Download Primary- when a women has not yet started her monthly periods and

Menstruation
Normal physiology

The main players in the female reproductive cycle are the pituitary, ovaries, and the uterus.
Their activities are closely coordinated each month. Each month one or other ovary releases a
single egg in an event called ovulation.

It is brought about by a series of complex interactions between the pituitary gland, uterus, and
the ovaries. The pituitary gland is under the control by a small section/ layer of the brain known
as the hypothalamus.

A new menstrual cycle begins when the nerve cells of the hypothalamus secrete a hormone
called gonadotropin-releasing hormone GnRH into the network of blood vessels that surround
the pituitary gland. Stimulated by pulses of gonadotropin releasing cells, the pituitary gland
secretes another hormone called follicle-stimulating hormone or FSH.

FSH travels in the bloodstream reaching the ovaries where it stimulates the formation and
growth of an ovarian follicle on one or other ovary the follicle consist of an egg and number of
surrounding cells that secrete estrogen hormones and fluid. FSH helps the egg to mature and
prepare it for release.

As the follicle matures the hypothalamus increases secretion of a GNRH. This in turn stimulates
the pituitary to secrete a second hormone which acts on the ovary this is luteinizing hormone or
LH.

Toward the middle of the cycle there is a sudden increase in blood level of LH (after 2-3 days of
high estradiol it is released) this acts as the trigger for ovulation. Within minutes of its release it
is guided by suction by the fringed opening by the outer end of the fallopian tube starting on its
5-6 day journey to the uterus via the Fallopian tube.

After the follicle ruptures it is converted into a yellow body known as the corpus luteum. Cells of
the corpus luteum secrete a hormone called progesterone, which brings about important
changes in the lining of the uterus. Preparing it for possible pregnancy. In fact the lining of the
uterus known as the endometrium undergoes changes in response to hormone levels during the
cycle.

In the first half of the cycle known as the follicular phase the developing follicle secretes
increasing amounts of estrogen hormone, which encourages regeneration of the endometrium.
After ovulation there are important changes in the endometrium aimed at making it suitable to
receive a fertilized egg. These changes are brought about by a secretion of progesterone from
the corpus luteum.

The secretion of progesterone is maintained for several days but if the egg is not fertilized in
that time the corpus luteum whither, and falling levels of progesterone and estrogen trigger the
shedding of the uterine lining as the menstrual flow. The cycle then starts again, but if the egg is
fertilized no menstruation occurs as a corpus luteum continues to function secreting
progesterone during the first three months of pregnancy. There after, numerous changes occur
to support the developing embryo.
Treatment- Progesterone is the most important hormone for implantation. It stops proliferation/
prevents hyperplasia (anti-mitotic). It also causes the glands in the lining of the endometrium to secrete
mucus.
Etc.






Duration of menstruation ranges 2-7 days. Average is 4 days (4+/-2 days).
Cycle is 28 days +/- 7 days
21 days= Polymenorrhea. <21 days then the cycles tend to be anovular and are associated with
dysfunctional uterine bleeding
35 days= Oligomenorrhea
Mean blood loss is 40ml+/- 20ml. blood loss >80 ml (menorrhagia/ hyper menorrhea) per cycle
is abnormal and frequently produces anemia.
Average loss of Fe in menses is 13 mg.
Dysfunctional uterine bleeding (DUB)

Etiology-A sub category of abnormal uterine bleeding. AUB is organic in origin (commonly
fibroid tumors, uterine polyps, or systemic disease) or a problem that is hormonal in origin
(known as DUB). DUB is irregular uterine bleeding that occurs in the absence of a recognizable
pelvic pathology, general medical disease, or pregnancy (organic etiology). DUB reflects a
disruption in the normal cyclic pattern of ovulatory hormonal stimulation to the endometrial
lining. Bleeding is unpredictable and can be light, heavy, prolonged, frequent or random.
o

DUB most commonly occurs when the ovaries do not release an egg. The changes in
hormone levels cause your period to be later or earlier and sometimes heavier than
normal. Anovulatory >ovulatory and polycystic ovarian syndrome is the most common
etiology for anovulatory. Ovulatory although less common is a functionality of
progesterone withdrawal.
Signs/ Symptoms Bleeding/ spotting from vagina between periods
 Periods that occur less than 28 days apart (MC) or more than 35 days apart
 Time between periods changes each month
 Heavier bleeding (passing clots, soaking through sanitary pad or tampon every hour for 2-3
hr in a row/10 a day
 Bleeding lasts for more days than normal or for more than 7 days
 Others caused from variation in hormones (hirsutism, hot flashes, mood swings, tenderness
and dryness of the vagina)
Labs/procedures- besides pelvic and Pap smear.





CBC
Serum/urine pregnancy test- rule out pregnancy first!
Blood clotting profile-PT/PTT
Hormone tests- FSH, LH, androgen levels, prolactin, progesterone
Pregnancy test


Thyroid function tests-TSH, free T3/T4, thyroid antibody
Possibly (Biopsy-cancer, pre-cancer, or infection), Hysteroscopy, transvaginal Ultrasound
Treatment- If close to first period and young then not treated unless very severe such as excessive blood
loss/anemia. The goal of tx however is to control the menstrual cycle




Birth control pills or progesterone only pills
Intrauterine device that releases the hormone progestin
Ibuprofen or naproxen taken just before the period starts
Iron supplements for women with anemia
If continue to want children may give meds to stimulate ovulation. If pt no longer wants children may
consider



Endometrial ablation or resection to remove the lining of the uterus (preoperative endometrial
biopsy to rule out cancer should be done prior to)
Hysterectomy (absolute cure)
Dilatation and curettage to remove polyps and diagnose certain conditions.
Complications-infertility, severe anemia, increased risk of endometrial cancer
Amenorrhea- The absence of menstruation (monthly period).
Primary- when a women has not yet started her monthly periods
and she has gone through other
normal changes that occur during puberty and is older than 15. Primary and secondary are same but
differ in time.

Etiology Most girls begin menstruating between ages of 9 and 18, with an average of 12.
Primary amenorrhea typically occurs when a girl is older than 15, if she has gone through other
normal changes that occur during pregnancy. Primary amenorrhea may even occur with or
without other signs of puberty.
o
o
o
Poorly formed genital organs-Narrow or blockage of cervix, imperforate hymen, missing
uterus or vagina, vaginal septum.
Hormonal problems-changes occur to brain where hormones are controlled to manage
the menstrual cycle. The ovaries are not working properly .
Any above problem may be due to- anorexia, chronic illness (CF/ heart dz), genital
disorders, infections that occur in the womb or after birth, other birth defects, poor
nutrition, tumors.

Blood test/labs-estradiol, FSH, LH, prolactin, TSH, T3, and T4. Others: 17 hydroxyprogesterone,
chromosome analysis, head CT/MRI scan, pelvic ultrasound, serum progesterone.

Treatment-Depends on the cause of the missing period. Primary amenorrhea caused by birth
defects may require medications (hormones) surgery, or both.
o If the amenorrhea is caused by a tumor in the brain (pituitary tumor)
 Meds can shrink tumor
 Surgery to remove it
 Radiation therapy is last resort.
o
o
o
o
If systemic dz, tx may resolve amenorrhea
If amenorrhea is due to anorexia or excessive exercise, with proper return to weight and
less exercise menorrhea will return to normal.
If menstruation can not be obtained, medicines can sometimes create a menstrual-like
situation (pseudomenstruation). Can help against osteoporosis as well.
Estrogen/ progesterone combinations are the mainstay of tx for hormonal imbalance.
CMDT has a whole list of them.
SecondarySecondary amenorrhea occurs when a woman who has been having normal menstrual cycles stops
getting her periods for 6 or more months.
Women who are pregnant, breastfeeding, or in menopause are not considered to have secondary
amenorrhea.

Etiology
Women who are taking birth control pills or who receive hormone shots such as Depo-Provera
may not have any monthly bleeding. When they stop taking these hormones, their periods may
not return for more than 6 months.
You are more likely to have amenorrhea if you:






Are obese
Exercise too much and for long periods of time
Have very low body fat (less than 15% - 17%)
Have severe anxiety or emotional distress
Lose a lot of weight suddenly (such as with strict or extreme diets or after gastric bypass)
Other etiology:
 Brain (pituitary) tumors
 Chemotherapy drugs for cancer
 Drugs used to treat schizo or psychosis
 Overactive thyroid
 PCOS
 Reduced function of the ovaries
Procedures such as a dilation and curettage can lead to scar tissue formation that may cause a
woman to stop menstruating. This is called Ashermans syndrome. Scarring may also be caused
by some severe pelvic infections.

Signs/ Symptoms
In addition to having no menstrual periods, other symptoms can include:






Breast size changes
Weight gain/loss
Discharge from the breast (galactorrhea) or change in breast size
Increased hair growth in a "male" pattern (hirsutism) and acne
Vaginal dryness
Voice changes
If amenorrhea is caused by a pituitary tumor, there may be other symptoms related to the
tumor, such as vision loss and headache.

Exams and Tests
A physical exam and pelvic exam must be done to check for pregnancy. A pregnancy test will be
done.
Blood tests may be done to check hormone levels, including:

Estradiol level





(FSH level)
(LH level)
Prolactin level
Serum hormone levels such as testosterone levels
Thyroid stimulating hormone (TSH)
Other tests that may be performed include:





CT scan or MRI scan of the head to look for tumors
Biopsy of the lining of the uterus
Genetic testing
Ultrasound of the pelvis or hysterosonogram
Treatment
Treatment depends on the cause of the amenorrhea. Normal monthly periods usually return
after the condition is treated.
A lack of menstrual period due to obesity, vigorous exercise, or weight loss may respond to a
change in exercise routine or weight control.
Dysmenorrhea


Primary dysmenorrhea- associated with menstrual cycles in the absence of pathologic findings.
Begins 1-2 after menarche onset.
o
Signs/ symptoms-Primary dysmenorrhea is low, midline, wave-like, cramping pelvic pain
that radiates to the back or inner thighs. Cramps may last a few days and are associated
with nausea, diarrhea, headache, and flushing. The pain is caused by uterine
vasoconstriction, anoxia, and sustained contractions mediated by prostaglandins.
o
TX- NSAIDS (Ibuprofen, ketoprofen, mefenamic acid, naproxen). Should start medication
1-2 days before expected menses. Symptom suppression is easily obtained through the
use of oral contraceptives, depot-medroxyprogesterone acetate, or the levonorgestrel
releasing IUD.
 Continuous use of oral contraceptives can be used to suppress menstruation
completely. If women do not wish to use hormonal contraceptives, they may
use other therapies such as local heat, thiamine 100mg/d orally, Vit E 200
units/d orally for 2 days prior and first 3 days of menses, or the use of a TENS
unit.
Secondary dysmenorrhea- menstrual pain for which an organic cause exists. Often associated
with endometriosis or uterine fibroids. Usually begins way after menarche in the 3-4th decade of
life. Hx/ PE may also suggest PID, adenomyosis, myoma, IUD use, cervical stenosis with
obstruction, or blind uterine horn (rare).
o
DX-Obtain cervical cultures to rule out infection. Pelvic imaging can detect fibroids
submucosal myomas, or adenomyosis, Cervical stenosis may result from induced
abortion. Laprascopy can be used to dx endometriosis or other abnormalities not
visualized by imaging.
o
TX- NSAIDs and oral contraceptives may give relief, particularly in endometriosis.
Danazol and GnRH agonists are effective in the treatment of endometriosis, although
use is limited by cost or side effects. Adenomyosis may respond to the same effective
hormonal tx as endometriosis, levonogestrol releasing intrauterine system, or uterine
artery embolization, but hysterectomy remains the definitive tx of choice if the women
is at the completion of childbearing.
Premenstrual syndrome (premenstrual tension)

Definition-A recurrent variable cluster of troublesome physical and emotional symptoms that
develop 7-14 days before the onset of menses and subside when menstruation occurs. Occurs in
50% of those premenstrual women ages 25-40 and are severe in some cases.

