Academic Courses
FACULTY OF CLINICAL MEDICINE AND SURGERY
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Topic One: Normal Fertility
Fertility is defined as the capacity to reproduce or the state of being fertile. A healthy couple having frequent intercourse have about an 18–20% chance of conceiving in a single menstrual cycle. As a species this makes us relatively infertile.
There is of course a cumulative increase in pregnancy rates over time as couples try for conception. Within 6 months 70% of couples will have conceived, after 12 months 80% and after 24 months 90% of couples will achieve a pregnancy.
The most important factor affecting fertility is female age, which is related to a decline in the quality and quantity of eggs. Female fertility tends to fall sharply over the age of 36, with a further dip after the age of 40. However, there is a considerable variation and biological age (or ovarian reserve) does not always precisely correlate with chronological age.
Male age is also an important factor; semen quality tends to fall in men over the age of 50, while frequency of intercourse tends to fall in men over the age of 40.
Both frequency and timing of sexual intercourse impact strongly on the chance of conceiving naturally. Couples having intercourse three times a week are three times more likely to conceive than couples having intercourse once a week. Maximum ‘efficiency’ is probably intercourse at least every alternate day. There should, however, be awareness among physicians and patients of the added stress and anxiety that ‘over medicalizing’ this advice can bring to couples.
Increased frequency of intercourse should be encouraged in the periovulatory period. Eggs are thought to be fertilizable for about 12–24 hours post ovulation, while sperm can survive in the female reproductive tract for up to 72 hours. Ovulation usually occurs about 14 days prior to menstruation, with the luteal phase being relatively stable at this length. The ‘fertile window’ for women will, therefore, be different depending on the average length of their menstrual cycle (e.g. for a woman with a 28-day menstrual cycle, her optimal fertile window will be between days 12 and 15).
External factors may influence the chance of conception. There is now strong evidence that smoking can decrease the quality and quantity of eggs and sperm. The role of alcohol and caffeine remains controversial, and there is no compelling evidence to totally abstain from these while trying to conceive, but moderation is probably sensible.
Body mass index (BMI) exerts a strong influence on fertility, with male and female BMI at both the high and low extremes associated with a reduced chance of conceiving. However, there is little evidence for so-called fertility diets to improve natural fertility.
Stress can have a direct influence on the hypothalamic–pituitary–ovarian (HPO) axis, interfering with regular ovulation, and may indirectly reduce conception by reducing libido and frequency of intercourse.
Factors Essential for Conception
- Healthy spermatozoa should be deposited high in the vagina at or near the cervix (male factor).
- The spermatozoa should undergo changes (capacitation, acrosome reaction) and acquire motility (cervical factor).
- The motile spermatozoa should ascend through the cervix into the uterine cavity and the fallopian tubes.
- There should be ovulation (ovarian factor).
- The fallopian tubes should be patent and the oocyte should be picked up by the fimbriated end of the tube (tubal factor).
- The spermatozoa should fertilize the oocyte at the ampulla of the tube.
- The embryo should reach the uterine cavity after 3–4 days of fertilization.
- The endometrium should be receptive (by estrogen, progesterone, IGF-l, cytokines, integrins) for implantation, and the corpus luteum should function adequately.
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Topic Two: Introduction to Infertility
Infertility is defined as failure to conceive within one or more years of regular unprotected coitus. Sterility implies an intrinsic inability to achieve pregnancy, whereas infertility implies a decrease in the ability to conceive and is synonymous with subfertility. Primary infertility applies to those who have never conceived, whereas secondary infertility designates those who have conceived at some time in the past.
Fecundity is the probability of achieving a live birth in 1 menstrual cycle. Fecundability is expressed as the likelihood of conception per month of exposure. Fertility, as well as infertility, of a woman or couple is best perceived as fecundability, as few infertile patients are sterile. It also allows for a direct comparison of treatment options over a more functional time frame.
Infertility is common and affects 10 to 15 percent of reproductive-aged couples. Of note, even without treatment, approximately half of women will conceive in the second year of attempting. Sterility affects 1–2% of couples.
Most couples are more
correctly considered to be subfertile, rather than infertile, as they
will ultimately conceive if given enough time. This concept of subfertility can
be reassuring to couples. However, there are obvious exceptions, such as the
woman with bilaterally obstructed fallopian tubes or the azoospermic male. In
general, infertility evaluation is for any couple that has failed to conceive
in 1 year. But, several scenarios may prompt earlier intervention. For example,
to delay
assessment in an anovulatory woman or a woman with a history of severe pelvic
inflammatory disease (PID) may not be appropriate. Of particular note, fecundability
is highly age-related, with a significant decrease beginning at approximately 32 years of age and more
rapid decline after age 37. This decline in conception rates is associated with
an increase in poor pregnancy outcomes, primarily due to increased aneuploidy
rates. Thus, most experts agree that evaluation is considered after only 6
months in women older than 35 years.
Causes of Infertility
Conception depends on the
fertility potential of both the male and female partner. The male is
directly responsible in about 30–40 percent, the female in about 40–55 percent
and both are responsible in about 10 percent cases. The remaining 10
percent, is unexplained, in spite of thorough investigations with modern
technical knowhow. It is also strange that 4 out of 10 patients of unexplained
category become pregnant within 3 years without having any specific treatment.
It is also emphasized that the relative subfertility of one partner may
sometimes be counterbalanced by the high fertility of the other.
Female and male factor infertility
Female factors that affect fertility include the following categories:
- Cervical: Stenosis or abnormalities of the mucus-sperm interaction
- Uterine: Congenital or acquired defects; may affect endometrium or myometrium; may be associated with primary infertility or with pregnancy wastage and premature delivery
- Ovarian: Alteration in the frequency and duration of the menstrual cycle—Failure to ovulate is the most common infertility problem
- Tubal: Abnormalities or damage to the fallopian tube; may be congenital or acquired
- Peritoneal: Anatomic defects or physiologic dysfunctions (eg, infection, adhesions, adnexal masses)
Male factors that affect fertility include the following categories:
- Pretesticular: Congenital or acquired diseases of the hypothalamus, pituitary, or peripheral organs that alter the hypothalamic-pituitary axis
- Testicular: Genetic or nongenetic
- Posttesticular: Congenital or acquired factors that disrupt normal transport of sperm through the ductal system
Factors that affect the fertility of both sexes include the following:
- Environmental/occupational factors
- Toxic effects related to tobacco, marijuana, or other drugs
- Excessive exercise
- Inadequate diet associated with extreme weight loss or gain
- Advanced age
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Topic Three: Evaluation of Patients with Infertility
Evaluation of infertility
Infertility is a problem that involves both partners. Diagnostic testing is unnecessary if the couple has not attempted to conceive for at least 1 year, unless the woman is age 35 years or older, or if they have a history of a male factor infertility, endometriosis, a tubal factor, diethylstilbestrol (DES) exposure, pelvic inflammatory disease, or pelvic surgery. A complete infertility evaluation is performed according to the woman's menstrual cycle and may take up to 2 menstrual cycles before the etiology is determined.
Obtain the following medical history and information from the couple:
• Copy of previous medical records
• Completed medical history questionnaire
• Details regarding the type of infertility (primary or secondary) and its duration
• History of previous pregnancies and their outcomes; pregnancy intervals; and detailed information about pregnancy loss, pregnancy duration, human chorionic gonadotropin (hCG) level, ultrasonographic data, and presence/absence of fetal heartbeat
• History of previous infertility evaluation/treatment, including details about frequency of intercourse, use of lubricants (eg, K-Y gel) that could be spermicidal, use of vaginal douches after intercourse, and presence of any sexual dysfunction
• Female menstrual history, frequency, and patterns since menarche, as well as history of weight changes, hirsutism, frontal balding, and acne
• Male medical history, including previous semen analysis results, history of impotence, premature ejaculation, change in libido, history of testicular trauma, previous relationships, history of any previous pregnancy in female partners, and the existence of offspring from previous female partners
• Couple’s history of sexually transmitted diseases (STDs); surgical contraception (eg, vasectomy, tubal ligation); lifestyle; consumption of alcohol, tobacco, and recreational drugs (amount and frequency); occupation; and physical activities
• Couple’s current medical treatment (if any), reason, and any history of allergies
• Complete review of systems to identify any endocrinologic or immunologic issue that may be associated with infertility.
Examination for infertility should include the following:
- Routine records of blood pressure, pulse rate, and temperature (if applicable)
- Height/weight findings to calculate body mass index; measure arm span when indicated
- Head and neck assessment: (1) The presence of exophthalmos can be associated with hyperthyroidism; (2) the presence of epicanthus, lower implantation of ears and hairline, and webbed neck can be associated with chromosomal abnormalities; (3) exclude thyroid gland enlargement/nodules, which may indicate thyroid dysfunction
- Breast evaluation: Assess breast development and seek any abnormal masses or secretions, especially galactorrhea
- Abdominal evaluation: Assess for presence of abnormal masses at hypogastrium level
- Thorough gynecologic evaluation: Assess for hair distribution, clitoris size, Bartholin glands, labia majora/minora, and any condylomata acuminatum or other lesions that could indicate the existence of venereal disease
- Speculum examination: Obtain a Papanicolaou test and cultures for gonorrhea, chlamydia, Ureaplasma urealyticum,Mycoplasma hominis; assess for cervical stenosis
- Bimanual examination: Establish direction of the cervix plus size/position of the uterus to exclude the presence of uterine fibroids, adnexal masses, tenderness, or pelvic nodules indicative of infection or endometriosis; assess for defects (eg, absence of vagina and uterus, vaginal septum)
- Extremities evaluation: Exclude malformation (eg, shortness of fourth finger, cubitus valgus), which can indicate chromosomal abnormalities and other congenital defects
- Dermatologic evaluation: Assess for the presence of acne, hypertrichosis, and hirsutism
The urologist usually examines the male partner if the patient's history of his semen analysis produces an abnormal finding. Attention should be directed to the following:
- Congenital abnormalities of the genital tract (eg, hypospadias, cryptorchid, congenital absence of the vas deferens)
- Testicular size, urethral stenosis, and presence of any varicocele
- Any previous inguinal hernia repair: Can indicate accidental ligation of spermatic artery
Laboratory, imaging, and/or surgical evaluation
Laboratory, radiologic, and/or surgical assessment of the female includes the following areas:
- Cervical: Postcoital test or Sims-Huhner test; no longer routine in standard infertility workup
- Uterine and endometrial: Hysterosalpingogram—most frequently used diagnostic tool to assess endometrial cavity (see the image below); pelvic ultrasonograms; saline infusion sonograms; pelvic magnetic resonance imaging; hysteroscopy; endometrial biopsy
- Tubal and peritoneal: Laparoscopy and hysterosalpingogram
- Ovarian: Progesterone levels and/or serial ultrasonography to assess ovulation; follicle-stimulating hormone and estradiol levels (or antral follicle counts, ovarian volume, inhibin B level, and antimüllerian hormone level) to assess ovarian reserve; clomiphene citrate challenge test for dynamic ovarian reserve testing
Laboratory evaluation of the male partner includes the following:
- Semen analysis: Volume, pH level, concentration, motility, morphology, WBC count
- Sperm function tests: (1) The acrosome reaction test with fluorescent lectins or antibodies, (2) computer assessment of the sperm head, (3) computer motility assessment, (4) hemizona-binding assay, (5) hamster penetration test, and (6) human sperm-zona penetration assay
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Topic Four: Treatment and Prevention of Infertility
Treatment of infertility
Treatment plans are based on the diagnosis, duration of infertility, and the woman's age. Management of any underlying female and/or male factors affecting fertility may include medical treatment (eg, pharmacotherapy), surgical intervention, or both.
