myomectomy is done, a decrease in size will be associated with a decrease in blood loss, and if a hysterectomy is planned, then perhaps a vaginal instead of an abdominal hysterectomy can be performed.
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• Myomectomy. This is a surgical procedure performed if the patient desires to main-tain fertility. The uterus is incised and the myoma removed through either a laparo-scopic or laparotomy approach. If the myomectomy incision entered the endometrial cavity, delivery of any subsequent pregnancy should be by cesarean section because of increased risk of scar rupture in labor.
• Embolization. This is an invasive radiology procedure in which a catheter is placedinto the vessels supplying the myoma. Microspheres are injected, causing ischemia and necrosis of the myoma.
• Hysterectomy. If the patient has completed her childbearing, definitive therapy is anabdominal or vaginal hysterectomy.
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