Signs/Symptoms-bloating, breast pain, ankle swelling, sense of increased weight, skin disorders,
irritability, aggressiveness, depression, inability to concentrate, libido change, lethargy, and food
changes. If mood or emotional symptoms predominate on top of physical symptoms it is termed
premenstrual dysphoric disorder PMDD. The pathogenesis of PMS/PMDD is still uncertain.
Current tx is empiric.

TX- Support for both the patients’ emotional and physical distress. Includes:
 Careful eval of pt

Pt keeping a daily diary of symptoms to rule out if its depression or other emotional
problems

Advise lifestyle habits: increased aerobic exercise and proper nutritional diet.

When physical symptoms predominate, spironolactone 100mg orally daily during the luteal
phase, is effective for reduction of bloating and breast tenderness. Oral contraceptive or
injectable progestin depot medroxyprogesterone acetate will decrease breast pain and
cramping. NSAIDs will reduce a number of symptoms.

When mood disorders predominate, several serotonin reuptake inhibitors (fluoxetine 20mg
orally) have been shown to be effective in relieving tension, irritability, and dysphoria.

When the above regimens are not effective, ovarian function can be suppressed with high
dose progestin (20-30mg oral medroxyprogesterone acetate or 150 mg depot
medroxyprogesterone every 3 months or GnRH agonist with add back therapy such as
conjugated equine estrogen 0.625 orally daily with medroxyprogesterone acetate, 2.5-5mg
orally.
Menopausal syndrome- Cessation of menses due to aging or to bilateral oophorectomy.
Elevation of FSH and LH levels. Hot flushes and night sweats. Decreased vaginal lubrication; thinned
vaginal mucosa with or without dyspareunia.

Etiology- The term menopause denotes the final cessation of menstruation, either as a normal
part of aging or as the result of surgical removal of both ovaries. It denotes a 1-3 year period
during which a woman adjusts to a diminishing and then absent menstrual flow and the
physiologic changes that may be associated-hot flushes, night sweats, and vaginal dryness. The
average age at menopause is 51. Premature menopause is defined as ovarian failure and
menstrual cessation before age 40.

Signs and symptoms Cessation of menstruation-Menstrual cycles generally become irregular as menopause
approaches. Anovular cycles occur more often. Menstrual flow usually diminishes in amount
owing to decreased estrogen secretion, resulting in less abundant endothelial growth.
Cycles become longer with missed periods. When no bleeding has occurred for 1 year, the
menopausal transition can be said to have occurred. Any bleeding after this time warrants
investigation by endometrial curettage or aspiration to rule out endometrial cancer.

Hot flushes- Occur as a result of the decrease in ovarian hormones. Flushes can begin
before the cessation of menses. They typically persist for 2-3 years and are more severe in
women who undergo surgical menopause. Occurring at night, they often cause sweating
and insomnia and result in fatigue on the following day.

Vaginal atrophy-With decreased estrogen secretion thinning of the vaginal mucosa and
decreased vaginal lubrication occur and may lead to dyspareunia. On PE there is a pale,
smooth vaginal mucosa and a small cervix and uterus. The ovaries are not normally palpable
after menopause.

Osteoporosis- May occur as a late sequelae of menopause.

Labs- Serum FSH and LH levels are elevated.

Treatment

Natural menopause- Education and support from health providers, midlife discussion
groups, and reading material will help most women having difficulty adjusting to
menopause.
o Vasomotor response-For women with moderate to severe vasomotor symptoms,
estrogen or estrogen/preogestin regimens are the most effective approach to
symptom relief. If the patient has had a hysterectomy, a progestin need not be
used.
o
Vaginal atrophy- Due to a lack of estrogen. Vaginal suppositories, patches, rings or
pills work well.
o
Osteoporosis-Women should ingest at least 800mg of calcium daily throughout life.
In addition 1200 mg of elemental calcium should be taken as a supplement at the
time of the menopause and thereafter; calcium supplements should be taken with
meals to increase to increase their absorption. Vit D 800 IU/d is necessary to
enhance the calcium absorption and maintain bone mass.
Risk of hormone therapy- Coronary heart events, increased risk of cognitive decline,
strokes, thromboembolic disease, gallstones, breast cancer along with increased mortality
of it.

o
Women who have been receiving long term estrogen/progestin hormonal replacement
therapy in the absence of complications should be encouraged to stop, especially if they
do not have menopausal symptoms.
o
The risks appear to be lower in women starting therapy at the time of menopause and
higher in previously untreated women starting therapy long after menopause. Therapy
should be individualized as the risk-benefit profile varies with age and individual risk
factors.
Surgical menopause- Abrupt hormonal decrease resulting from oophorectomy generally
results in severe vasomotor symptoms and rapid onset of dyspareunia and osteoporosis
unless treated. If not contraindicated, estrogen replacement is generally started
immediately after surgery. Conjugated estrogen or estrogen sulfate at 1.25mg orally or
estradiol at 2 mg orally given for 25 days of each month. After age 45-50 years this dose can
be tapered to 0.625 mg of conjugated estrogens or equivalent.
Contraception
Oral contraceptive –MC primary method used in women, # 2 is female sterilization and #3 is condom
use.
1. Combined- The primary mode of action is suppression of ovulation. Pills can be initially started
on the first day of the menstrual cycle or any day during the cycle. But on any other day during
the cycle a back up method should be used. If an active pill is missed and no intercourse has
taken place in past 5 days, should take two pills immediately and a backup method should be
used for 7 days. If intercourse occurred in the previous 5 days, emergency contraception should
be used immediately, and the pills restarted the following day. The Estrogen/ progesterone
combination prevents ovulation by interrupting the feedback loop of sex hormone production.
This decreases the amount of endometrial proliferation and thickens cervical mucous. The most
important effect is to prevent ovulation by suppression of hypothalamic gonadotropin releasing
factors (prevents pituitary secretion of FSH and LH).

Benefits- Lighter menses, reduced anemia, dysmennorhea unlikely, functioning ovarian
cysts, ovarian and endometrial cancer, salpingitis and ectopic pregnancy are all less likely.
Acne is usually improved. The frequency of developing myomas is lower. There is a
beneficial effect on bone mass. The predictability of menstrual cycles is favorable as well.

Monophasic- A constant dose of Estrogen (ethanyl estradiol or mestranol) is given with a
constant dose of progesterone, which aims for a less risk of breakthrough bleeding.

Triphasic- developed to minimize the amount of progesterone dose often combined with
variable estrogen dose (more risk for breakthrough bleeding).

Contraindications- at increased risk for myocardial infarction, thromboembolic diseae,
cerebrovascular disease in those taking estrogen dose 50mcg or grater. Non-estrogen
contraceptive is warranted in increased hypercoagulable disease states(DVT, MI, stroke).

Adverse effects- Contraceptives may worsen depression, cause hypertension with extended
use, elude to severe headaches, and impair the quantity and quality of breast milk. Nausea
and vomiting may occur during the first few months of pill use. Weight gain may occur as
well. Fatigue and decreased libido can occur as well as chloasma (tan or dark brown skin
discoloration).

Drug-drug interactions- Rifampin is the only antibiotic proven to decrease serum ethinyl
estradiol and progestrin levels in women taking oral contraceptives (including Ortho Evra
and Nuva Ring) a nonhormonal contraceptive method is recommended in these women. In
spite of other anecdotal reports of oral contraceptive failure, other antibiotics have not
been proven to affect the pharmacokinetics of ethinyl estradiol. For women taking ABX
other than rifampin with oral contraception, back-up contraception is not required.
o
Anticonvulsants-including phenytoin, carbamazepine, barbituates, primidone,
topiramate, or oxcarbazepine should not use hormonal contraception (with the
exception of depo-medroxyprogesterone acetate.
o
Antiretroviral-especially ritonavir may significantly reduce the efficacy of combined
oral contraceptives. Contraceptives may also increase the toxicity of the retroviral.
2. Transdermal/ Mucosal methods- The patch and ring avoid hepatic first pass effect. Wathc for
increased risk of thromboembolism since the lower overall dos 15-20mcg of ethinyl estradiol has
higher systemic absorption these ways.

Ortho Evra- Patch that delivers 20mcg of ethinyl estradiol and 150 mcg of norelgestromin
daily

Nuva Ring- delivers 15 mcg ethinyl estradiol and 120mcg of etonogestrel daily.
3. Progesterone only methods-

Mini-pill-Noreyhindrone. Safe to use during lactation. Does not reliably suppress ovulation
but promote cervical mucous thickness and decrease in endometrial proliferation to help
prevent implantation. Less effective than combination.

Injectable- Depo-provera-depo Sub-Q provera 104 (Depo-Medroxyprogesterone Acetate).
Dosed every 90 days. Usually amenorrhea 20% risk for spotting as well. Usually results in a
longer interval to resumption of normal fertility >90% in 2 years, 50% in 6-12 months. Bone
density loss- likely reversible.