Ovulation induction is the appropriate treatment for infertile patients who have dysfunction of the hypothalamic-pituitary-ovarian axis. The ovulation induction agents used include clomiphene citrate, hMG, hCG, recombinant FSH, and recombinant LH.
Clomiphene citrate (Clomid): The standard dose of CC is 50 mg PO qd for 5 days, starting on the menstrual cycle day 3-5 or after progestin-induced bleeding. As an antiestrogen, CC requires that the patient have some circulating estrogen levels; otherwise, the patient will not respond to the treatment. The CC response is monitored using pelvic ultrasonography starting on menstrual cycle day 12. The follicle should develop to a diameter of 23-24 mm before a spontaneous LH surge occurs.
The principal indications for CC use are oligomenorrhea, especially polycystic ovarian syndrome (PCOS), and for patients with slight menstrual irregularities. Its use has been extended to assisted reproduction technologies.
The use of CC is contraindicated in cases of ovarian cyst, pregnancy, and liver disease. Its use is controversial in patients with a history of breast cancer.
Assisted Reproductive Technologies
Assisted reproductive technologies used to treat infertility include the following:
- In vitro fertilization (IVF)
- Gamete intrafallopian transfer (GIFT)
- Zygote intrafallopian transfer ZIFT)
- Intracytoplasmic sperm injection (ICSI)
- Intrauterine insemination (IUI)
- Sperm, oocyte, or embryo cryopreservation
Assisted fertilization techniques used clinically include ICSI and assisted hatching.
Alternative treatment plans
If pregnancy has not been established within a reasonable time, consider further evaluation and/or an alternative treatment plan, such as use of donor oocyte, sperm, or embryo, or the use of a gestational carrier or surrogate mother.
Prevention of Infertility
Prevention of infertility is difficult to achieve and thus discuss, as a couple isn’t really aware of the diagnosis until they try to achieve pregnancy. Although difficult to do, there are a few steps one can take to possibly decrease risk of infertility.
Although infertility is
defined as the failure to achieve pregnancy after 12 months or more, earlier evaluation may be justified depending on one’s history and is warranted for
women over the age of 35. Because fertility is related to aging in women and perhaps
in men after the age of 50, one should be aware of these risks when considering
delaying childbearing. Therefore, it is the responsibility of the primary care
provider or gynecologist to openly discuss fertility and aging during a
well-woman visit. The new techniques of oocyte cryopreservations hold a great
promise for women who would like to delay childbearing and should be addressed
with women to increase awareness.
Weight extremes have also been associated with infertility in women, mainly due
to anovulation. Thus a healthy lifestyle may improve fertility for women with ovulatory
dysfunction. However, beyond what has been mentioned previously, there is little evidence that
dietary variations enhance fertility. Women should also be advised to take folic acid supplement (at least
400 μg daily) when trying to conceive.
Smoking has a substantial adverse effect on female fertility demonstrated by a recent meta-analysis and also causes abnormalities in male semen parameters. Thus couples who smoke and are trying to conceive should be advised accordingly. Moderate alcohol and caffeine consumption has no adverse effect on fertility; however. higher levels of alcohol and recreational drugs should be discouraged for couples trying to conceive.
Lastly, couples trying to conceive should be advised to avoid using vaginal lubricants as these can be toxic to sperm based on their effect demonstrated in vitro. If needed, it may be better to recommend mineral oil, canola oil, or hydroxyethylcellulose-based lubricants.
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Topic One: Further Reading
1. DeCherney, A., Nathan, L., Goodwin, T.W., Laufer, N. and Roman, A. (2007) Current Diagnosis and Treatment: Obstetrics and Gynecology, 10th Edition. New York: McGraw-Hill
2. Chamberlain, G. (2007) Obstetrics by Ten Teachers, 20th Edition. Oxford: Oxford University Press
3. Cunningham, F.G., Leveno, K.L., Bloom, S.L., Hauth, J., Gilstrap, L.C. and Wenstrom, K.D. (eds) (2005) Williams Obstetrics, 22nd Edition. New York, McGraw Hill
4. Toy, E., Baker, B., Ross, P. and Jenning, J. (2012) Case Files: Obstetrics and Gynecology, 4th Edition. London, McGraw Hill Medical
5. Medscape and other internet resources.Click here to access Unit one Content..
Topic Two: Historical Development of Nutrition and Dietetics
History of nutrition can be explained in three
eras.
- Chemical analysis era (1700-1900).
Dr. James Lind, a physician in the British Navy, performed the first scientific experiment in nutrition. At that time, sailors were sent on a long voyage for years and they developed scurvy (a painful, deadly bleeding disorder). Only nonperishable foods such as dried meat and breads were taken on the voyages, as fresh foods wouldn’t last. In his experiment, Lind gave some sailors sea water, others vinegar and the rest limes. Those given the lime were saved from scurvy.
Antoine Lavoisier, the father of nutrition and chemistry discovered the actual process by which food is metabolized. He also demonstrated where animal heat comes from. In his equation, he describes the combination of food and oxygen in the body and the resulting off of heat and water.
Justus Liebig of Germany, a pioneer in early
plant growth studies, was the first to point out the chemical makeup of
carbohydrates and proteins. Carbohydrates were made of sugars, fats were fatty
acid and proteins were made up of amino acids.
2. Biological era (1900-1955)
E.V McCollum, while working for the U.S department of agriculture at the University of Wisconsin, developed an approach that opened the way to the widespread discoverer of nutrients. He decided to work with rats. Using this procedure, he discovered the first fat soluble vitamin, vitamin A.
Dr. Casmir Funk was the first to coin the term ‘vitamin’ as vital factors in the diet. He wrote about this unidentified substance present in food, which could prevent diseases of scurvy, beriberi and pellagra. The term vitamin is derived from the words vital and amines, because vitamins are required for life and they were originally thought to be amines- compounds derived from ammonia.
William Rose discovered the essential amino acids, the building blocks of protein.
3. Molecular / cellular era (1955- present)
The roles of essential nutrients as part of bodily processes have been brought to light. For example, more became known about role of vitamins and mineral as components of enzymes and hormones that work within the body.
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Topic Three: Professional requirements for nutritionists and dieticians.
The scope of practice is determined by:
- Education
- Training
- Credentialing
- Demonstrated and documented competence to practice
An individual with a certificate becomes a community nutrition technician, Diploma- community nutrition officer and degrees- nutritionists/dieticians
Registration is with the Kenya Nutritionist and Dietitian Institute (KNDI)- Regulatory body
- Management is also defined as the process by which resources are mobilized, combined and coordinated to effectively to achieve organizational objectives.
- It is a process that utilizes organizational resources in the most effective and efficient manner, in order to attain stated organizational objectives.
Efficiency and Effectiveness
- Efficiency in management refers to optimal utilization of organization resources with minimal wastage. It is also the relationship between achieving objectives and consumption of resources.
Management versus Administration
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Topic 1: Benign and Malignant Conditions of the Vulva
BENIGN CONDITIONS OF THE VULVA
Benign epithelial disorders of the vulva include several inflammatory, ulcerative, and blistering disorders, as well as pigmentary changes involving the vulvar region.
Inflammatory diseases involving the vulvar region include the following:
• Lichen sclerosus
• Squamous cell hyperplasia (with and without atypia)
• Lichen simplex chronicus (localized neurodermatitis)
• Primary irritant dermatitis
• Fixed drug eruption
• Reiter disease
• Lupus erythematosus
• Darier disease
• Aphthosis and Behçet disease
• Pyoderma gangrenosum
• Plasma cell vulvitis
• Vulvar vestibulitis
Blistering diseases involving the vulvar region include the following:
• Familial benign chronic pemphigus (Hailey-Hailey disease)
Pigmentary changes involving the vulvar region include the following:
• Lentigo, lentiginosis, and benign vulvar melanosis
• Postinflammatory hyperpigmentation
• Postinflammatory hypopigmentation
• Vitiligo
• Vulvar melanosis
Benign tumors, hamartomas, and cysts involving the vulvar region include the following
• Bartholin and Skene duct cysts
• Acrochordon (fibroepithelial polyp)
• Fibroma, fibromyoma, and dermatofibroma
• Lipoma
• Hidradenoma
• Syringoma
• Hemangioma
• Angiokeratoma
• Heterotopic sebaceous glands and sebaceous gland hyperplasia
• Papillomatosis (papillary vulvar hirsutism)
• Schwannoma
• Angiomyxoma: a benign and aggressive mesenchymal tumor
Congenital malformations involving the vulvar region include the following:
• Ambiguous external genitalia
• Congenital labial hypertrophy
Atrophy of the vulva may also occur.
VULVAL INTRAEPITHELIAL NEOPLASIA (VIN)
Vulvar intraepithelial neoplasia, or VIN, is a precancerous skin condition on the vulva. It occurs when there are changes in the cells of the skin covering the vulva. VIN is not cancer. However, if the changes become more severe, cancer of the vulva may develop after many years. Also known as dysplasia, VIN can range from mild to severe.
Aetiology
The exact cause is not known, however it has been linked to:
- Human papillomavirus (HPV), a common infection
- Herpes simplex virus
- Granuloma inguinale, a sexually transmitted disease (STD)
- Smoking
- Immunosuppression
- Chronic vulvar irritation
Clinical Features
Symptoms vary but may include:
- Chronic vulvar itching
- Burning, tingling or soreness in the vulva area
- Change in appearance of the affected area, including areas of redness or white, discolored skin
- Slightly raised skin lesions; some may appear darkened like a mole or freckle
- Pain during sex
In rare cases, there may be no symptoms initially.
Diagnosis may include:
- A physical exam
- A colposcopy, an office procedure that uses a special microscope (colposcope) to closely examine the tissue for abnormal areas
- A biopsy of the affected area. A local anesthetic is given to numb the area. A small sample of vulva tissue is then taken and the cells are examined under a microscope.
Prevention
Lifestyle habits that may help prevent VIN or detect it early include:
- Practicing safe sex
- Vaccinating girls with the HPV vaccine before their first sexual contact
- Regular exams for early detection and treatment, preventing cancer of the vulva from developing
Treatment
Treatment varies depending on how abnormal the skin cells are, the size of the affected area, and the estimated risk of the area developing into vulvar cancer. Treatment options include:
- Steroid cream to reduce inflammation and control symptoms, with close monitoring
- Surgery to remove the abnormal tissue
- Laser therapy to destroy targeted areas of abnormal cells, using a beam of light
- Diathermy, which uses a tiny electrical current to cut out the affected areas
- Topical chemotherapy cream to remove abnormal cells
- Vulvectomy (removal of the whole vulva) in rare cases where the affected areas are very large
VIN can recur after treatment, therefore regular follow-up appointments are highly recommended.
MALIGNANT VULVAR LESIONS
The most common etiology of vulvar cancer involves infection with the Human Papilloma Virus (HPV). In this group of women there is an association with high-risk sexual activity, increased rates of tobacco use, and younger age. The remaining cases are seen mostly in elderly patients, does not have an apparent association to HPV infection, is not preceded by vulvar dysplasia, and is commonly found adjacent to chronic dystrophic or inflammatory lesions. There are also a small proportion of vulvar cancers classified as melanoma, sarcoma, or basal cell lesions.
Epidemiology
Vulvar cancer accounts for approximately 5% of all female genital malignancies. It occurs in about 2.5 per 100,000 women-years in developed countries but is 2-3 times more frequent in underdeveloped countries. With the exception of the rare sarcomas, this cancer appears most frequently in women aged 65-75 years, and, in some series, almost half of the patients are aged 70 years or older. Vulvar cancer can appear in younger patients, and, in some large cancer referral institutions, approximately 15% of all vulvar cancers occur in women younger than 40 years. These young patients tend to have early microcarcinomas, which may be associated with diffuse intraepithelial neoplasia of the vulva.
Prevention
Although there is no screening for vulvar neoplasia or vulvar cancer, immunization with the quadrivalent or 9-valent HPV vaccine and smoking cessation have been shown to decrease the rates of disease.
MELANOMA
Melanoma is the second most common invasive cancer occurring in the vulva, but its occurrence is rare. Melanoma probably arises from a lesion containing a junctional or compound nevus. Consider pigmented lesions on the vulva suspicious if they are blue-black in color, have a jagged or fuzzy border, are raised or ulcerated, or are larger than approximately 1 cm. Melanomas may be misdiagnosed as undifferentiated squamous carcinoma, particularly if they are amelanotic. Most melanomas are located on the labia minora or clitoris, and prognosis is related to the size of the lesion and the depth of invasion.
Approximately 3% of all melanomas are located in the genital tract. Melanoma of the vulva accounts for 5-7% of invasive vulvar cancers and has an estimated annual incident rate of 1 per 1,000,000 women. The disease can affect women of all ages but is more common in the older population, with almost half of the patients aged 70 years or older. More than 90% of melanomas occur in white women.
PAGET DISEASE
Paget disease of the vulva is rare. It occurs in women in the seventh decade of life but can occur in young patients. Symptoms of pruritus and tenderness or identification of a vulvar lesion occur most frequently. The patient may experience symptoms for several years before seeking medical advice. The lesion may be localized to one labium or involve the entire vulvar epithelium. It may extend to the perirectal area, buttocks, inguinal area, or mons. It has been observed extending into the vagina.
Vulvar lesions usually are hyperemic, and they may be demarcated sharply and thickened with foci of excoriation and induration. The vulvar skin may be thick, leading to the impression of leukoplakia with the cake icing effect. This classic finding almost is pathognomonic for Paget disease. The lesion is usually superficial and is considered an intraepithelial lesion, although an underlying adenocarcinoma may be associated with Paget disease. Older literature suggests that underlying adenocarcinoma occurs in about a quarter of cases, but more recent data find less association of Paget disease with an underlying adenocarcinoma.
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Topic 2: Benign and Malignant Conditions of the Cervix
BENIGN TUMORS OF THE CERVIX
Endocervical polyps
Endocervical polyps are the most common benign neoplasms of the cervix. They are focal hyperplastic protrusions of the endocervical folds, including the epithelium and substantia propria. They are most common in the fourth to sixth decades of life and usually are asymptomatic but may cause profuse leukorrhea or postcoital spotting.
Grossly, they appear as typical polypoid structures protruding from the cervical os. At times, endometrial polyps protrude through the cervical os. They cannot be distinguished from endocervical polyps by gross appearance. Microscopically, a variety of histologic patterns are observed, including (1) typical endocervical mucosal, (2) inflammatory (granulation tissue), (3) fibrous, (4) vascular, (5) pseudodecidual, (6) mixed endocervical and endometrial, and (7) pseudosarcomatous.
Treatment is removal, which can usually be accomplished by twisting the polyp with ringed forceps if the pedicle is slender. Smaller polyps may be removed with punch biopsy forceps. Polyps with a thick stalk may require surgical removal.
Smooth muscle tumors (leiomyomas)
These benign neoplasms may originate in the cervix and account for approximately 8% of all uterine smooth muscle tumors. They are similar to tumors in the fundus. When located in the cervix, they usually are small, ie, 5-10 mm in diameter.
Symptoms depend on size and location. Microscopically, leiomyomas resemble the typical smooth muscle tumor found in the uterine corpus. Treatment is required only for those patients who are symptomatic. The cervical leiomyoma is usually part of the spectrum of uterine smooth muscle tumors.
Endometriosis
When present in the cervix, endometriosis is usually an incidental finding. However, it may present as a mass or abnormal bleeding, particularly postcoital. Grossly, it may appear as a bluish-red or bluish-black lesion, typically 1-3 mm in diameter. Diagnosis is made by colposcopy and colposcopically directed biopsy but at times is difficult. Microscopically, the implants are typical endometriosis, consisting of endometrial glands, endometrial stroma, and hemosiderin-laden macrophages. The implants usually gain access to the cervix during childbirth or previous surgery. Management is expectant in almost all instances.
CERVICAL INTRAEPITHELIAL NEOPLASIA (CIN)
CIN, formerly called dysplasia, refers to premalignant lesions of the cervix. It means disordered growth and development of the epithelial lining of the cervix.
There are various degrees of CIN. Mild dysplasia, or CIN I, is defined as disordered growth of the lower third of the epithelial lining. Abnormal maturation of the lower two-thirds of the lining is called moderate dysplasia, or CIN II. Severe dysplasia, CIN III, encompasses more than two thirds of the epithelial thickness with carcinoma in situ (CIS) representing full-thickness dysmaturity. While histologically evaluated lesions are characterized using the CIN nomenclature, cytologic smears are classified according to the Bethesda system, which was most recently revised in 2001.
Briefly, atypical squamous cells are divided into those of undetermined significance (ASC-US) and those in which a high-grade lesion cannot be excluded (ASC-H). Low-grade squamous intraepithelial lesion (LSIL) encompasses cytologic changes consistent with koilocytic atypia or CIN I. High-grade squamous intraepithelial lesion (HSIL) denotes the cytologic findings corresponding to CIN II and CIN III. CIN may be suspected because of an abnormal cytologic smear, but the diagnosis is established by cervical biopsy. Spontaneous regression, especially of CIN I, occurs in a significant number of patients, allowing for expectant management with serial cytologic smears in the reliable patient. A certain percentage of high-grade lesions will progress to an invasive cancer if left untreated.
PATHOGENESIS
The epidemiologic risk factors for CIN are similar to those for cervical cancer and include multiple sexual partners, early onset of sexual activity, a high-risk sexual partner (history of multiple sexual partners, human papillomavirus [HPV] infection, lower genital tract neoplasia, or prior sexual exposure to someone with cervical neoplasia), a history of sexually transmitted infections (STIs), cigarette smoking, human immunodeficiency virus (HIV) infection, acquired immunodeficiency syndrome (AIDS), other forms of immunosuppression, multiparity, and long-term oral contraceptive pill use.
HPVs are a prime etiologic factor in the development of CIN and cervical cancer. In fact, most of the above behavioral and sexual risk factors for cervical neoplasia become statistically insignificant as independent variables after adjusting for HPV infection. Analyses of cervical neoplasia lesions show the presence of HPV in more than 80% of all CIN lesions and in 99.7% of all invasive cervical cancers. The 2 most common high-risk HPV types are HPV-16, found in 50–70% of cervical cancers, and HPV-18, found in 7–20% of cases.
There are about 130 HPV types, about 30–40 of which infect the anogenital epithelium. Based on their malignant potential, HPV subtypes are categorized into low-risk and high-risk types. Low-risk HPV types (eg, types 6, 11, 42, 43, and 44) are associated with condylomata and low-grade lesions (CIN I), whereas high-risk HPV types (e.g. types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, and 68) are associated with invasive cancer in addition to high-grade lesions (CIN II and CIN III).
More than 90% of immunocompetent women will have a spontaneous resolution of their HPV infection over a 2-year period, and only approximately 5% will have cytologically detectable CIN. About 10% of women will have a persistent high-risk HPV infection, which places them at increased risk for developing CIN II/III and cervical cancer.
Prevention
A. HPV Vaccination
Three HPV vaccines are currently approved by the Food and Drug Administration (FDA), a quadrivalent vaccine (Gardasil 4) against HPV-16, -18, -6, and -11; a bivalent vaccine (Cervarix) against HPV-16 and -18 and a nanovalent Gardasil 9 against HPV types 6, 11, 16, 18, 31, 33, 45, 52 and 58. These HPV vaccines are prophylactic and not therapeutic. Thus, immunization with HPV vaccine is most effective in female or male individuals who have not been infected with HPV (eg, before sexual debut).
B. Screening for CIN & Cervical Cancer
Following the implementation of population-based screening programs and treatment of preinvasive and early invasive disease, there has been a 75% reduction in the incidence and mortality of cervical cancer in developed countries. It is critical that women, whether vaccinated or not, follow current cervical cancer screening guidelines.
For the Kenyan screening programme, this guideline recommends the following:
1. HPV testing is
recommended as the primary screening method for women above 30 years of age.
2. Where HPV testing is not yet available, or loss-to-follow-up is a risk, then
Visual Inspection with Acetic acid (VIA) or Visual Inspection with Acetic acid
and Visual Inspection with Lugol’s iodine (VIA/VILI) is recommended as the
primary screening method
3. Pap smear is
recommended as a primary screening method in the following situations:
a. For women not eligible for VIA or VIA/VILI because their squamo-columnar
junction (SCJ) is not visible, and HPV screening not accessible
b. As a primary test in women under 30 years of age
c. As a co-test with HPV in HIV positive women where the resources are available
CERVICAL CANCER
Cervical cancer is the third most common malignancy in women worldwide, and it remains a leading cause of cancer-related deaths for women in developing countries. The incidence of invasive cervical cancer has declined steadily in developed countries over the past decades mainly due to mass screening with Papanicolaou (Pap) tests, which permit detection and treatment of preinvasive disease. Internationally, more than 500,000 new cases are diagnosed each year; rates vary widely, ranging from an annual incidence of 4.5 cases per 100,000 in Western Asia to 34.5 per 100,000 women in Eastern Africa. In industrialized countries with well-established cytology screening programs, the incidence of cervical cancer ranges from 4 to 10 per 100,000 women.
Clinical Findings
Abnormal vaginal bleeding is the most common symptom of invasive cancer and may take the form of a blood-stained leukorrheal discharge, scant spotting, or frank bleeding. Leukorrhea, usually sanguineous or purulent, odorous, and nonpruritic, is frequently present. A history of postcoital bleeding may be elicited on specific questioning.