Implantable- Nexplanon/ Implanon (etonogestrel) 68mg used long term up to 3 years.
Subcutaneous placement and removal- A newer rod vinyl polymer compared to the usual
silicone.
4. Intra Uterine Device (IUD)-Implantable chemical eluting device that prevents pregnancy by
prevention of fertilization (acts as a spermicidal, disrupts the intra-uterine lining, thickening of
cervical mucous, and inhibition of ovulation). There is an increased risk for PID if pt develops
STD. There is also an increased risk of ectopic pregnancy if pregnancy occurs. No decrease in
fertility after removal.
 Mirena- Levonogestrel releasing IUD- Low doses of progesterone with some systemic
absorptiom. Decreases menstrual bleeding nad lasts up to 5 years.

Paragard copper device- causes uterus to release leukocytes and prostaglandins which are
spermicidal and make the uterine lining inhospitable. Associated with increased menstrual
bleeding but is hormone free and effective up to 10 years.

Contraindications- Pregnancy, acute PID, postpartum endometriosis or infected abortion in
the past 3 months, noted or suspected uterine or cervical malignancy, genital bleeding of
unknown origin.

Complications- Increased PID risk leading to infertility if infection occurs, risk of perforation
during insertion, wilson’s dz, copper allergy.
5. Barrier methods- perfect use is important for good efficacy.
 Diaphragm- latex flecible dome placed over cervix used with spermicidal jelly

Cervical cap- smaller tighter fitting latex dome

Sponge impregnated with nonoxynol-9 spermicide- single use. Failure rates re similar to the
cap but ok for repeated use up to 24 hrs. There are issues with timing, failure rates, and risk
for toxic shock; no STD protection.

Male condoms- perfect use with spermicide close to 95%. No spermicide with animal skin
condoms.. Male condoms are cheap and affordable, protct from many sexually transmitted
infections making them most used barrier device.

Female condoms- not widely available and more difficult to use.
6. Sterilization Femaleo Tubal ligation- excision to interrupt passage of egg through the fallopian tubes to
the uterus
o Essure-steel/nickel coil, trans cervical placement into tubes, use backup method x 3
months and confirm tubal blockage via hysterosalpingogram. Permanent with some
success at reversal. There is some risk for ectopic pregnancy and the essure may be
done without general anesthesia. Essure is a highly effective method of
contraception without any long term hormone exposure/ drug interaction potential.

Maleo Vasectomy-surgical ligation/ excision of the vas deferens. 1-3 month back up
method to ensure no residual sperm.
Contraceptive based on awareness of fertile periods
Calendar/ Rhythm method- reliable if regular and predictable menstruation. It requires periods
of abstinence. There is perfect use with effectiveness comparable to barrier methods.

Symptothermal method- daily measurement of basal body temperature. A slight decrease
indicates ovulation.
Emergency contraception-to prevent pregnancy after unprotected intercourse within 72 hours. Plan B.
Next choice- Levonogestrel. Works by inhibiting or delaying ovulation, disruption of endometrial lining. If
menses is delayed by 3 weeks or more assume pregnancy. Use barrier method or abstinence until end of
cycle. IUD insertion within 5 days of unprotected sex results in effective contraception. RU
486(mifepristone) usually is used as abortive therapy.
Endometriosis-The aberrant growth of endometrial tissues outside the lining of the uterus. Most
commonly found in the dependent parts of the pelvis (ie. Fallopian tubes, ovaries or the tissue lining
your pelvis-perimetrium or peritoneum). However, it can appear anywhere within the abdominal
cavity.9-10% of women. MC in high achieving “type A”, nulliparous women.30-40% of infertile women
will have endometriosis. Some pt’s have severe dz where the endometriosis and adhesions grow like
KUDZU.

Hypothesis-The cause of endometriosis remains unknown. Retrograde menstruation (most
widely accepted)-menstrual blood containing endometrial cells flows back through the fallopian
tubes, takes root and grows outside the endometrium. Lymphatics and vascular metastasis- the
bloodstream is responsible for carrying endometrial cells to other sites in the body. Genetic
predisposition-familial distribution. Iatrogenic dissemination-during surgery endometrial tissue
contaminates portions of the abdomen.

Pathophysiology-ectopic endometrial tissue responds to normal hormonal stimulation (but
more unpredictably). The endometrial cells respond to estrogen and progesterone w/
proliferation and secretion. During menstruation, the ectopic tissue bleeds, which causes
inflammation of the surrounding tissues. The inflammation causes fibrosis, leading to adhesions
and produce pain and infertility.

Signs & symptoms-pelvic pain (dysmenorrhea) pain normally begins 2-7 days before menses
peaks and may increase in severity until menstrual flow slackens. Severity of pain is NOT
indicative of extent of dz. Abnormal uterine bleeding, and infertility (main three) othersdyspareunia, rectal pain w/ bleeding (colonic), suprapubic pain and hematuria (bladder).

PE- Pelvic examination-difficult to ID and palpate endometrial tissue but secondary cysts may be
located. May also note uterine retroversion w/ decreased uterine mobility. Cervical motion
tenderness and/ or adnexal mass or tenderness. Most women w/ endo have a normal pelvic US.
Transvaginal US-does not obtain the dx however it can identify cystic structures, CT/MRI of
limited value as well. Laparoscopy-The only definitive way to dx endometriosis is via laparoscopy
or laparotomy. Direct visualization of endometrial tissue confirms the dx; bx help as well.

Management and TX of endometriosis-2 main goals of tx-Improvement of pain, to promote
fertility.
o Medical management-can help decrease pain but may not increase likelihood of
pregnancy. Most therapies are designed to inhibit ovulation over 4-9 months and lower
the hormone levels thus preventing cyclic stimulation of endometionic implants and
inducing atrophy.
 Pain meds-Ibuprofen/ NSAID’s

Hormonal therapy-An androgen, such as danazol (danocrine) to help suppress
menstruation by inhibiting LH/FSH. Oral/ injectable contraception (for those w/
minimal or mild sx’s). Gonadotropin releasing hormone(GnRH) Agonists (seems
counterintuitive since they overstimulate LH and FSH receptors of the anterior
pituitary. But over stimulation leads to a down regulation of these receptors,
resulting in a decrease in LH/FSH secretion- Leuprolide acetate 3.75mg IM
(Lupron) once monthly for up to 6 months(one option).

Surgical-effective in both reducing pain and promoting fertility.conservative
surgery( LAP exporation)-removal of implanted endometrial tissue, scar tissue,
and adhesions. (total hysterectomy- including both ovaries(TAH w/ BSO)
definitive tx option for those w/ severe pain and no longer desire childbearing.
Uterine Fibroids-AKA fibromyomas, leiomyomas, or myomas.The most common benign
neoplasm of the female genital tract. Benign growths that occur on the uterus- develop from the uterine
myometrium and lead to a round, firm, and often multiple uterine tumor composed of smooth muscle
and connective tissue.

S&S- Asymptomatic to significantly symptomatic, heavy prolonged/ irregular menstrual bleeding
(anemia), dyspareunia, infertility, pelvic pain or pressure, urinary incontinence, Acute
ABD/pelvic pain-out grows the available blood supply or ruptures.

Etiology-Genetic alterations-many fibroids contain alterations in genes that code for uterine
muscle cells. Hormonal-excess in estrogen and progesterone. Additional substances-insulin like
growth factor may be related to fibroid growth.

DX-MC found during routine pelvic exam- irregularly shaped uterus or masses, always check
serum pregnancy. Transabd/transvaginal US-confirms the dx and determine location and size of
fibroids. Hysterosonography-TVUS w/ saline to expand the uterine cavity. Hysteroscopy-Easily
performed during an office visit to visualize the walls of the uterus and fallopian tubes.

Management/Tx- Identification, awareness, and watchful waiting.
 GnRH Analogs-Depo leuprolide 3.75 mg IM once monthly can be used preoperatively for 3-4
months to induce reversible hypogonadism, which temporarily reduces the size of myoma,
suppresses further growth, and reduces surrounding vascularity prior to surgical
intervention. GnRH agonist rapidly suppresses pituitary gonadotropin release, which leads
to a profound hypoestrogenemia, and a 50% reduction in uterine volume.

Oral/ injectable contraception-typical hormonal changes shrinks fibroid tissue.

Surgical-Myomectomy-removal of fibroids more commonly indicated for pt’s of childbearing
years. Hysterectomy.
Ovarian cyst-Usually a fluid filled sac on an ovarian structure. Common in reproductive years. Often
related to ovulation. Usually unilateral. Most cysts resolve spontaneously over the next few menstrual
cycles.

Follicular cysts-mature follicle that fails to rupture

Corpus luteum cyst-result from bleeding into center of corpus luteum.

Theca-lutein cysts-associated w/ elevated levels of chorionic gonadotropin. (ie.
Choriocarcinoma, clomiphene therapy, hydatiform mole or rarely w/ normal pregnancy.
S&S-may be asymptomatic, change in menstrual cycle, pelvic pain, dyspareunia, abnormal vaginal
bleeding. Possible adnexal mass on bimanual exam. BEWARE!-that a ruptured cyst w/ bleeding can
present as an acute abdomen w/ decreased systolic bp.
Workup/TX for ovarian cysts-Check b-HCG for pregos, Pelvic US for acute processes. If adnexal mass
(cystic structure) has not resolved in 6-8 weeks, then evaluate for malignancy via laparoscopic
cystectomy. CT abdomen/ pelvis to look for metastasis or possible primary lesion.
Urinary Incontinence
Prevalence increases with age. More
greater the likelihood of incontinence.
Consequences of UI



Social isolation
Depression
Rash/ decubitus ulcer
Falls/ fractures
debilitated the



Infections
Increased likelihood of
admission
Caregiver stress
Bladder physiology-Age related changes





Decreased bladder capacity
Increased involuntary bladder contractions
Increased post void residual
Increased nocturia
Gender-related change
Neurology of Urination



Parasympathetic tone (cholinergic) causes detrusor constriction and bladder emptying. Pelvic
nerves S2-S4.
Sympathetic tone (adrenergic) facilitates storage of urine. Beta-adrenergic receptors in
detrusor, alpha adrenergic in the internal sphincter. Hypogastric nerve Tll-L2
Somatic (voluntary control) via the pudendal nerve
Continence requirements
Mobility, Manual dexterity, cognitive ability to want to go to the bathroom, motivation to stay dry,
Balance and coordination (muscles and nerves): Bladder smooth muscle and urethral sphincter
mechanisms, Sympathetic & parasympathetic nervous systems.
#’s to remember
Abnormal PVR>200, normal void 80% of bladder volume, Capacity 300-600ml, First urge 150cc, normal
urine velocity 20-25ml/sec, empty bladder within 20 seconds. PVR should be less than 50 cc.
Reversible causes (transient)-DIAPPERS
Delirium (transition inhibition), Infection, atrophic vaginitis, pharmacy, psychological, excess urine
output, restricted activity (functional incompetence), stool impaction.
Serious causes of incontinence
Lesions of the brain and spinal cord, cancer of the bladder or prostate, bladder stones, hydronephrosis.
Established causes

Urge incontinence (Detrusor overactive)-medical hx (leakage w/out stress maneuvers or urinary
retention, preceded by intense urge to urinate), Little PVR increased contraction on refilling.