Pelvic pain, often unilateral and radiating to the hip or thigh, is a manifestation of advanced disease, as is the involuntary loss of urine or feces through the vagina, a sign of fistula formation. Weakness, weight loss, and anemia are characteristic of the late stages of the disease, although acute blood loss and anemia may occur in a bulky or ulcerating stage I lesion.
Physical examination findings include a grossly normal-appearing cervix with preclinical disease. As the local disease progresses, physical signs appear. Infiltrative cancer produces enlargement, irregularity, and a firm consistency of the cervix and eventually of the adjacent parametria. The growth pattern can be endophytic, leading to a barrel-shaped enlargement of the cervix, or exophytic, where the lesion generally appears as a friable, bleeding, cauliflower-like lesion of the portio vaginalis.
Ulceration
may be the primary manifestation of invasive carcinoma; in the early stages,
the change
often is superficial, so that it may resemble an ectropion or chronic
cervicitis. With further progression of the disease, the ulcer becomes deeper
and necrotic, with indurated edges and a friable, bleeding surface. The
adjacent vaginal fornices may become involved next. Eventually, extensive parametrial
involvement by the infiltrative process may produce a nodular thickening of the
uterosacral and cardinal ligaments with resultant loss of mobility and fixation
of the cervix.
Clinical Staging
It
is important to estimate the extent of the disease not only for prognostic
purposes, but also for
treatment planning. Clinical staging also affords a means of comparing methods
of therapy for various stages of the disease worldwide. The classification
adopted by FIGO is the most widely used staging system (Table 48–3). Cervical
cancer is staged by clinical examination and evaluation of the bladder, ureters,
and rectum. If the lesion is clearly confined to the cervix by office
examination, only chest radiography and evaluation of the ureters by IVP or CT
scan with intravenous contrast are necessary to assign the stage. If it is not
possible to evaluate the extent of local disease in the office, examination under
anesthesia with cystoscopy and proctoscopy may be necessary. Although CT scan,
MRI, lymphangiography, and PET scan may offer information helpful for treatment
planning, these findings do not change the FIGO stage of disease. The FIGO
stage of disease is also not changed by surgicopathologic findings of
metastatic disease at the time of radical hysterectomy or lymphadenectomy.
Management
The treatment of cervical cancer frequently requires a multidisciplinary approach. Involvement of a gynecologist oncologist, radiation oncologist and medical oncologist may be necessary.
The treatment of cervical cancer varies with the stage of the disease, as follows:
Stage 0: local ablative or excisional measures such as cryotherapy, laser ablation and LEEP; surgical removal (cold knife conization) is preferred in that it allows further pathologic evaluation to rule out microinvasive disease. After treatment, these patients require lifelong surveillance.
Stage IA1: The treatment of choice is surgery: total hysterectomy, radical hysterectomy, and conization are accepted procedures. Lymph node dissection is not required if the depth of invasion is less than 3 mm and no lymphovascular invasion is noted.
Stage IA2, IB or IIA: Combined beam radiation with brachytherapy and radical hysterectomy with bilateral pelvic lymphadenectomy for patients with stage IB or IIA disease; radical vaginal trachelectomy with pelvic lymph node dissection is appropriate for fertility preservation in women with stage IA2 disease and those with stage IB1 disease whose lesions are 2 cm or smaller.
Stage IIB, III or IVA: Cisplatin-based chemotherapy with radiation is the standard of care.
Stage IVB and recurrent cancer: Individualized therapy is used on a palliative basis; radiation therapy is used alone for control of bleeding and pain; systemic chemotherapy is used for disseminated disease.
Prognosis
The prognosis in patients with cervical cancer depends on the disease stage. In general, the 5 year survival rates are as follows:
Stage I: >90%
Stage II: 60-80%
Stage III: Approx. 50%
Stage IV: <30%
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Topic 3: Benign and Malignant Conditions of the Uterus
BENIGN CONDITIONS OF THE UTERUS
FIBROIDS
Leiomyomas
of the uterus (or uterine fibroids) are benign tumors that
arise from the overgrowth of smooth muscle and connective tissue in the uterus.
Histologically, a monoclonal proliferation of smooth muscle cells occurs. A
genetic predisposition to leiomyoma growth exists. Uterine leiomyomas
(fibroids) are the most common benign gynecologic tumors. They primarily affect
women of reproductive age, and the estimated incidence of fibroids is over 70%
by 50 years of age.
Rarely, uterine leiomyomas may undergo malignant degeneration to become a sarcoma. The true incidence of malignant transformation is difficult to determine, because leiomyomas are common, whereas malignant leiomyosarcomas are rare and can arise de novo. The incidence of malignant degeneration is less than 1.0% and has been estimated to be as low as 0.2%.
Pathophysiology
Although myomas are common, relatively few actually cause symptoms. Whether symptoms are present depends largely on a combination of size, number, and location of the myomas. In general, myoma growth is a result of the stimulation of estrogen, which is present until menopause. Over time, previously asymptomatic myomas may grow and become symptomatic. Conversely, many myomas begin to shrink as menopause removes the estrogen stimulation and many myoma-related symptoms resolve spontaneously shortly after menopause.
Myomas are generally categorized by location. Intramural myomas are entirely or mostly contained within the myometrium. Subserosal myomas project outward from the uterus. Submucosal myomas project into the endometrial cavity. Pedunculated myomas are attached to the uterine wall by stalks and can be directed into either the peritoneal or the uterine cavity
Presentation
Most leiomyomata are small and do not cause symptoms. Many are found as incidental findings after an obstetric or gynecologic ultrasonographic examination or after a routine pelvic examination.
However, myomas can cause a number of symptoms. They can cause menstrual irregularities, particularly menorrhagia. This bleeding usually begins gradually and progressively worsens as the responsible myoma enlarges. A regular menstrual pattern should be still discernible despite the development of heavier or prolonged bleeding. If no regular pattern is noted, an alternative etiology such as chronic anovulation is more likely.
Some patients present with progressive pelvic pressure, pelvic pain, or low back pain. The differential diagnoses for such symptoms is diverse; however, if they are noted in someone with a medium- or large-sized uterus (>14-15 weeks' size), the myomas are more likely to be contributing. Some fibroid uteri can grow out of the pelvis and into the abdomen, where they can be palpated by the patient. This can be disturbing, even if the patient is having mild or no symptoms. Some are visible, distorting the abdominal wall and, at times, making the patient appear pregnant.
Secondary Changes in Fibroids
1. Degenerations
a) Hyaline – most common – 65%, affects all sizes of fibroid except the tiny ones. The feel is soft, elastic in contrast to firm.
b) Cystic – occurs following menopause. Common in interstitial fibroid.
c) Fatty (myoxomatous) – found at or near menopause. Fat globules are deposited in muscles cells.
d) Calcification - 10% - calcaneus. Usually sub serous. Precipitation of calcium carbonate or phosphates within tumor
e) Red - occurs in large fibroids during 2nd half of pregnancy & puerperium
2. Atrophy- following menopause due to loss of support from estrogen they reduce in size.
3. Necrosis- inadequate supply leads to central necrosis of the tumor
It’s present in submocous polyp or pedunculated sub serous.
4. Infection- usually happens following delivery or abortion.
5. Vascular changes- dilatation of the vessels or telengiactasis or dilatation of lymphatic channels cause is unknown.
6. Sarcomotous change- less than 0.1% turn malignant. Usually leiomyosarcoma
Management
Medical Therapy
Management of symptomatic uterine fibroids includes a number of nonsurgical approaches. Of note, treatment is usually strictly for patient comfort, and withholding treatment is reasonable in patients with no symptoms or with mild, well-tolerated symptoms. While medical treatment does not currently allow a permanent cure for fibroids, therapy with nonsteroidal anti-inflammatory drugs, oral contraceptive pills, progesterone modulators, progestins and estrogens, and gonadotropin-releasing hormone (GnRH) analogs is often attempted.
Surgical Therapy
A number of surgical therapies are available for the management of myomas, including hysterectomy, abdominal myomectomy, laparoscopic myomectomy, and hysteroscopic myomectomy. Myomas are most commonly treated with hysterectomy. The traditional procedure is abdominal myomectomy, although laparoscopic myomectomy is an acceptable option for experienced laparoscopic surgeons.
ADENOMYOSIS
Adenomyosis is a common, but poorly understood, condition that affects women of all age groups. It is defined as the presence of ectopic nests of endometrial glands and stroma within the myometrium, surrounded by reactive smooth muscle hyperplasia. Adenomyosis is a common cause of dysmenorrhea, menorrhagia, and chronic pelvic pain, but is often underdiagnosed.
The pathophysiology of adenomyosis development remains poorly understood. Adenomyosis may be present either as diffuse, scattered individual glands, or focal collections of glandular tissue. The most widely accepted theory for the origin of adenomyosis is an abnormal invagination of the basalis layer of the endometrium into the adjacent myometrial layer.
Diagnosis
Currently, adenomyosis remains a largely clinical diagnosis. Definitive diagnosis of adenomyosis requires a histologic exam of uterine tissue. Typically this step is circumvented in women desiring future fertility or who wish to preserve their uterus. Increasing availability and technological advances in imaging such as ultrasound, CT and MRI scans have improved evaluation for adenomyosis, but it still remains largely under-diagnosed until the time of hysterectomy. It is important both to maintain a high clinical suspicion for adenomyosis throughout the evaluation, as it may shape management options moving forward.
Treatment
The most important factor when considering treatment of a patient with adenomyosis is her desire for future fertility. The only definitive treatment for symptoms associated with adenomyosis is hysterectomy; however, this is not an option for patients who desire future fertility and may not be an option for patients who are poor surgical candidates.
Medical Care
The medications most commonly used to treat symptoms of adenomyosis are anti-inflammatory medications and hormonal therapies. The most common class of anti-inflammatory medications used to treat menorrhagia are non-steroidal antiinflammatory drugs. These inhibit formation of prostaglandins, which are considered the primary mechanism of action in uterine pain. Hormonal therapies cause ovarian suppression, mainly through negative feedback on the hypothalamic-pituitary-ovarian axis. By suppressing ovarian function, hormonal stimualtion of adenomyotic tissue is suppressed.
Hysterectomy
Hysterectomy is currently considered the only definitive management for adenomyosis, and is still the recommended method if desired future fertility is not a factor. In many instances, adenomyosis is incidentally noted on histologic exam.
ENDOMETRIAL HYPERPLASIA
Endometrial hyperplasia involves the proliferation of endometrial glands that results in a greater than normal gland-to-stroma ratio. This results in varying degrees of architectural complexity and cytologic atypia. The clinical significance of this diagnosis is progression to or concurrent endometrioid endometrial adenocarcinoma.
The classification of endometrial hyperplasia has had numerous terminologies. The classification below was the most commonly used system historically and was used by the World Health Organization (WHO) and the International Society of Gynecologic Pathologists since 1994. This system characterizes the glandular architectural pattern as simple or complex and describes the presence or absence of nuclear atypia.
- Simple hyperplasia - Increased number of glands but regular glandular architecture
- Complex hyperplasia - Crowded irregular glands
- Simple hyperplasia with atypia - Simple hyperplasia with presence of cytologic atypia (prominent nucleoli and nuclear pleomorphism)
- Complex hyperplasia with atypia - Complex hyperplasia with cytologic atypia
Clinical Features
The most common clinical presentation of patients with endometrial hyperplasia is abnormal uterine bleeding, whether in the form of menorrhagia, metrorrhagia, or postmenopausal bleeding. It can be associated with uterine hemorrhage, requiring emergent medical or surgical interventions, loss of fertility, and blood transfusion therapy. Others present with abnormal vaginal discharge or Pap smear results showing glandular abnormalities. The abnormal Pap smear result may be atypical glandular cells or presence of atypical endometrial cells.
Diagnosis of endometrial hyperplasia is usually made by sampling the endometrial cavity with an endometrial biopsy in the office.
Treatment & Management
The accurate diagnosis of hyperplasia type is vital for appropriate treatment based on risk of cancer without over or under treatment. Once a tissue diagnosis of endometrial hyperplasia is made, treatment depends on the type of hyperplasia, the patient's symptoms such as severity of bleeding, surgical risks, and wish for future childbearing. Progestins can effectively treat endometrial hyperplasia to control bleeding and prevent progression to cancer. They can serve as prevention of recurrence in those with continued risk factors. Benign hyperplasia responds well to progestins. More than 98% of women with hyperplasia treated with cyclic progestins experienced regression of the disease in 3-6 months. However, atypical hyperplasia or EIN lesions should undergo hysterectomy for definitive diagnosis and treatment if they have completed childbearing and are reasonable surgical candidates due to a 42% risk of concurrent endometrial cancer.
ENDOMETRIAL CARCINOMA
Endometrial cancer is the most common gynaecologic malignancy in developed countries and is second after cervical malignancy in developing countries. The peak incidence of onset is in the seventh decade, but 25% of cancers occur in premenopausal women, and the disease has even been reported in women ages 20–30 years.
Most endometrial carcinomas arise on the background of
endometrial hyperplasia and are well differentiated tumours. There are 2 major
types of endometrial cancer. Type I tumours are more
common (85%) and tend to occur in younger women. These are associated with
either endogenous or exogenous unopposed oestrogen exposure and usually consist
of a low-grade or well-differentiated tumour with a favourable prognosis. Type
II tumours grow independent of oestrogen, are associated with endometrial
atrophy, and occur in an older population.
Clinical Findings
Abnormal bleeding occurs in approximately 80% of
patients and is the most important and early
symptom of endometrial carcinoma. An abnormal vaginal discharge, especially
after menopause or intermittent spotting, is reported by some patients. During
the premenopausal years, the bleeding is usually described as excessive flow at
the time of menstruation. However, bleeding may occur as intermenstrual
spotting or premenstrual and postmenstrual bleeding. Approximately 5–10% of patients
with postmenopausal bleeding have underlying cancer, but the probability
increases with age and depends on underlying risk factors. Approximately 10% of
patients complain of lower abdominal cramps and pain secondary to uterine
contractions caused by detritus and blood trapped behind a stenotic cervical os
(hematometra). If the uterine contents become infected, an abscess develops and
sepsis may occur.
Physical examination is usually unremarkable but may
reveal medical problems associated with
advanced age. Speculum examination may confirm the presence of bleeding, but
because it may be minimal and intermittent, blood might not be present.
Atrophic vaginitis is frequently identified in these elderly women, but
postmenopausal bleeding should never be ascribed to atrophy without a histologic
sampling of the endometrium to rule out endometrial carcinoma. Bimanual and rectovaginal
examination of the uterus in the early stages of the disease will be normal
unless hematometra or pyometra is present. If the cancer is extensive at the
time of presentation, the uterus may be enlarged and may be misdiagnosed as a
benign condition such as leiomyomata. In advanced cases, the uterus may be
fixed and immobile from parametrial extension.
Treatment
The mainstay of
treatment is surgery, including a total hysterectomy with bilateral salpingo-oophorectomy
and staging with pelvic and periaortic lymphadenectomy. Further postoperative
therapy depends on the particular histologic characteristics and the extent of
the tumour.
The majority of endometrial cancer cases are diagnosed at an early stage and
can be treated with
high cure rates. The most important treatment modality is surgery with total
hysterectomy, bilateral salpingo-oophorectomy, and staging, including pelvic
and periaortic lymphadenectomy. Primary radiation therapy is used only in
patients with medical contraindications for surgery or advanced pelvic disease.
It has been repeatedly demonstrated that radiation therapy can cure endometrial
carcinoma in some patients. However, radiation therapy averages about a 20%
lower cure rate compared to surgery in stage I disease. Primary chemotherapy is
used infrequently and mostly in patients with metastatic disease. High-dose
progesterone therapy, commonly with
medroxyprogesterone acetate or megestrol acetate, may be used for patients who
are inoperable or in younger patients who elect for fertility preservation. The
overall response to high-dose progesterone therapy is up to 75% in grade 1
endometrial cancer cases limited to the endometrium. To verify that the patient
is responding to therapy, regular endometrial sampling needs to be performed.
Prognosis
The overall
prognosis is considerably better than for the other major gynaecologic cancers
with 5-year survival rates of 96%, 67%, and 17% for local, regional, and distant
disease at diagnosis, respectively. The most important prognostic factors for
endometrial cancer are stage, histologic type, grade, myometrial invasion, and
the presence of lymphovascular space invasion.
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Topic 4: Benign and Malignant Conditions of the Ovaries
BENIGN CONDITIONS OF THE OVARIES
Ovarian Cysts
An ovarian cyst is a sac filled with liquid or semiliquid material that arises in an ovary. The number of diagnoses of ovarian cysts has increased with the widespread implementation of regular physical examinations and ultrasonographic technology. The discovery of an ovarian cyst causes considerable anxiety in women owing to fears of malignancy, but the vast majority of ovarian cysts are benign.
These cysts can develop in females at any stage of life, from the neonatal period to postmenopause. Most ovarian cysts, however, occur during infancy and adolescence, which are hormonally active periods of development. Most are functional in nature and resolve without treatment.
However, ovarian cysts can herald an underlying malignant process or, possibly, distract the clinician from a more dangerous condition, such as ectopic pregnancy, ovarian torsion, or appendicitis. (On the other hand, there may be an inverse relationship between ovarian cysts and breast cancer).
Signs and symptoms
Most patients with ovarian cysts are asymptomatic, with the cysts being discovered incidentally during ultrasonography or routine pelvic examination. Some cysts, however, may be associated with a range of symptoms, sometimes severe, including the following
- Pain or discomfort in the lower abdomen
- Severe pain from torsion (twisting) or rupture - Cyst rupture is characterized by sudden, sharp, unilateral pelvic pain; this can be associated with trauma, exercise, or coitus. Cyst rupture can lead to peritoneal signs, abdominal distention, and bleeding (which is usually self-limited)
- Discomfort with intercourse, particularly deep penetration
- Changes in bowel movements such as constipation
- Pelvic pressure causing tenesmus or urinary frequency
- Menstrual irregularities
- Precocious puberty and early menarche in young children
- Abdominal fullness and bloating
- Indigestion, heartburn, or early satiety
- Endometriomas - These are associated with endometriosis, which causes a classic triad of painful and heavy periods and dyspareunia
- Tachycardia and hypotension - These may result from hemorrhage caused by cyst rupture
- Hyperpyrexia - This may result from some complications of ovarian cysts, such as ovarian torsion
- Adnexal or cervical motion tenderness
- Underlying malignancy may be associated with early satiety, weight loss/cachexia, lymphadenopathy, or shortness of breath related to ascites or pleural effusion
Diagnosis
Per ACOG guidelines, transvaginal ultrasound is the preferred imaging modality for assessment of a suspected pelvic mass.
The definitive diagnosis of all ovarian cysts is made based on histologic analysis. Each cyst type has characteristic findings.
Management
Many patients with simple ovarian cysts found through ultrasonographic examination do not require treatment. In a postmenopausal patient, a persistent simple cyst smaller than 10 cm in dimension in the presence of a normal CA125 value may be monitored with serial ultrasonographic examinations.
Pharmacologic therapy
Oral contraceptive pills (OCPs) protect against the development of functional ovarian cysts. Existing functional cysts, however, do not regress more quickly when treated with combined oral contraceptives than they do with expectant management.
Laparotomy and laparoscopy
Persistent simple ovarian cysts larger than 10 cm (especially if symptomatic) and complex ovarian cysts should be considered for surgical removal. The surgical approaches include an open technique (laparotomy) or a minimally invasive technique (laparoscopy) with very small incisions. The latter approach is preferred in cases presumed benign. Removing the cyst intact for pathologic analysis may mean removing the entire ovary, though a fertility sparing surgery should be attempted in younger women.
Bilateral oophorectomy
Bilateral oophorectomy and, often, hysterectomy are performed in many postmenopausal women with ovarian cysts, because of the increased incidence of neoplasms in this population.
OVARIAN CANCER
Majority of adnexal cancers arise from the surface epithelial cells of the ovary (epithelial ovarian cancer [EOC]). Fewer ovarian cancers develop from the remaining cell types (sex cord-stromal, germ cell, or mixed cell type tumors), and even fewer adnexal cancers arise from the fallopian tubes, although recent evidence has shown that they account for a greater percentage than previously thought. The categories of ovarian cancers are depicted in the table below:
Clinical Findings
Early-stage EOC is associated with poorly defined or vague symptoms, which often are not severe enough to prompt a woman to seek medical attention. For later stage disease, which accounts for more than 70% of all diagnoses, the most common symptoms include an increased abdominal girth, pelvic or abdominal pain, bloating, urinary symptoms of frequency or urgency, or early satiety. Occasionally patients will have nausea or anorexia secondary to ascites or bowel metastases. Patients may also present with dyspnoea due to pleural effusions. Rarely do patients present with paraneoplastic phenomena such as subacute cerebellar degeneration, seborrheic keratoses (sign of Leser-Trelat), Trousseau’s syndrome (migratory thrombophlebitis), or hypercalcemia of malignancy.
Approximately 15% of
reproductive-age patients will present with menstrual abnormalities.
Abnormal vaginal bleeding may occur in the presence of a synchronous
endometrial carcinoma or as a consequence of metastatic disease to the lower
genital tract. Excess androgens or oestrogens may be present due to stimulation
of normal theca, granulosa, or hilar cells that surround the neoplasm or due to
secretion by a germ cell tumour or sex cord-stromal tumour. Ovarian stromal
hyperplasia or hyperthecosis may also be associated with excess androgen
production.
A pelvic exam will often reveal a solid, fixed, irregular adnexal mass.
Unilateral, cystic masses in reproductive-age women are benign in up to 95% of
cases. These masses, particularly when <6–8 cm in size, are observed through
a menstrual cycle because many represent functional cysts that spontaneously
resolve. An enlarging mass or one that is associated with pain merits prompt
intervention. A cystic, somewhat immobile adnexal mass may represent a
hydrosalpinx or tubo-ovarian abscess. Fixed, bilateral masses and firm masses
with nodularity are suggestive of, but not diagnostic of, an ovarian malignancy.