Overflow incontinenceo Detrusor underactive- Least common. Strain to void, low output, incomplete emptying,
nocturia.Causes: LMN problem/ damage, autonomic neuropathy, medications, or
fibrosis of detrusor, remember meds, increased PVR.
o
Outlet obstructive-mechanical obstruction-prostate, urethral stricture, cystocele.
Symptoms: hesitancy, frequency, increased PVR.

Stress incontinence (outlet incompetence)-F>M. secondary to pelvic floor laxity or urethral
sphincter dysfunction. Primary cause (males): radical prostatectomy. Symptoms: dribble,
aggravated by increased intra-abdominal pressure. Normal PVR.

Mixed incontinence-Characteristics of urgency and stress incontinence.
Evaluation
HX-Sx’s, bladder or voiding diary, fluid intake, Meds, use of pads or protective devices, previous
tx’s, expectations

PE-rectal and pelvic exams.
TX general principles-DX-reversible cause? Remember: mixed incontinence, management of
comorbidities. Consider social history.
Incontinence tx’s
Behavioral approacheso For cognitive intact-Pelvic floor exercises (kiegel), bladder training, Biofeedback,
electrical stimulation.
o For cognitively impaired-Habit training, timed voiding, prompted voiding, improved
toilet access, manage fluid and diet, proper undergarments.

Pharmacological approaches
o Anticholinergics/ Antimuscarinics agents: Promote bladder relaxation, decrease urgency
with behavioral therapy.
 Oxybutinin- Ditropan
 Tolterodine- Detrol
 Fesoterodine
 Trospium-Sanctura
 Solifenacin- Vesicare
 Darifenacin- Enablex

o
Alpha adrenergic agonists-Mechanism: relax smooth muscle, decrease urine flow
resistance.
 Selective a1 agents (Prazosin, Alfuzosin-uroxactral)
 Long acting a1 agents (terazosin-hytrin, doxazosin-cardura)
 Long-acting a1a subtype selective agents (tamsulosin-flomax)
o
o
o
Estrogens: little/ no evidence to support use.
Serotoninergic/ norepinephrine drugs
5-alpha-reductase inhibitors
 Finasteride- proscar
 Dutasteride- 24vodart
Specific tx’s:
o Detrusor overactive- bedside commode, bladder training, (Oxybutinin, imipramine,
dicyclomine, propantheline, estrogen)
o Detrusor underactive- intermittent catheterization, Bethanacol (weak evidence), Foley
catheter.
TX strategies





Urge-bladder training, meds, surgery, sacral nerve stimulation.
Stress:-kegel’s and bladder training, meds, surgical procedures
Overflow-intermittent, indwelling, or supra pubic catheter
Misc-pessaries, vaginal cones, periurethral injections, biofeedback, compression devices.
Indications for chronic indwelling catheter in long-term care-urinary retention, short term care,
palliative care, patient preference
Referral to urology-uncertain dx, tx failure, hematuria w/out infection, comorbidities.
Domestic violence- Intimate partner violence

Intimate partner violence is a pattern of abusive behavior by a person who is in some type of
intimate relationship with the victim.

The abuse can be physical sexual or emotional and can include economic deprivation. IPV is
common but is often not diagnosed in part because patience try to hide the abuse.

Rates are higher when measured an emergency departments.

Risk factors for abuse include being young, being pregnant, being single, divorced, or separated,
alcohol or drug abuse in the victim or the partner, smoking, and being poor.
Evaluation

Clinicians must be alert to clues that suggested abuse including an explanation of the injuries
that do not fit with what is being seen. These may include frequent visits to the emergency
department and somatic complaints such as chronic headache, abdominal pain, and fatigue.

The patient may be vague about some of her symptoms and May avoid Eye contact. It is critical
that the patient has the opportunity to speak with the clinician alone.

Physical examination often reveals injuries in the central area of the body. As with any situation
of expected abuse bruises that are in various stages of healing may be an important clue. Post
dramatic stress disorder, depression anxiety, and alcohol or others substance-abuse can develop
in victims. Somatization is also very common.

Several instruments have been developed to screen for IPV. These include HITS, (hurt insult
threatens screen) tool, the woman abuse screening tool, the partner violence screen, and abuse
assessment screen, and the woman's experience with battering scale.

Inclusion of one question in the context of the medical history," Have you ever been hit, kicked,
punched her otherwise hurt by someone within the past year? If so b whom?" Has shown to
increase identification of IPV. Women preferred written questionnaires over face-to-face
interview.

Screening for IPV has been advocated by many experts, although no evidence has improved
outcomes. The USPSTF has concluded that there is insufficient evidence to recommend for or
against universal screening for IPV, since there is currently no evidence that screening improves
outcomes. However, clinician should remain on High alert for clues to IPV among patients.
Interventions for IPV
Interventions can include encouraging the woman to leave the abusive situation, ensuring that
she has a safe place to go, and counseling so that she can adequately assess her risk of danger
and create a plan for safety.
When to refer
Victims should be referred to social services so that they can provide information on local
resources. In general, mandatory reporting of IPV or suspicion of it in adult women who are
competent is not required in most states. However, mandatory reporting by physicians is
required in California, Colorado, Kentucky, Mississippi, Ohio, and Rhode Island.
Sexual assault- Women neither secretly want to be raped nor do they expect, encourage, or
enjoy rape. Rape is always a terrifying experience in which most victims fear for their lives. The rapist is
usually a hostile man who uses sexual intercourse to terrorize and humiliate a woman. Knowledge of
state laws and collection of evidence requirements are essential for clinicians evaluating possible rape
victims.
General considerations



It is essential that persons treating rape victims recognize the nonconsensual and violent nature
of the crime.
95% of rape victims are women and penetration may be vaginal, anal, or oral by the penis hand,
or a foreign object.
The assailant may be unknown to the victim or more frequently, may be an acquaintance or
even the spouse.
Rape represents an expression of anger, power, and sexuality on the part of the rapist.
Consequently, all victims suffer some psychological aftermath( anxiety disorder, PTSD etc.).
Some even acquire sexually transmitted diseases or become pregnant.
Rape trauma syndrome- 2 principle phases

Immediate/acute- Shaking, sobbing, and restless activity lasts a few days to a few weeks. Pt
experiences shame, guilt, or anger.

Late/chronic- develop weeks to months later. The lifestyle and work patterns of the individual
may change. Sleep disorders or phobias often develop.
General office procedures
Secure written consent. If police are to be notified, do so, and obtain advice on the preservation
and transfer of evidence.

Obtain and record the history in the patients own words. Note the details of the assault and
whether the pt is calm, agitated or confused. Also record whether the patient came directly to
the hospital or whether she bathed or changed her clothing.

Have the pt disrobe while standing on a white sheet. Hair, dirt, and leaves, underclothing, and
any torn or stained clothing should be kept as evidence.

Examine the pt, noting any traumatized areas that should be photographed.

Perform a pelvic exam and appropriate laboratory tests as needed (STI’s/Pregnancy etc.).

Transfer clearly labeled evidence directly to the clinical pathologist in charge or to the
responsible laboratory technician in the presence of witnesses so that the rules of evidence will
not be breached.
Treatment
Give analgesics or sedatives if indicated. Give emergent contraception and available antibiotics
to prevent against STD’s. Due to psychological manifestations it is important for the patient
along with family and friends have a source of ongoing counseling and psychological support.

All women who seek care for sexual assault should be referred to a facility that has expertise in
the management of victims of sexual assault and is capable of performing expert forensic
examination, if required.
Infertility
A couple is said to be infertile if pregnancy does not result after 1 year of normal sexual activity without
contraception.
Initial testing- During the initial interview, the clinician can present an overview of infertility and discuss
a plan of study. Separate private consultations are then conducted, allowing appraisal of psychosexual
adjustment without embarrassment or criticism. Pertinent details must be obtained (prior pregnancies/
STD’s). Pay particular attention to cigarette, alcohol, and recreational drug use in male fertility.
Prescription meds may impair male motility. Scrotal hyperthermia can cause this as well. The
gynecologic history should include menstrual pattern, the use and types of contraceptives, douching,
libido, sex techniques, frequency and success of coitus, and correlation of intercourse with the time of
ovulation. General physical and genital examinations are performed on the female partner and a basic
lab panel is obtained. Note that luteal phase serum progesterone above 3ng/ml establishes ovulation. A
semen analysis to rule out a male factor for infertility should be completed. Semen should be examined
within 1-2 hours after collection. If the sperm count is abnormal, further evaluation includes physical
examination of the male partner and a search for exposure to environmental and workplace toxins,
alcohol or drug abuse.
Further testing
Intracytoplasmic sperm injection is the treatment option available for sperm deficiencies except
for azoospermia(absence of sperm).

Screening pelvic ultrasound and hysterosalpingography to identify uterine cavity or tubal
anomalies should be performed.

Absent or infrequent ovulation requires additional laboratory evaluation.
o
o
o
o
Elevated FSH and LH levels indicate ovarian failure causing premature menopause.
Elevated LH levels in the presence of normal FSH levels confirms the presence of
polycystic ovaries.
Elevation of prolactin levels suggest a pituitary adenoma.
A markedly elevated FSH on the 3rd day of menses suggests inadequate ovarian reserve.
In addition a Clomiphene Citrate challenge test with measurement of FSH on day 10
after administration from day 5-9 should be completed to determine if diminished
ovarian reserve indicates a need for donor eggs.

Ultrasound monitoring of folliculogenesis may reveal the occurrence of unruptured luteinized
follicles.

If all the above testing is normal, the patient is diagnosed with unexplained fertility.
Treatment-Fertility may be restored by treatment of endocrine abnormalities; particularly
hypothyroidism or hyperthyroidism ABX tx of cervicitis may be of value. Microsurgical relief of tubal
obstruction due to salpingitis or tubal ligation will reestablish fertility in a number of cases.