Laboratory Findings
The best characterized tumour marker in EOC is cancer antigen-125 (CA-125). CA-125 is a secreted glycoprotein present in foetal amniotic and coelomic epithelium, and its level can be detected in serum using immunoassay. The accepted upper limit of normal is 35 IU/mL, but this is a rather arbitrary cut-off. CA-125 is elevated in many patients with ovarian cancer, especially with serous histology, but is also elevated in other malignancies such as pancreatic, colon, breast, stomach, fallopian, or endometrial cancer. In addition, it is also elevated in certain benign conditions such as endometriosis, leiomyoma, or pelvic inflammatory disease, although rarely above 200 IU/mL. Therefore, it can be a useful adjunct in postmenopausal women, but not very useful in premenopausal women given the low incidence of EOC and greater incidence of benign lesions. Additionally, a normal CA-125 does not exclude the diagnosis of cancer and does not represent a reason to delay surgery.
In young girls and adolescents presenting with an adnexal mass, serum AFP, lactate dehydrogenase (LDH), and hCG should be measured as potential biomarkers given the greater likelihood of a malignant germ cell tumour.
Imaging Studies
Pelvic ultrasound helps
delineate the presence of a benign or malignant adnexal mass, and a number of
different scoring systems have been used, although there is no standardized
system
for evaluation of ovarian masses. Typical characteristics of ovarian cancer
include a solid component, which is often nodular or papillary, septations, and
ascites. Angiogenesis accompanying malignancy results in vascular abnormalities
and increased blood flow compared with the vascular architecture and patterns
of blood flow in non-malignant lesions. The addition of colour flow Doppler
studies that evaluate the vascular patterns of adnexal masses improves the
sensitivity and specificity of the radiographic diagnosis of benign and
malignant lesions. However, even when combined with laboratory or physical
findings, ultrasound is limited in making a definitive diagnosis, and surgery
is required to document malignancy histologically.
Treatment and prognosis
Surgical staging and tumour removal are required for all patients, unless the performance status of the patient limits surgical intervention. Initial surgical staging provides the definitive histologic diagnosis as well as the extent of disease. Obtaining the true stage of disease allows appropriate treatment and subsequent prognosis. The different types of ovarian cancers have different treatment approaches. Treatment modalities that are commonly used may include: surgery, chemotherapy, radiotherapy, hormonal or a combination of the several modalities.
Ovarian cancer is the third most common gynaecologic malignancy, yet the most common cause of death in women with such a malignancy due to late presentation and diagnosis. The following table shows the overall survival of patients with epithelial ovarian cancer (EOC).
Prevention
The
lifetime risk of ovarian cancer in the general population is 1.7%, and the
majority of known risks factors are not amenable to change, with age, early
menarche (prior to age 12), and late menopause (after age 50) being the most
prominent.
Endometriosis is an independent risk factor of EOC; malignant transformation occurs in approximately 2.5% of patients, who are typically younger. Nulligravidity is a major risk factor for EOC.
Certain protective
factors have been identified. The use of oral contraceptive pills (OCPs)
decreased the risk of ovarian cancer, with increasing protection conferred by
longer duration of use. The risk is reduced to half by 15 years of use, and the
protection persists after discontinuing
medication, although the effects become attenuated over time. Low-dose OCPs,
with ≤ 35 μg of
ethinyl estradiol are as effective as the higher dose OCPs. Women who have
undergone tubal ligation were found to have a decreased risk by about a third
to a half, with the effect being synergistic with a history of OCP use.
However, caution must be taken when suggesting this as a preventive measure, especially
in patients with hereditary syndromes because occult malignancies within the
fallopian tubes are often present in women carrying a genetic mutation.
Breastfeeding and progesterone use have also been shown to have a protective
effect.
Prevention by screening
methods is currently not possible. The lack of sensitivity or specificity of available
testing negates their use to identify women at risk of developing ovarian
cancer, and
therefore, screening by any modality is not recommended.
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Topic 5: Introduction to Breast Conditions
BREAST ABSCESSES AND MASSES
Breast masses are broadly classified as benign or malignant. Common causes of benign breast lesions include fibrocystic disease, fibroadenoma, intraductal papilloma, and abscess. Malignant breast disease encompasses many histologic types that include, but are not limited to, in situ ductal or lobular carcinoma, infiltrating ductal or lobular carcinoma, and inflammatory carcinoma. The main concern of many women presenting with a breast mass is the likelihood of cancer. Reassuringly, most breast masses are benign.
Breast infections are divided into lactational and nonlactational infections and puerperal versus nonpuerperal, depending on their association with pregnancy. The process may be confined to the skin overlying the breast, or it may result from an underlying lesion (eg, sebaceous cyst), as in hidradenitis suppurativa.
Causes
Malignant
Risk factors for females include the following:
- Age older than 40 years
- Family history of a first-degree relative with breast cancer
- Menarche before age 12 years
- Menopause after age 55 years
- Nulliparity
- First pregnancy after age 30 years
- Therapeutic radiation over chest before age 30 years
- Prediagnosis hormone replacement therapy remains controversial
- A history of smoking tobacco products for more than 15 years
- BRCA1 and BRCA2 mutations (responsible for approximately 5% of all breast cancers; inherited in an autosomal dominant fashion; women with mutations in either of these genes have a lifetime risk of breast cancer of 60%-85% and a lifetime risk of ovarian cancer of 15%-40%)
- Paget disease of the breast
Risk factors for males are as follows:
- BRCA1 and BRCA2 mutations
- Klinefelter syndrome: 20- to 50-fold greater lifetime risk
- Cowden syndrome
- Hormonal imbalance and increased estrogen levels, including liver disease and testicular abnormalities
- Environmental exposures, including to ionizing radiation, electromagnetic radiation, polycyclic aromatic hydrocarbons, alcohol, and red meat, have been studied in relation to male breast cancer, but none has convincingly been found to be associated with incidence across studies.
Exercise has been shown to decrease the risk of breast cancer in women at high risk for developing a malignancy. However, further studies are needed to verify this association and its relationship to preventing breast cancer in women on tamoxifen therapy (standard treatment for preventing breast cancer recurrence).
Alcohol consumption has not been shown to increase the risk of developing breast cancer.
Benign
Developmental breast lesions
Prepubertal and peripubertal developmental breast lesions may include abnormalities of embryology and gynecomastia.
Abnormalities of embryology include polythelia (accessory nipples) and polymastia (supernumerary breasts).
Gynecomastia is characterized by excessive development of breast tissues in males. It can be physiologic or pathologic in teens.
Neonatal breast hypertrophy is a common transient condition that results from elevation of maternal hormones, seen in up to 90% of all newborns.
Non-developmental breast lesions
Fibrocystic changes
Breast lobules may dilate and form cysts of varying sizes, due to hormonal changes in the menstrual cycle. Cysts are found in about 1 in 3 women aged 35-50 years. Rupturing of the cysts can cause scarring and inflammation that leads to fibrotic changes, which feel rubbery, firm, or hard.
Hyperplasia
Hyperplasia is caused by an overgrowth of cells that line the ducts or lobules. About 1 in 4 women have mild or usual hyperplasia. About 1 in 25 women have atypical hyperplasia (associated with an increased risk of malignancy).
Adenosis
An increase in the number of glands.
Fibroadenoma
Fibroadenoma is the most common cause of breast mass in women younger than 35 years and comprises 91% of all solid breast masses in females younger than 19 years. These arise from the terminal duct lobular unit and appear clinically as singular, firm, rubbery, smooth, mobile, painless masses ranging in size from 1-5 cm. They may grow to a large size, thereby affecting the contours of the overlying skin and overall shape of the breast. Ultrasonography reveals a well-defined hypoechoic homogeneous mass 1-20 cm in diameter. Fibroadenomas appear as multiple masses in 10%-15% of patients.
Phyllodes tumor
Phyllodes tumor is also known as cystosarcoma phyllodes or giant fibroadenoma. Although generally benign, a malignant variant occurs in 10% of cases. Incidence is highest among women aged 40-60 years. Phyllodes tumor is also the most common primary breast malignancy in adolescents. The most common presentation is that of a large (average 5 cm), solitary, firm, breast nodule. Ultrasonographic findings of the mass may appear identical to those of a fibroadenoma with well-circumscribed borders and small cysts.
Papillary adenoma of the nipple
Papillary adenoma is also known as erosive adenomatosis of the nipple, adenoma of the nipple, florid papillomatosis of the nipple, and subareolar duct papillomatosis of the nipple. This is believed to arise from terminal lactiferous ducts. Incidence is highest among women aged 40-50 years. It commonly presents with unilateral serous or bloody nipple discharge that increases before menses.
Vascular lesions
Vascular lesions are usually benign. The most common form is hemangioma. Surgical excision may be required.
Infectious
Breast abscess
Puerperal breast abscesses most often contain S aureus and streptococcal species. Methicillin-resistant S aureus (MRSA) has become increasingly common. The overall rate of breastfeeding cessation among patients with breast abscess was 41% in a US cohort and did not differ between MRSA and MSSA infections. In a US cohort, 81% of S aureus–confirmed cultures were MRSA pulsed-field type USA 300–0114. Nonpuerperal abscesses typically contain mixed flora (S aureus, streptococcal species) and anaerobes. Diabetes is strongly associated with incidence and clinical outcomes of breast abscesses in nonlactating women. One study demonstrated a 72% prevalence of diabetes in women with nonpuerperal abscesses. Cigarette smoking is a debated risk factor but has been shown to have a strong association with development of nonpuerperal mastitis. Primary breast abscess has also been reported to be more common in African Americans and those with obesity, and a possible association with inadequate vitamin A supplementation has also been described. Nipple piercing has been associated with increased risk of developing subareolar breast abscess.
Mastitis
Mastitis occurs in up to 33% of lactating women, with its highest incidence within 6 weeks postpartum or while weaning breastfeeding. Periductal mastitis comprises 3%-4% of all benign lesions of the breast. It may be associated with milk stasis caused by ineffective positioning of the baby, limited feeding, or restricted feeding.
Of infective mastitis cases, S aureus is the most common cause. Streptococci, enterococci, S epidermidis, Peptostreptococcus species, Prevotella species, and Escherichia coli are less common causes. True fungal mastitis is rare and should prompt evaluation for coexisting diabetes mellitus. In infants, infections with Shigella, E coli, and Klebsiella species have been reported. Mastitis that is refractory to appropriate treatment should prompt evaluation for tuberculous mastitis.
Prognosis
Breast mass: Prognosis varies from excellent in patients with a fibroadenoma to poor in those with inflammatory breast cancer. Influencing factors include tumor size, histology, nodal involvement, distant metastases, and comorbid conditions.
Breast abscess: Unfortunately, the recurrence rate of breast abscess is high (39%-50%) when treated with standard incision and drainage, and studies have shown even higher recurrence rates in women undergoing fine-needle aspiration. Nonpuerperal abscesses recur more frequently, especially when associated with non-staphylococcal species (>50% recurrence rate). Studies of patients with fistulectomy show lower recurrence rates.