Induction of ovulationo Clomiphene citrate- Stimulates gonadotropin release, especially LH. Consequently
plasma estrone and estradiol also rise, reflecting ovarian follicle maturation. If estradiol
rises sufficiently, an LH surge occurs to trigger ovulation. After a normal period one
should give 50 mg of clomiphene orally daily for 5 days. If ovulation does not occur, the
dosage is increased to 100 mg daily for five days. If ovulation still does not occur repeat
with 150mg then 200mg. Add 10,000 units of chorionic gonadotropin 7 days after
clomiphene.
o
Letrozole- aromatase inhibitor, appears to be as effective as clomiphene for ovulation
inductionnin women with PCOS. Dose 5-7.5 mg daily starting day 3 of menstrual cycle.
o
Bromocriptine- used only if PRL levels are elevated and there is no withdrawal bleeding
following progesterone administration. Initial dose is 2.5 mg orally once daily increased
to two or three times daily in increments of 1.25 mg. the drug is discontinued once
pregnancy has occurred.
o
Human menopausal gonadotropin (hMG) or recombinant FSH- indicated in cases of
hypogonadotropism and most other types of anovulation resistant to clomiphene
treatment. Refer to infertility specialist.
o
Artificial insemination in Azoospermia- If azoospermia is present, artificial insemination
by a donor usually results in pregnancy, assuming female function is normal. Frozen
sperm is currently preferable to fresh (frozen can be held pending cultures and blood
tests).
o
Assisted reproductive technologies-These techniques are complex and require a highly
organized team of specialists. All of the procedures involve ovarian stimulation to
produce multiple oocytes, oocyte retrieval and handling oocytes outside the body. With
IVF, the eggs are fertilized in vitro and the embryos transferred to the uterine fundus. In
the event of a multiple gestation pregnancy, a couple may consider selective reduction
to avoid the medical issues related to multiple births. This issue should be discussed
with the couple before embryo transfer.
OBGYN
PREGNANCY COMPLICATIONS
Abortion
 Spontaneous Abortion: Any loss of fetus < 20 weeks. Occurs in 10-25% of all
pregnancies. (However this is underestimated and it is probably 2/3 miscarry)
 1st trimester abortion most likely CHROMOSOMAL and most are evident by the
12th week.
 2nd trimester abortion most likely due to STRUCTURAL cause (Incompetent
Cervix)
 Types of Spontaneous Abortions
o Complete: Complete expulsion of products of conception (POC), NO
GESTATIONAL SAC in uterus, OS is CLOSED
o Incomplete: Partial expulsion of POC, some tissue is passed with blood,
OS is OPEN
o Inevitable: NO EXPULSION of sac, but there is usually bleeding and the
OS is OPEN.
o Threatened: Vaginal bleeding before 20 weeks, NO tissue is passed, OS is
closed.
o Missed abortion: Retention of the POC, usually no VB, may have
brownish discharge. NO fetal heart tones, sac is irregular, lacunae from
degenerating villi
TX of spontaneous abortion:
o Based on pt preference and diagnosis.
o Complete: Send placenta for pathology report
o Incomplete, blighted ovum, inevitable, missed: Expectant(let patient
miscarry on their own and POC will usually pass); D&C or Misoprostol.
Make sure to monitor for fever or prolonged VB
 Make sure to give Rh neg mothers RhoGAM if there is any
bleeding
o Threatened: Expectant management and pelvic precautions. 50/50
chance of viability

2nd trimester abortions
o Present with painless dilation and effacement of Cx
o Fetal membranes bulge & exposed to vaginal flora, trauma Infection &
vaginal discharge common
o Inc. Cx estimated to cause 15% of all 2nd trimester losses
Risk factors of Inc. Cervix:
o Hx of cervical surgery (cone Bx/LEEP or dilation of cervix)
o Hx of cervical lacerations with vaginal delivery
o Uterine anomalies
o Hx of DES exposure (now rare)
o Family history of Incompetent cx
TX:
o If pre-viable (<23-24wk) elective TOP or expectant management with
bed rest & pelvic rest
o May be a candidate for “rescue cerclage”
o Consider cerclage at 13-14 wks in future pregnancies
o McDonald Cerclage (@ cervico-vaginal junction most common)
o Shirodkar (higher up and buried)
o Abdominal (with history of prior failed cerclage)
o If dx unclear based on hx, may follow with serial TVUS to assess cervix q
1-2 wk from 16-24 wk
o Placement of cerclage only if clinically indicated

Recurrent Abortions
o Unknown cause in up to 50% of PTs. 3 or more SAb or 2 or more SAb for
women over 35.
Causes: (M/C SLE, Hypothyroidism, or DM)
o Genetic Abnormalities (usually parental; 70% karyotype abnormality)
o Hormonal and Metabolic Disorders
 Thyroid
 DM
 Luteal Phase Defect (corpus luteum doesn’t make
enough Progesterone. Give IVF patient progesterone
until 10wks
o Uterine Anomalies – more common in 2nd trimester
 Incompetent cervix
 Asherman’s Syndrome (uterine synechiae)
 Fibroids
o Infectious CausesLike if they have a previous septic abortion (sporadic
not recurrent abortions)
o Environmental
 Smoking, ETOH, Organic Solvents
o Thrombophilias
 Factor V Leiden, Prothrombin G20210A mutation
 Protein C, s and antithrombin III deficiency
o Autoimmune Disorders
 Antiphospholipid antibody syndrome – associated with
SLE and other AI diseases. Suspect if any thrombotic
event or recurrent abortions.
 Thyroid antibodies (anti-thyroglobulin, thyroid
peroxidase antibodies)


Antinuclear Antibodies (ANA)
Alloimmune Disorders (NK cells) (placenta is
semiallogenic tissue so may be attacked by maternal NK
cells)
**2/3 of subsequent pregnancies will be normal; most causes of recurrent abortions are
not identifiable and TX depends on etiology

Obstetric
Hemorrhage





Induced Abortion – termination of pregnancy before viability intentionally,
whether for medical purposes or personal decision.
o Approximately ½ of pregnancies are unintentional
o Medical Abortifacients are used up to 9 weeks usually consisting of
Mifepristone (antiprogesterone Ru-486) + Misoprostol (Cytotec
prostaglandin).
o Surgical: up to 15 weeks you use Manual Vacuum Aspiration (MVA) and
after 15 weeks it is completed by D&C
Leading cause of maternal death
3rd trimester bleeding occurs in 3-4% of pregnancies may be obstetric or nonobstetric
Major causes of antepartum hemorrhage include:
o Placenta previa (20%)
o Placental abruption (30%)
o Uterine Rupture
Placenta Previa: Abnormal implantation of placenta over the internal cervical os
o Signs/Symptoms: Sudden profuse PAINLESS bleeding usually after 28 wks
as the lower uterine segment thins and disrupts attachment
o Risks: Prior C/S, Uterine surgery, Multiparity, Multiple gestation,
Smoking, Hx of placenta previa
 Complete: Covers the os
 Partial: Covers portion of the os
 Marginal: At the edge of the os
 Low lying: Implanted on lower uterine segment
o Fetal Complications: Preterm, PROM, IUGR, Vasa Previa, congenital
abnormalities
o Accreta: Abnormal invasion into the uterine wall (5-15% of the time).
Usually asymp unless it invades the bladder or bowel
 Accreta: superficial attachment & invasion
 Increta: invades myometrium
 Percreta: penetrates myometrium to uterine serosa
o Dx: U/S, vaginal exam is CI, speculum exam to assess bleeding
o Tx: Stabilize the PT and if acute hemorrhage  C/S
 Admit, Non Stress Test, 2 large bore IVs
 Labs: cbc, type & cross, DIC panel, Kleihauer-Betke if Rh –
 Prepare for bleeding and PTD (MgSO4 and steroids)
 Consider amnio for Fetal lung maturity if < 37 and consider C/S
Placental Abruption: Premature separation of a normally implanted placenta
from the uterine wall. 50% before labor and after 30 wks
o

Ectopic
pregnancy






Signs/Symptoms: Sudden PAINFUL bleeding with uterine pain and
contractions, with 50% showing fetal distress
o Risks: HTN, Prior abruption, Advanced maternal age, Multiparity, DM,
Connective tissue dz, Cocaine/smoking, short cord/Circumvallate
placenta, trauma, PROM, ROM w/ polyhydraminos
 30% of 3rd trimester VB; Risk increases in future pregnancy
o Dx: bleeding, firm uterus; Tocometer (frequent or tetanic contractions);
FHR non reassuring due to hypoxia
o Tx: Stabilize the PT and deliver if hemorrhaging or non reassuring FHR
 Admit, Non Stress Test, 2 large bore IVs
 Labs: cbc, type & cross, DIC panel, Kleihauer-Betke if Rh –
 Prepare for bleeding and PTD (MgSO4 and steroids)
 Consider tocolysis and steroid if <34 wks
 Consider amnio for Fetal lung maturity if < 37 and consider C/S
 Vaginal delivery is preferred as long as bleeding is controlled and
no abnormal FHR.
Uterine Rupture
o Signs/Symptoms: Sudden onset of intense abdominal pain +/- vaginal
bleeding.
o Risks: Prior uterine surgery, excessive Pitocin, Grand Multiparity, Marked
uterine distention, Abnormal fetal lie, Large fetus, External version,
Trauma
 Potential OB catastrophe, most occur during labor and 90%
associated w/ prior uterine scar
o Tx: Stabilize the PT immediate laparotomy and delivery of fetus
 Discourage future pregnancies
 No future Trial of Labor (must have C/S)
 Deliver future pregnancy by C/S consider amniocentesis @36
wks for Fetal Lung Maturity
Pregnancy implants outside the uterine cavitypositive hGC
Incidence in 1:100 pregnancies
No bleeding, just severe pain, just one side with palpation
Risks:
o Hx of STD/PID
o *****Prior ectopic ***** (25%-->Underlying tubal disease, often post
STD)
o Previous tubal surgery
o Prior pelvic or abdominal surgery
o Endometriosis
o IVF
o Antiretroviral therapy
o DES exposed with congenital anomalies
o Use of IUD for birth control: Almost no chance of getting pregnant with
IUD; if they do, then the risk of that pregnancy being ectopic is higher.
Hx
o Unilateral pelvic/abdominal pain +/- vaginal bleeding
PE
o
o
adnexal mass, tender; uterus SGA; +/- VB; +/- peritoneal Sx
Shock with rupture
 DX
LABS: bhCG levels lower than expectedQuantitative bhCG is best lab to get
o Inappropriate rise
 > 66% in 48 hr &
 At least double in 72hr
 But 15 % of inappropriately rising bhCG can be normal
pregnancy
 Use the same lab
o +/- anemia and  WBC
o Progesterone level
 <5 ng/ml: ectopic or nonviable pregnancy
 >25 ng/ml: 97% with normal IUP
US: 20-30 % NO sonographic abnormality
o Adnexal mass or gest sac, fluid in pelvis, no IUP with yolk sac are classic
findings
• Pseudosac often confused with IUP
o Seen in 10-20% of ectopics, decidual cast
• Small risk of IUP + ectopic with ART = heterotopic pregnancy
• Should see IUP if bhCG 1,500-2,000 and FHR should be seen if beta > 5,000
mIU/mL
Surgical TX:
• Laparoscopic surgery
• Salpingostomy – hole in tube
• Salpingectomy –resect tube
• Fimbrial expression – “milking out of the tube”
• Exploratory laparotomy – if unstable
Medical TX:
• Methotrexate inhibits rapidly growing cellsMild side effects
• Single IM dose 50mg/sq meter
• Resolution of ectopic in ~70-95% of cases
• Tubal patency rates by HSG ~70-85% after MTX
Criteria for Methotrexate Rx:
o Hemodynamically stable
o No evidence of rupture
o Ectopic< 3-4 cm in diameter
o No contraindication to MTX
o Compliant with f/up
o No cardiac activity
o Bhcg < 15,000
*After treatment, risk of persistent ectopic
o After laparatomy 3-5% of cases
o After LSC range 3-20% (avg. 5-15%)
o Follow weekly bhCG until negative
*After 1 ectopic:
o Recurrent ectopic risk 20-25%
o
Gestational
diabetes