Mastitis: Most patients experience resolution within 2-3 weeks. All patients with symptoms that have not resolved within 5 weeks should be evaluated for resistant infection or malignancy.
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Further Reading
1. DeCherney, A., Nathan, L., Goodwin, T.W., Laufer, N. and Roman, A. (2007) Current Diagnosis and Treatment: Obstetrics and Gynecology, 10th Edition. New York: McGraw-Hill
2. Chamberlain, G. (2007) Obstetrics by Ten Teachers, 20th Edition. Oxford: Oxford University Press
3. Cunningham, F.G., Leveno, K.L., Bloom, S.L., Hauth, J., Gilstrap, L.C. and Wenstrom, K.D. (eds) (2005) Williams Obstetrics, 22nd Edition. New York, McGraw Hill
4. Toy, E., Baker, B., Ross, P. and Jenning, J. (2012) Case Files: Obstetrics and Gynecology, 4th Edition. London, McGraw Hill Medical
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Topic 1: Obstetrical Complications
At the end of this unit, the learner should be able to demonstrate understanding of the following conditions:
- Amniotic Fluid Embolism
- Pregnancy Trauma
AMNIOTIC FLUID EMBOLISM
Amniotic fluid embolism (AFE) is a life threatening obstetric emergency characterized by sudden cardiorespiratory collapse and disseminated intravascular coagulation.
Incidence of amniotic fluid embolism (AFE) is estimated at 1 case per 8,000-30,000 pregnancies. The true incidence is unknown because of inaccurate diagnoses and inconsistent reporting of nonfatal cases.
The diagnosis of AFE has traditionally been made at autopsy when fetal squamous cells are found in the maternal pulmonary circulation; however, fetal squamous cells are commonly found in the circulation of laboring patients who do not develop the syndrome. The diagnosis is essentially one of exclusion based on clinical presentation. Other causes of hemodynamic instability should not be neglected.
Amniotic fluid embolism (AFE) is considered an unpredictable and unpreventable event with an unknown cause. Reported risk factors for development of AFE include multiparity, advanced maternal age, male fetus, and trauma.
Complications
- Pulmonary edema is a common occurrence in survivors. Pay close attention to fluid input and output.
- Left heart failure may occur. Some sources recommend inotropic support.
Treat DIC with blood components. Consider activated factor VIIa for severe hemorrhage. Bilateral uterine artery embolization has been successful in controlling blood loss in 2 reported cases.
Clinical Presentation
The classic history is that a woman in the late stages of labor becomes acutely dyspneic with hypotension. There may be a preceding period of agitation or a sense of impending doom. Altered mentation may or may not be present. She may experience seizures quickly followed by cardiac arrest. If undelivered, the fetus will demonstrate loss of heart rate variability followed by decelerations and ultimately a terminal bradycardia. Massive DIC-associated hemorrhage follows and then death. Most patients die within an hour of onset.
The classic triad of AFE is hypoxia, hypotension and coagulopathy. The following signs and symptoms are indicative of possible AFE:
- Hypotension: Blood pressure may drop significantly with loss of diastolic measurement.
- Dyspnea: Labored breathing and tachypnea may occur.
- Seizure: Tonic clonic seizures are seen in 50% of patients.
- Cough: This is usually a manifestation of dyspnea.
- Cyanosis: As hypoxia/hypoxemia progresses, circumoral and peripheral cyanosis and changes in mucous membranes may manifest.
- Fetal bradycardia: In response to the hypoxic insult, fetal heart rate may drop to less than 110 beats per minute (bpm). If this drop lasts for 10 minutes or more, it is a bradycardia. A rate of 60 bpm or less over 3-5 minutes may indicate a terminal bradycardia.
- Pulmonary edema: This is usually identified on chest radiograph.
- Cardiac arrest
- Uterine atony: Uterine atony usually results in excessive bleeding after delivery. Failure of the uterus to become firm with bimanual massage is diagnostic.
- Coagulopathy or severe hemorrhage in absence of other explanation (DIC occurs in 83% of patients.)
- Altered mental status/confusion/agitation
Differential Diagnoses
• Abruptio Placentae
• Anaphylaxis
• Aortic Dissection
• Aspiration
• Cholesterol Embolism
• Myocardial Infarction
• Pulmonary Embolism (PE)
• Septic Shock
Laboratory Studies
There are no laboratory tests to either confirm or refute the diagnosis of AFE. Laboratory values are useful in providing supportive measures for the patient.
Arterial blood gas (ABG levels
Expect changes consistent with hypoxia/hypoxemia, such as the following:
• Decreased pH levels (reference range = 7.40-7.45)
• Decreased PO2 levels (reference range = 104-108 mm Hg)
• Increased PCO2 levels (reference range = 27-32 mm Hg)
• Base excess increased
CBC with platelets
Hemoglobin and hematocrit levels should be within reference ranges.
Thrombocytopenia is rare. If platelets are less than 20,000/µL, or if bleeding occurs and platelets are 20,000-50,000/µL, transfuse platelets at 1-3 U/10 kg/d.
Coagulation studies
Prothrombin time (PT) is prolonged because clotting factors are used up. Values are institution specific, but intervention is indicated when the PT is 1.5 times the control value. Administer fresh frozen plasma (FFP) to normalize the PT.
Activated partial thromboplastin time (aPTT) may be within reference ranges or shortened.
Rotational thromboelastometry (ROTEM) has been used as a point of care test to guide management of the coagulopathy. [35]
Fibrinogen level
If fibrinogen level is less than 100 mg/dL, administer cryoprecipitate. Each unit of cryoprecipitate raises the fibrinogen level 10 mg/dL.
Type and screen
Blood type and screen in anticipation of the requirement for a transfusion.
Electrocardiography
A 12-lead ECG may show tachycardia, ST segment and T-wave changes, and findings consistent with right ventricle strain.
Histologic Findings
On autopsy, blood vessels in the lungs may show evidence of fetal debris (eg, squamous cells, vernix, mucin).
Management
Medical Care
Admit the patient with amniotic fluid embolism (AFE) into the intensive care unit (ICU).
Treatment is supportive and includes the following:
- Administer oxygen to maintain normal saturation. Intubate if necessary.
- Initiate cardiopulmonary resuscitation (CPR) if the patient arrests. If she does not respond to resuscitation, perform a perimortem cesarean delivery.
- Treat hypotension with crystalloid and blood products. Use pressors as necessary.
- Avoid excessive fluid administration. During the initial phase, right ventricular function is suboptimal. Excess fluid may overdistend the Right ventricle which could increase the risk of a right sided myocardial infarction.
- Consider pulmonary artery catheterization in patients who are hemodynamically unstable.
- Continuously monitor the fetus. Deliver immediately following cardiac arrest if gestational age is ≥ 23 weeks.
- Early evaluation of clotting status and early initiation of massive transfusion protocols is recommended.
- Treat coagulopathy with FFP for a prolonged aPTT, cryoprecipitate for a fibrinogen level less than 100 mg/dL, and transfuse platelets for platelet counts less than 20,000/µL.
- Lim and colleagues reported a case of AFE in which the coagulopathy was treated with activated recombinant factor VIIa. The range of doses to treat serious bleeding is from 20-120 mcg/kg.
- Hemodialysis with plasmapheresis and extracorporeal membrane oxygenation (ECMO) with intra-aortic balloon counterpulsation have been described in case reports with successful outcomes in treating AFE patients with cardiovascular collapse. The use of anticoagulation during ECMO may worsen bleeding in patients with AFE. Use of ECMO is not routinely recommended.
Surgical Care
Perform emergent cesarean delivery in arrested mothers who are unresponsive to resuscitation.
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Topic 1: Obstetrical Complications [Cont'd]
PREGNANCY TRAUMA
The pregnant trauma patient presents a unique challenge because care must be provided for two patients—the mother and the fetus. Anatomic and physiologic changes in pregnancy can mask or mimic injury, making diagnosis of trauma-related problems difficult. Care of pregnant trauma patients with severe injuries often requires a multidisciplinary approach involving an emergency clinician, trauma surgeon, obstetrician, and neonatologist.
Pathophysiology
To evaluate the pregnant patient, the various physiologic changes that occur during pregnancy must be understood. Because balance and coordination are most adversely affected during the third trimester, the frequency of accidental injury is greatest during this period. Although the pregnant patient's blood pressure decreases during pregnancy, changes may not be as great as traditionally thought. Systolic blood pressure changes by only 2-4 mm Hg, while diastolic pressure decreases by 5-15 mm Hg in mid-trimester. In addition, the resting heart rate usually increases by only 10-15 beats per minute. Thus, tachycardia or hypotension in the pregnant trauma patient should not be attributed solely to the gravid state.
Blood flow to the uterine arteries is normally maxillary vasodilated, so blood delivery to the uterus is maximal in the normal physiologic state. Maternal hypovolemia may result in vasoconstriction of the uterine vasculature. The third trimester fetus can adapt to a decrease in uterine blood flow and oxygen delivery by diverting blood distribution to the heart, brain, and adrenal glands. Because fetal hemoglobin has a greater affinity for oxygen than does adult hemoglobin, fetal oxygen consumption does not decrease until the delivery of oxygen is reduced by 50%. Thus, maternal shock may have a significant impact on the developing embryo/fetus.
Direct fetal injury is relatively uncommon because the maternal soft tissues, uterus, placenta, and amniotic fluid all tend to absorb and distribute the energy of the blow. The most common cause of fetal death is maternal shock, which is associated with a fetal mortality rate of 80%. This explains why efforts to assess fetal well-being are secondary to resuscitation of the mother.
Placental abruption is the second most common cause of fetal death, with fetal mortality rates as high as 30-68%. Placental abruption occurs when shearing forces lead to a separation of the rigid placenta from the elastic uterus. Up to 30-50% of patients with major traumatic injuries and as many as 5% of patients with minor injuries have placental abruption after trauma. Blunt injury in pregnancy does not appear to pose higher risk for death than it does in nonpregnant patients, with most deaths occurring as a result of either head injury or hemorrhage.
Fetal mortality and overall maternal morbidity remains exceedingly high (73% and 66%, respectively) following penetrating abdominal injury.
Causes
Causes of traumatic injuries in pregnancy are similar to those in the general population; blunt injury trauma is the most common cause.
• Motor vehicle accidents (MVAs) account for 49% of injuries.
• Falls account for 25% of injuries (may be related to physiologic changes that result in loss of balance).
• Assaults account for 18% of injuries.
• Guns account for 4% of injuries.
• Burns account for 1% of injuries.
Risk factors for trauma in pregnancy include simply pregnancy itself, younger age, drug use, alcohol use, and history of intimate partner violence.
Clinical Presentation
Features of the pregnant patient's history may include the following:
- Mechanism - Direct abdominal trauma, weapons, seatbelt use, proper or improper (The American College of Obstetrics and Gynecology emphasizes that both the lap belt and shoulder harness be worn with the lap belt passing below the abdomen and over the anterior superior iliac spine and symphysis pubis and the shoulder harness passing between the patient's breasts).