Infertility risk 25-30%
Diabetes in Pregnancy
Priscilla White Classification: not used as much anymore
o A1 diet controlled GDM (gestational diabetes mellitus)
o A2 GDM controlled with insulin; polyhydramnios, macrosomia, prior stillbirth
o B DM onset > 20 yo; duration < 10y
o C onset 10-19 yo; duration < 20 y
o D juvenile onset dur > 20 y
o F nephropathy
o R retinopathy
o M cardiomyopathy
o T renal transplant
Etiology : impairment in carbohydrate metabolism that manifests during pregnancy ;
50% in subsequent preg ; many get DM later in life.
Risk Factors: >25 yo, obesity, family history, high risk ethnicity, prev infant >4000 g,
prev. stillborn, prev. polyhydramnios, recurrent Ab
Associated with: 4x more pre eclampsia, 2x more S Abs, inc. infection,
polyhydraminos, macrosmia, c/s, pp hemorrhage, fetal death
Risk of Fetal anomalies: Transpostion of the great vessels, sacral agenesis,
macrosomia, still birth

DX: O’Sullivan Oral Glucose Challenge Test “Glucola” (50 g glucose) @28
o > 140 then need 3 hr OGTT.
o 100g 3hr OGTT (need 2/4): fasting 95, 1hr 180, 2 hr 155, 3 hr 140
Management: ADA 1800 – 2200 kcal/d diet; glucose checks, insulin if necessary,
deliver @ 38-40 w oral glucose tolerance test after delivery in six weeks to screen for
Post Partum DM (OGTT fasting >126, 2hr >200)
o Diet: Carbohydrate restriction (35-40% of daily caloric intake)
o Exercise: Regular exercise has been shown to improve glycemic control in
women with GDM.
o Self-monitoring of blood glucose
o Oral agents such as Metformin or Glyburide
o Addition of insulin therapy to achieve and maintain euglycemia when diet and
exercise fail
Antepartum care:
o U/S in first trimester to confirm gestational age
o U/S at 18-20 weeks for fetal anatomy assessment
o Maternal glycemic control by self-monitoring and of fetal growth and
development by ultrasound are essential during evaluation
o @ 30-32 w US q 4w (look for IUGR, polyhydramnios), kick counts, Non stress
test (NST), Biophysical profiles (BPP) – Make sure to monitor fetal growth
Consider delivery at 38 weeks if macrosomia or poorly controlled DM and consider
C/S if fetus is >4250-4500g
Watch for neonatal hypoglycemia after delivery

Overt (Pregestational DM)
Initial assessment ideally done prior to conception try to achieve normal HgA1c













Pregnancy
induced
hypertension





before conception
Assessment of other end-organ damage
Comprehensive eye examination
Renal function
Thyroid studies (T1DM)
ECG (older than 30 yo or DM more than 5 years)
Urinalysis and Culture (TOC if Tx)Asymptomatic bacteruria 3X more common
Begin prenatal vitamins with additional folate
U/S in first trimester to confirm gestational age
U/S at 18-20 weeks for fetal anatomy assessment
Maternal glycemic control by self-monitoring and of fetal growth and development
by ultrasound are essential during evaluation
Common medical condition that affects 20-30% of populationSustained BP >
140/90
Second leading cause of maternal mortality in the United States
Complicates 5-8% of all pregnancies
Associated with Intrauterine Growth Restriction (IUGR)
Classification
1. Chronic hypertension (CHTN)
2. Preeclampsia-Eclampsia
3. Preclampsia super imposed on CHTN
Gestational hypertension
o History of Hypertension prior to pregnancy or recognized during first half of
pregnancy
o Hypertension evident before 20 weeks gestation
o Does not worsen appreciably during pregnancy
o High blood pressure lasts longer than 12 weeks postpartum
 Complete Comprehensive History and Physical
 Exclude underlying disorders
 Laboratory
 CBC, CMP
 UA and Culture
o 24 hour urine (baseline)
o Urinary catecholamines (pheochromocytoma)
 Diagnostic Tests
 EKG (LVH)
 Fetal ultrasound early (confirm date and anatomy) then q 4 weeks for growth
assessment
 TX:
 Avoid alcohol and tobacco
 Consider dietary sodium restriction
 Avoid rigorous activity
 Medications
o Required if BP is sustained at or above 160/105 Threshold if no end-organ
involvement





Preeclampsia/ecl
ampsia







o 140/90 as threshold if evidence of renal involvement
o Target goal: 130-150 / 80-100 mmHg
Methyldopa (Aldomet) – initiation
o Previously used as a first line agent in pregnancy by many clinicians.
Labetalol (Never use Atenolol)
o BB that is safe during pregnancy and crosses the placental boarder in very
small amounts.
Nifedipine (Procardia)
o CCB that is safe in pregnancy.
ACEI contraindicated in all trimesters
Sustained BP > 150 / 100
o Initiate medications
o Frequent prenatal visits (q2-4wk)
o Effectiveness of medications
o Proteinuria monitoring
o Fetal monitoring (32 wks)
o Early delivery (39 wks)
1. Preeclampsia - 2-8% of all pregnancies (250,000/yr)
2. Preeclampsia and eclampsia account for 10-15% of maternal deaths worldwide
3. Hypertension - 17.6% of maternal deaths in the U.S.
The cause of preeclampsia remains unknown
ETIOLOGY: vasospasm; inc. thromboxane; inadequate trophoblast invasion of spiral
arteries; immune mediated maternal reaction
Recurrence of pre eclampsia in subsequent pregnancy is 25 – 33%
Risks: First pregnancy or new partner, Multifetal gestation, Hx of PIH, CHTN, Medical
Dz: pregestational DM, vascular or autoimmune dz, nephropathy, APLS, Obesity,
AMA >35 or too young < 20yo, African American ethnicity
Prolongation of gestation, even in severe preeclampsia, offers the best option for
improving neonatal outcome with an acceptable level of maternal risk
Ambulatory management of preeclampsia (no severe features) is acceptable with
some caveats
Magnesium sulfate should be used for seizure prophylaxis in cases of severe
preeclampsia and/or impending eclampsia
Types
A. Mild Preeclampsia:
o BP > 140/90mmHg [ or >30/15 ]
o Proteinuria: >300mg/24 hr or > 1-2+ on dipstick
o Non-dependent edema
B. Severe Preeclampsia: (some findings)
o Proteinuria: > 5gm/24 hr or > 3-4+ on dip
o Cvascular: BP > 160/110mmHg
o Neuro: HA, visual changes (blurry, scotomata)
o Pulmonary: Edema
o Renal: ARF with rising creatinine or oliguria (<400ml/24hr or < 30ml/hr)
o
o
o
o
GI: RUQ pain, elevated LFTs
Heme; hemolytic anemia, platelets < 100K, DIC
Fetal: IUGR, abnormal umbilical artery dopplers
HELLP SYNDROME:
o ~10% of pts with severe PIH will develop HELLP syndrome
o ~80% of pts develop HELLP after diagnosis with PIH
o Stillbirth (10-15%), Neonatal death (20-25%), Proteinuria
o Hemolysis – uric acid, LDH & total bilirubin
o Elevated LFTs - AST, ALT
o Low Platelets < 100K +/- DIC
C. Eclampsia: Seizure
o Presence of new-onset grand mal seizures in woman with PIH
o Other etiologies for seizures include: AVM, ruptured aneurysm, idiopathic …
more likely to be diagnosis when eclampsia occurs after 48-72 hrs postpartum
Fetal Complications: IUGR, prematurity, dec blood flow to placenta; abruption/fetal
distress, oligohydramnios
 Prematurity related complications
 Acute Uteroplacental insufficiency (UPI)
o Placental infarcts and/or abruption
o Intrapartum fetal distress
o Stillbirth (in severe cases)
 Chronic UPI
o Asymmetric & symmetric IUGR
o Oligohydramnios
Management – Delivery is the cure (if need to deliver stabilize and give betamethasone
for 48hrs then deliver)
 Bed rest
 Fetal surveillance
 Laboratory testing
 Antihypertensives (if BP >160/110)
o Hydralazine: 5-10mg dose iv q 15-20mins until desired response achieved
o Labetalol: 20mg iv bolus dose followed by 40mg if not effective w/in 10min 
80mg q 10mins to max total dose of 220mg
 Timing of delivery (34wks severe; 37 mild) Delivery at >37wk if worsening PIH
 Mode of delivery (want vaginal b/c they won’t tolerate blood loss very well)
 Anesthesia (No epidural b/c drop BP)
 Goal is to prevent eclampsia
 With severe HELLP/eclampsia deliver as soon as possible
 Consider expectant management for 48hr to let steroids  Fetal Lung Maturity then
deliver
 Use of Magnesium Sulfate
 Antenatal surveillance and close f/up usually outpatient or in-house
 Start MgSO4
o 4gm load – 2gm/hr maintenance  continue 12-24 hrs postpartum

Preterm expectant management:
o Bed rest
o Betamethasone if < 34 wks
Post-partum management
 CBC with platelets
 Serum creatinine and BUN
 24 hour urine for protein
 Baseline transaminases
Optional – LDH, uric acid
Gestational
trophoblastic
disease
 Hydatidiform MolePartial Mole or Complete Mole
 Invasive Mole
 Gestational Choriocarcinoma
 Placental Site Trophoblastic Tumor
*Hydatidiform moles
 90% of molar pregnancies are benign
o Complete (classic): molar degeneration with no associated fetus
o Incomplete (Partial): molar degeneration with an abnormal fetus
 Complete Mole: Result from fertilization of an empty egg
o All chromosomes are paternal; Most common pattern 46,XX
o Sperm penetration with duplication
o Trophoblastic proliferation with hydropic degeneration
o Higher malignant potential than partial moles- 20%
o Quant bhCG extremely high (>100,000mIU/mL)
o Incidence: 1:1000 pregnancies
 Highest rate: Asians in the Far East 1:200
 Lowest rate: Black women in U.S.
Risks:
o Age less than 20 or greater than 40
o Higher in areas with diet deficient in b-carotene and folic acid
o Higher incidence among women with Hx of prior SAbs or GTD
Pelvic US:
o “snowstorm” pattern due to swelling of villi
o No fetus in uterus
o +/- Theca Lutein ovarian cysts
TX:
o Immediate evacuation
o D&E  by suction curettage
o IV pitocin to minimize blood loss
o Consider hysterectomy if completed childbearing
o 3-5% develop recurrent Dz even after hysterectomy
F/U:
o 95-100% cure rate15-25% persistent disease
o Serial bhCG weekly until 3 consecutive negatives then monthly for 1 yr
o Contraception during follow-up

Incomplete: Normal egg fertilized by 2 sperm
o Triploid karyotype (2 sets from father); M/C 69,XXX (80%)
o Focal hydropic villi and trophoblastic hyperplasia of syncitial layer coexist
with fetus
o Almost always benign
o 90% present with incomplete or missed Ab
o Usually dx later and less severe than complete mole
o Physical Exam can be normal and Dx by US
TX:
o Immediate evacuation of uterine contents
o Follow up weekly bhCG until neg x 3 then monthly for 1 yr
o Contraception during follow up
Good Prognostic Factors
Age < 40
Post mole
< 4 mo from antecedent pregnancy
Bhcg < 40,000
No brain or liver mets
No prior chemotherapy
Sensitive to chemotherapy
 Methotrexate or Actinomycin D
 Good prognosis GTD: single agent
 Poor prognosis GTD: multi-agent
 Choriocarcinoma
o Malignant necrotizing tumor; 25% after molar pregnancy; 50% after
normal term pregnancy; 25% after SAb, EAb or ectopic
o Often metastatic: Lungs, vagina, brain, & liver
o Rare in US 1:20,000 pregnancies:  incidence in Asia
o Often presents with Sx of metastatic disease
TX:
o Same as for invasive moles; Follow up: same as for others
 Placental Site Trophoblastic Tumors (PSTTs)
o Extremely rare; Arise from any type of pregnancy
o Absence of villi and proliferation of cytotrophoblasts
o Spread by invasion into myometrium & blood vessels
o Usually present with VB & persistent + bhCG
o Not sensitive to chemo
**Hydatidiform moles generally benign; Invasive moles usually don’t metastasize
**GTD treated with chemo except PSTT
POSTPARTUM CARE
Postpartum
 Leading cause of perinatal maternal death.
hemorrhage
 > 500ml following vaginal delivery; > 1000ml following C/S
 Etiology:
o Uterine Atony - the inability of the uterus to contract and may lead to
continuous bleeding. Retained placental tissue and infection may contribute to
uterine atony. Uterine atony is the most common cause of postpartum
o
o
o
o
o
o
o

Endometritis/
Chorioamnionitis

hemorrhage
o Trauma - trauma from the delivery may tear tissue and vessels leading to
significant postpartum bleeding
o Retained Placenta
o Coagulopathy
Management (stages from California Maternity Quality Care Collaborative)
o Stage 0: normal - treated with fundal massage and oxytocin.
o Stage 1: more than normal bleeding
o Establish large-bore intravenous access, assemble personnel
o Increase oxytocin, consider use of methergine, perform fundal massage
o Prepare 2 units of packed red cells.
o Stage 2: bleeding continues
o Check coagulation status, assemble response team, move to OR
o Place intrauterine balloon, administer
additional uterotonics(misoprostol, carboprost tromethamine)
o Consider: uterine artery embolization, dilatation and curettage,
and laparotomy with uterine compression stitches or hysterectomy.
o Stage 3: bleeding continues
o Activate massive transfusion protocol, mobilize additional personnel,
o Recheck laboratory tests, perform laparotomy, consider hysterectomy.
Chorioamnionitis
o Def: infection of amniotic fluid
o Requires delivery; increased risk with inc. length of rupture of membranes
o S/S: fever > 38 c, inc WBC, tachycardia, uterus tender, foul discharge; signs of
maternal fever or fetal/maternal tachycardia
o TX: Ampicillin and Gentamycin, add Clindamycin if c/s, DELIVERY
o Most common cause of neonatal sepsis

Perineal
laceration/episio
tomy care
Endometritis
o Risk factors: compromised abortions, medical instrumentation, retention of
placental fragmentprolonged labor, PROM, more c/s than vag delivery
o Organisms: polymicrobial  anerobes/aerobes like E Coli/Group B
Strep/Bacteroides
o S/S: uterine tenderness, foul discharge
o TX: gentamycin and clindamycin (continue until 24-48 h afebrile)
1. First degree laceration: Skin only
2. Second degree lacerations: Skin + Mucosa
3. Third degree lacerations: Skin+ mucosa+ perineal body + anal sphincter
4. Fourth degree lacerations: 3rd + rectal mucosa
The perineal body, located between the vagina and the rectum, is formed predominantly
by the bulbocavernosus and transverse perineal muscles (Figure 1). The puborectalis
muscle and the external anal sphincter contribute additional muscle fibers.
The internal anal sphincter provides most of the resting anal tone that is essential for
maintaining continence. Laceration of this sphincter is associated with anal incontinence.
Surgical Principles
Obstetric perineal lacerations are classified as first to fourth degree, depending on their
depth. A rectal examination is helpful in determining the extent of injury and ensuring
that a third- or fourth-degree laceration is not overlooked.
Repair of the perineum requires good lighting and visualization, proper surgical
instruments and suture material, and adequate analgesia. Compared with surgical repair
using catgut or chromic suture, repair using 3-0 polyglactin 910 (Vicryl) suture results in
decreased wound dehiscence and less postpartum perineal pain.
Local anesthesia can be used for repair of most perineal lacerations. However, general or
regional anesthesia may be necessary
Severe perineal lacerations involving the anal sphincter complex pose a surgical
challenge. There is a 20 to 50 percent incidence of anal incontinence or rectal urgency
after repair of third-degree obstetric perineal lacerations. These DON’T require
immediate repair so an inexperienced physician can delay the procedure for a few hours
until appropriate support staff are available.
With severe perineal lacerations irrigate copiously to improve visualization and reduce
the incidence of wound infection. Because these lacerations are contaminated by stool, a
single dose of a second- or third-generation cephalosporin may be given intravenously
before the procedure is started.
Repair of Second-Degree Perineal Lacerations
Repair of a second-degree laceration requires approximation of the vaginal tissues,
muscles of the perineal body, and perineal skin. The steps in the procedure are as
follows:
Second-degree perineal laceration.
The apex of the vaginal laceration is identified. For lacerations extending deep into the
vagina, a Gelpi or Deaver retractor facilitates visualization.
An anchoring suture is placed 1 cm above the apex of the laceration, and the vaginal
mucosa and underlying rectovaginal fascia are closed using a running unlocked 3-0
polyglactin 910 suture. If the apex is too far into the vagina to be seen, the anchoring
suture is placed at the most distally visible area of laceration, and traction is applied on
the suture to bring the apex into view. The running suture CAN BE LOCKED FOR
HEMOSTASIS, if needed.
The sutures must include the rectovaginal fascia (Figure 4), which provides support to
the posterior vagina. The running suture is carried to the hymenal ring and tied proximal
to the ring, completing closure of the vaginal mucosa and rectovaginal fascia.
The muscles of the perineal body are identified on each side of the perineal
laceration (Figure 5). The ends of the transverse perineal muscles are reapproximated
with one or two transverse interrupted 3-0 polyglactin 910 sutures (Figure 6)
2nd degree perineal laceration
Repair of transverse perineal muscles
A single interrupted 3-0 polyglactin 910 suture is then placed through the
bulbocavernosus muscle(Figure 7). The torn ends of the bulbocavernosus muscle are
frequently retracted posteriorly and superiorly. Use of a large needle facilitates proper
suture placement.
Repair of bulbocavernosus muscle
If the laceration has separated the rectovaginal fascia from the perineal body, the fascia
is reattached to the perineal body with two vertical interrupted 3-0 polyglactin 910
sutures (Figure 8)
Reattachment of rectovaginal septum to muscles of
perineal body.
When the perineal muscles are repaired anatomically as described above, the overlying
skin is usually well approximated, and skin sutures generally are not required. Skin
sutures have been shown to increase the incidence of perineal pain at three months
after delivery.15 [Evidence level B, uncontrolled trial] If the skin requires suturing,
running subcuticular sutures have been shown to be superior to interrupted
transcutaneous sutures.16 The 4-0 polyglactin 910 sutures should start at the posterior
apex of the skin laceration and should be placed approximately 3 mm from the edge of
the skin.
An alternative approach to repair of the perineal body muscles is a running suture that is
continued from the vaginal mucosa repair and brought underneath the hymenal ring.
However, we prefer the interrupted approach because it facilitates a more anatomic
repair, allowing reapproximation of the bulbocavernosus muscle and reattachment of
the vaginal septum with minimal use of sutures.
Repair of Fourth-Degree Perineal Lacerations
Repair of a fourth-degree laceration requires approximation of the rectal mucosa,
internal anal sphincter, and external anal sphincter (Figure 9)
.Fourth-degree perineal laceration.
A Gelpi retractor is used to separate the vaginal sidewalls to permit visualization of the
rectal mucosa and anal sphincters. The apex of the rectal mucosa is identified, and the
mucosa is approximated using closely spaced interrupted or running 4-0 polyglactin 910
sutures (Figure 10). Traditional recommendations emphasize that sutures should not
penetrate the complete thickness of the mucosa into the anal canal, to avoid promoting
fistula formation. The sutures are continued to the anal verge (i.e., onto the perineal
skin).
Repair of rectal mucosa.
The internal anal sphincter is identified as a glistening, white, fibrous structure between
the rectal mucosa and the external anal sphincter (Figure 11). The sphincter may be
retracted laterally, and placement of Allis clamps on the muscle ends facilitates repair.
The internal anal sphincter is closed with continuous 2-0 polyglactin 910 sutures.
Internal sphincter and external anal sphincter.
The external anal sphincter appears as a band of skeletal muscle with a fibrous capsule.
Traditionally, an end-to-end technique is used to bring the ends of the sphincter
together at each quadrant (12, 3, 6, and 9 o'clock) using interrupted sutures placed
through the capsule and muscle (Figure 12). Allis clamps are placed on each end of the
external anal sphincter. We use 2-0 polydioxanone sulfate (PDS), a delayed absorbable
monofilament suture, to allow the sphincter ends adequate time to scar together.
Recent evidence suggests that end-to-end repairs have poorer anatomic and functional
outcomes than was previously believed.
End-to-end technique repair external sphincter.
An alternative technique is overlapping repair of the external anal sphincter. Colorectal
surgeons prefer to use this method when they repair the sphincter remote from
delivery.14,17 The overlapping technique brings together the ends of the sphincter with
mattress sutures (Figure 13) and results in a larger surface area of tissue contact
between the two torn ends. Dissection of the external anal sphincter from the
surrounding tissue with Metzenbaum scissors may be required to achieve adequate
length for the overlapping of the muscles. The suture is passed from top to bottom
through the superior and inferior flaps, then from bottom to top through the inferior and
superior flaps. The proximal end of the superior flap overlies the distal portion of the
inferior flap. Two more sutures are placed in the same manner. After all three sutures
are placed, they are each tied snugly, but without strangulation. When tied, the knots
are on the top of the overlapped sphincter ends. Care must be taken to incorporate the
muscle capsule in the closure.
Overlapping technique repair external sphincter.
Postpartum Care
Sitz baths and an analgesic such as ibuprofen. If a woman has excessive pain in the days
after a repair, she should be examined immediately because pain is a frequent sign of
infection in the perineal area. After repair of a third- or fourth-degree laceration, we
include several weeks of therapy with a stool softener, such as docusate sodium
(Colace), to minimize the potential for repair breakdown from straining during
defecation.
Prevention
The incidence of severe perineal trauma can be decreased by minimizing the use of
episiotomy and operative vaginal delivery. A Cochrane review demonstrated that liberal
use of episiotomy does not reduce the incidence of anal sphincter lacerations and is
associated with increased perineal trauma.
Episiotomy:



Normal
physiology

Indications:
o There is a serious risk to the mother of second- or third-degree tearing
o In cases where a natural delivery is adversely affected, but a Caesarean section is
not indicated
o "Natural" tearing will cause an increased risk of maternal disease being vertically
transmitted
o The baby is very large
o When perineal muscles are excessively rigid
o When instrumental delivery is indicated
o When a woman has undergone FGM (female genital mutilation), indicating the
need for an anterior and or mediolateral episiotomy
o Prolonged late decelerations or fetal bradycardia during active pushing
o The baby's shoulders are stuck (shoulder dystocia), or a bony association (Note
that the episiotomy does not directly resolve this problem, but it is indicated to
allow the operator more room to perform maneuvers to free shoulders from the
pelvis)
Types:
o Medio-lateral: The incision is made downward and outward from midpoint
of fourchette either to right or left. It is directed diagonally in straight line which
runs about 2.5 cm away from the anus (midpoint between anus and ischial
tuberosity).
o Median: The incision commences from centre of the fourchette and extends on
posterior side along midline for 2.5 cm.
o Lateral: The incision starts from about 1 cm away from the centre of fourchette
and extends laterally. Drawback include chance of injury to Bartholin's duct; thus
some practitioners have totally condemned it.
o J-shaped: The incision begins in the centre of the fourchette and is directed
posteriorly along midline for about 1.5 cm and then directed downwards and
outwards along 5 or 7 o'clock position to avoid the anal sphincter. This is also not
done widely
Episiotomy has been shown to not be as effective and has led to more tears.
Perineal lacerations are also increased with use of forceps rather than vacuum
delivery.
Puerperium is the period following childbirth which the body tissues, specially the
pelvic organs revert back to the pre-pregnant state both anatomically and
changes of
puerperium










physiologically.
o Involution is the process whereby the reproductive organs return to their
nonpregnant state.
Duration: puerperium begins as soon as the placenta is expelled and lasts for
approximately 6 weeks
o The period is arbitrarily divided into – Immediate- within 24 hours; Early- upto 7
days; Remote- upto 6 weeks.
Uterus becomes firm and retracted and measures about 20 X 12 X 7.5 cm and weighs
about 1000 g
o At the end of the first week, it weighs 500g
o By the 6 weeks, it weighs approx. 50g.
Cervix contracts slowly. External os will be two fingers wide for a few days but by the
end of first week, narrow down to admit the tip of finger only.
o It never returns back to the nulliparous state, usually remains slightly open and
appear slitlike or stellate
Muscles - there is a reduction of the myometrial cell size. Withdrawal of estrogen
and progesterone lead to increase in the activity of the uterine collagenase and the
release of the proteolytic enzyme.
Blood vessels - The arteries are constricted by contraction of its wall and thickening
of the intima followed by thrombosis. New blood vessels grow inside thrombi. There
is also degeneration of the elastic tissues.
Endometrium - The superficial layer becomes necrotic and is sloughed. The basal
layer adjacent to the myometrium remains intact and is the source of new
endometrium.
o By the 10th day: Regeneration of the epithelium is completed.
o By the day 16: the endometrium is restored.
o At about 6 weeks: the endometrium of placental site is restored
Placental site involution - Complete extrusion of the placental site takes up to 6
weeks.
o When this process is defective, late-onset puerperal hemorrhage may occur.
o Size of placental site immediately after delivery is approx. the size of the palm,
but it rapidly decreases thereafter.
Vagina takes a long time(4-8 weeks) to involute. It regains its tone but never to the
virginal state.
o The mucosa remains delicate for the first few weeks
o Rugae partially reappear at third week.
o The introitus remains permanently larger than the virginal state.
Abdominal Wall as a result of ruptured elastic fibers in the skin and prolonged
distension caused by the pregnant uterus, remains soft and flaccid for several weeks
Lochia - the vaginal discharge beginning the first night during puerperium.
o The discharge originates from the uterine body, cervix and vagina.
o Odor and reaction: it has an offensive fishy smell and is alkaline at first then acid
towards the end.
o Color – red for 1-4 days; the color is yellowish or pink or pale brownish days 5-9;
white days 10-15 days.
o Duration: may extend up to 3 weeks.
o 1. Persistence of red lochia means subinvolution













o 2. Offensive lochia means infection
o 3. In severe infection with septicaemia, lochia is scanty and not offensive
Insulinaze causes the diabetogenic effects of pregnancy to be reversed.
Estrogen and progesterone levels decrease. The estrogen levels in nonlactating
women begin to increase by 2 weeks after birth.
Lactating and non-lactating women differ in the time of the first ovulation.
o In women who breast feed, prolactin levels remain elevated into the sixth week
after birth.
o Prolactin levels decline in nonlactating women, reaching the prepregnant range
by third week.
Menstruation: If the woman does not breast fed her baby, the menstruation returns
by 6th week following delivery in about 40% and by 12th week in 80% of cases.
Ovulation: In non-lactating mothers, may occur as early as 4 weeks and in lactating
mothers about 10 weeks after delivery.
o A women who is exclusively breastfeeding, the contraceptive protection is about
98% up to 6 months postpartum. Thus, lactation provides a natural method of
contraception.
o Non-lactating mother should use contraceptive measures after 3 weeks and the
lactating mothers after 3 months of delivery.
Urinary system - Because of relative insensitivity to the raised intravesical pressure
due to trauma sustained to the nerve plexus during delivery, the bladder may be
overdistended without any desire to pass urine.
Blood and fluid changes - Diuresis b/t second and fifth day after birth, as well as
blood loss at birth, reduce the added volume accumulated during pregnancy and it
returns to normal by first or second week after birth.
The white blood cell count sometimes reaches 30,000/L, with the increase
predominantly due to granulocytes. Normally, during the first few postpartum days,
hemoglobin concentration and hematocrit fluctuate moderately.
Cardiac Output: Remains elevated for 24 to 48 hrs postpartum and declines to
nonpregnant values by 10 days.
The GI system - Digestion and absorption begin to be active again soon after birth,
but passage of stool through the bowel may be slow because of the still present
effect of relaxin on the bowel. Bowel evacuation may be difficult because of the pain
of episiotomy sutures or hemorrhoids.
Weight loss - Rapid diuresis and diaphoresis during 2nd to 5th days after birth result
in weight loss of 5 lb (2 to 4kg), in addition to approx. 12 lb (5.8 kg) lost at birth.
Lochia flow- 2-3 lb(1kg) loss
o Total weight loss- 19 lb
Integumentary system - Stretch marks in women’s abdomen still appear reddened
and may be even more prominent than pregnancy. Excessive pigment on face and
neck (Chloasma) and on abdomen (Linea nigra) barely detectable in 6 weeks time.
o Diastasis recti (Overstretching and separation of the abdominal musculature) if
present, the area will be slightly indented.
o Abdominal wall and ligaments require 6 weeks time to return to normal
Lactation - midway through pregnancy, she begins secreting colostrum, a thin,
watery, prelactation secretion, which continues the first 2 postpartum days. On the
third day, her breasts become full and feel tense (primary engorgement) or tender as

milk forms within breast ducts.
o When breast milk forms, the milk ducts become distended. The nipple secretion
changes from the clear colostrum to bluish white which is typical color of breast
milk.
Vital sign changes
o Temperature – may have a slight increase in temperature during the first 24
hours after birth. Occasionally, when breasts fill with milk on the third or fourth
postpartum day, temperature rises for a period of hours from increased vascular
activity.
o Pulse - after initial tachycardia associated with labor and delivery, a bradycardia
often develops in the early puerperium. During the postpartal period it is usually
slower than normal (60 and 70 bpm). As diuresis diminishes blood volume and
causes blood pressure to fall, the pulse rate increases and returns to normal in 1
weeks.
o Blood pressure - Systolic and diastolic blood pressures remain unchanged from
late pregnancy values until about 12 weeks post partum, after which they
increase. Within 2 weeks post partum, systemic vascular resistance increases by
30%