- Last menstrual period (LMP) and estimated date of confinement (EDC)
- Uterine contractions
- Fetal movement
- Premature rupture of membranes
- Vaginal bleeding
- History of depression, substance abuse, or several ED visits (These factors may suggest intimate partner violence, which is not dependent on age, race, marital status, or socioeconomic class. A review of 13 studies found the prevalence of intimate partner violence to range from 0.5% to 20.1 %.)
- Infants with mothers who have childhood histories of abuse/neglect, particularly those with unresolved trauma and trauma-specific reflective function, appear to be disproportionately insecure and exhibit attachment disorganization.
Laboratory Studies
Laboratory studies in the evaluation of the pregnant trauma patient may include the following:
• Determination of CBC: Pregnancy-induced leukocytosis peaks to levels of 12,000-18,000 per cubic millimeter during the third trimester. During labor, levels as high as 25,000 per cubic millimeter may occur.
• Determination of electrolyte and glucose levels
• Blood typing and cross matching
• Rhesus (Rh) blood group determination (Administer Rho(D) immune globulin [RhoGAM] if the mother is Rh negative)
• Urine pregnancy testing, if the status is unknown in a female of reproductive age with trauma
• Urinalysis
• Assessment of coagulation profile (Most coagulation factors rise throughout pregnancy, although laboratory values remain unchanged except for fibrinogen levels, which nearly double in value.)
Ultrasonography
• Assess fetal viability and for multiple gestations.
• Assess the size, gestational age, and position of the fetus.
• Ultrasonography can depict free intraperitoneal fluid or hemorrhage in the mother. The focused assessment with sonography for trauma (FAST) examination has become routine in many trauma centers and has been shown to have high sensitivity and accuracy in the hands of emergency clinicians and trauma surgeons.
Management
Patients who have minor trauma and who are at less than 20 weeks' gestation do not require specific intervention or monitoring. All pregnant women beyond 20-24 weeks' gestation who have direct or indirect abdominal trauma should undergo at least 4 hours of cardiotocographic monitoring. Resuscitation of the more serious trauma patient must focus on the mother because the most common cause of fetal death is maternal shock or death. It is important to remember that the mother will maintain her vital signs at the expense of the fetus. Because plasma volume is increased 50% and the mother is able to shunt blood away from the uterus, maternal shock may not manifest itself until maternal blood loss exceeds 30%. During the initial ABC assessment, the fetus is addressed only during evaluation of circulation.
If the patient is more than 20-24 weeks' pregnant, the patient should be tilted 15° to the left. Alternatively, one person may be designated to manually displace the uterus to the left. If the patient does not require spinal immobilization, then she can be asked to assume the left lateral decubitus position.
Admission and discharge criteria for pregnant trauma patients
Hospitalization is warranted in pregnant trauma patients with the following:
- Abnormal obstetric findings, such as vaginal bleeding
- Abnormal fetal heart rate tracings (eg, variable decelerations)
All serious trauma victims who are beyond 23 weeks EGA require 24 hours of fetal monitoring.
Discharge criteria include no abnormal obstetric findings and normal fetal heart tracings.
Instruct the patient to return in the event of decreased fetal activity, vaginal bleeding, uterine contractions and/or cramping, or spontaneous premature rupture of the membranes.
Transfer
Transfer the patient to a level I trauma center with obstetric and neonatal intensive care units (NICUs).
Consultations
The pregnant patient with serious traumatic injury requires a multidisciplinary team, which includes an obstetrician, trauma surgeon, and neonatologist.
Complications
Complications of pregnancy trauma include the following:
- Exsanguination: Dramatic increases in uterine blood flow (60 to 600 mL/min) may result in rapid exsanguination if there is avulsion of the uterine vessels or rupture of the uterus.
- Retroperitoneal hemorrhage: A common complication of pelvic fracture due to the tremendous increase in vascularity resulting from pregnancy.
- Uterine rupture: Enlargement of the uterus makes it susceptible to direct abdominal trauma. This rare complication is estimated to complicate 0.6% of traumatic injury. Uterine rupture is associated with a fetal mortality rate approaching 100%. Maternal mortality of 10% is usually a result of associated injuries.
- Rupture of amniotic membranes can lead to chorioamnionitis, preterm labor, and cord prolapse.
- Amniotic fluid embolism (may lead to acute respiratory distress syndrome)
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Topic 2: Gynaecological Complications
By the end of this topic, the learner should be able to demonstrate understanding of the following conditions:
- Gynaecological fistulae
- Uterine Inversion
- Uterine Prolapse
FISTULAE
Definition: Communication between hollow structures
Pathophysiology
Principles and phases of wound healing after injury.
Ø Tissue damage and necrosis stimulate inflammation
Ø Process of cell regeneration begins
Ø Formation of new blood vessels [angiogenesis]at injury site
Ø 3 to 5 days after injury, fibroblasts proliferate and subsequently synthesize and deposit extracellular matrix.
Ø This fibrosis phase determines final strength of healed wound
Ø Collagen deposition peaks about seven days after injury and continues for a number of weeks.
Ø Subsequent maturation and organization of the scar (remodeling) augments wound strength
Ø Phases interdependent and intrinsically involved in wound healing.
Ø Disruption in sequence leads to fistula formation
Ø Most fistulae occur 1 – 3 weeks after injury when tissues are most vulnerable to alterations in healing environment e.g.:
• Hypoxia
• ischemia
• immunosuppression : malnutrition, radiation and chemotherapy
• Wound edges eventually epithelialize forming a chronic fistula tract.
Classification (Anatomical)
• Urethrovaginal Fistula
• Urethrocervical Fistula
• Vesicovaginal Fistula [VVF]
• Vesicocervical Fistula
• Vesicouterine Fistula
• Ureterovaginal Fistula
• Ureterocervical Fistula
• Ureterouterine Fistula
• Rectovaginal fistula [RVF]
New Classification
- Divides fistulae into four main types, depending on distance of fistula’s distal edge from external urethral meatus
- The four types further sub-classified by:
o Size of fistula
o Extent of associated scarring
o Vaginal length
o Special considerations
Type 1: Distal edge >3.5cm from external urethral meatus
Type 2 Distal edge >2.5 – 3.5cm from external urethral meatus
Type 3: Distal edge 1.5 – 2.5cm from external urethral meatus
Type 4: Distal edge <1.5cm from external urethral meatus
Subtypes
Ø size <1.5cm in largest diameter
Ø Size 1.5 – 3cm in largest diameter
Ø Size >3cm in largest diameter
Further sub-typing
- None or only mild fibrosis and/or vaginal length normal
- Moderate or severe fibrosis and/or reduced vaginal length and/or capacity
- Special considerations e.g. post radiation, ureteric involvement, circumferential or previous repair
Aetiology
1. Congenital
Rare
Thought
to be due to either of below
o abnormal fusion of ureteric bud and caudal end of mullerian duct with urogenital sinus or
o Incorporation of an aborted ureteric bud into a future wolffian duct remnant
Usually
associated with other renal or urogenital abnormalities
2. Acquired
a) Obstetric trauma
• Obstructed labour leading to prolonged compression effect on the bladder base between the presenting part and the symphysis pubis followed by ischemic necrosis of the tissues, which slough off leading to fistulous communication
• Use of instruments e.g. vacuum
• Caeserian section
b) Pelvic Surgery
- Hysterectomy (laparoscopic commonest cause followed by abdominal, then vaginal)
c) Radiotherapy
• Induces endarteritis, which leads to tissue necrosis and subsequent fistula
• Most fistulae occur within weeks or months but may present upto 20 years after
d) Malignancy
• Due to tissue necrosis and deterioration
e) Trauma and Foreign body
• Trauma during sexual activity or sexual assault
• FBs such as neglected pessary and vesicle calculi
• FBs introduced during surgery e.g.
o Collagen injected transurethrally
o Synthetic materials used in urethral sling procedures
f) Miscellaneous
• Infections e.g.
o Lymphogranuloma venerum
o Urinary tuberculosis
o Inflammatory bowel disease
o Autoimmune
• Risk factors that interfere with wound healing e.g.
o Poorly controlled diabetes
o Peripheral vascular disease
o Chronic steroid use
o Malignancy
Clinical Presentation
• Continuous leakage of urine
• Perineal skin excoriation
• Ammonia smell
Diagnosis
1. Proper and thorough history and Physical examination
• Obstetric deliveries
• Prior surgeries
• Previous management of fistula
• Treatment of pelvic malignancy (surgery and irradiation)
2. Investigations
1. Cystourethroscopy
• Allows
o Localization of fistula,
o Determination of its proximity to ureteric orifices
o Assessment of surrounding mucosa viability
2. Voiding cystourethrography
Demonstrate leakage into vagina and help confirm presence, location and numbers of fistulae
3. Intravenous urography [IVU][pyelography]
• Assesses
o Integrity of upper collecting system
o Ureteric involvement in the fistula
4 . Retrograde pyelography
• Same is IVU
5. Phenazopyridine hydrochloride (pyridium) and three swab test
• Agent taken orally
• A gauze packed in vagina serially
• If most proximal gauze is coloured with orange dye then ureteric involvement suspected
• If both orange and blue dyes seen, then both bladder and ureter(s) typically involved.
6. EUA and Dye Instillation
• Methylene blue or indigo carmine instilled.
7. Moir’s three tampon test
useful in differentiating between a uretero-vaginal and a vesico-vaginal fistula and in identifying the level of a vesico-vaginal fistula.
Management of VVF
1. Conservative.
• For small fistulae (2 – 3 mm diameter): Continuous bladder drainage with catheter.
• If no closure within 4 weeks, then unlikely to do so probably
Possible reasons
o Secondary to collagen deposition
o Epithelialization of fistulous tract
o Inflammation and irritation of bladder due to continuous drainage
2. Surgery
a) General Principles
• Appropriate pre and intraoperative preparation
• Timely repair
• Multilayer, tension – free closure
• Assessment of adequate surrounding tissue viability
• Post operative bladder drainage
b) Factors affecting cure rates.
• Viability of surrounding tissue
• Duration of fistula
• Prior irradiation
• Surgical technique
• Surgeon experience
c) Timing of repair
• Immediate unless severe infection or acute signs of inflammation present
• If identified within 24 – 48 hrs can be repaired immediately
• Intervention individualized between quality of life and tissue viability
d) Route of Surgical Repair
- Dictated by ability to gain access
I) Vaginal
• Associated with
o Shorter operation times
o Decreased blood loss
o Less morbidity
o Shorter hospital stay
Classical technique
• Excision of fistulous tract
• Undermining and widely mobilizing vaginal epithelium
• Bladder mucosa closed
• Closure of two layers of fibro-muscular tissue.
• Confirmation of water tight repair
• Vaginal epithelium re-approximated
• Bladder (Nelaton) catheter for 14 days
II) Abdominal (transperitoneal) – Used in situations where.
• Fistula located proximal with a narrow vagina
• Fistula close to ureteral orifices
• Concomitant ureteral fistula present
• Unsuccessful repair or recurrent fistula
• Vaginal wall rigid with minimal mobility
• Fistula large or complex in configuration need for an abdominal interposition graft
Similar mobilization
iii) Laparoscopic
- Evidence – based support limited.