Danil Hammoudi.MD
Sinoe Medical Association

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USMLE STEP 2 PART VI

GYNECOLOGY OBSTECTRICS



GENERALITY:


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Quiz Results

 1. 40 million Americans currently have:

a) HIV/AIDS
b) herpes <-- correct answer
c) chlamydia <-- your answer

Herpes affects more people in the United States than any other sexually transmitted disease. It's currently estimated that 40 million Americans have herpes. Chlamydia, however, chalks up more new cases in the United States each year than any other STD: there are about 4 million new cases of chlamydia each year, as compared with 500,000 new cases of herpes. See FAQ for more surprising information about STD infection rates in the United States. If you want to speak with someone about herpes, call the National Herpes Hotline at 919-361-8488, Monday-Friday, 8am-7pm ET. If you want to speak with someone about HIV/AIDS, call the National AIDS Hotline at 800-342-AIDS, 7 days a week, 24 hours a day.
 2. Women who've had an STD are at increased risk for:

a) infertility <-- correct answer
b) HIV/AIDS <-- correct answer
c) cervical cancer <-- correct answer

Unfortunately, all of these answers are right. Women who have had an STD are at increased risk for infertility, AIDS, and cervical cancer. To learn more about the long-term health risks associated with particular STDs, check out Nothing But the Facts. If you want to speak with someone about HIV/AIDS, call the National AIDS Hotline at 800-342-AIDS, 7 days a week, 24 hours a day.
 3. Which of the following bacterial STDs do experts call "the silent epidemic"?

a) scabies
b) chlamydia <-- correct answer
c) trichomoniasis

The bacterial STD chlamydia has been called a "silent epidemic" because 75% of women and 50% of men with the disease experience no symptoms. It's especially prevalent among young people. Untreated chlamydial infections in women often result in another "silent epidemic" -- pelvic inflammatory disease (PID), a leading cause of infertility. To learn more about chlamydia, see Nothing But the Facts. If you want to speak with someone about STDs, call the National STD Hotline at 800-227-8922, Monday-Friday, 8am-11pm ET.
 4. Which of the following groups is at greatest risk for STDs?

a) men under 25
b) women under 25 <-- correct answer
c) men 25-40

The highest rates of STD infection occur among women 15 to 19 years of age, but people of all ages, ethnicities, and income levels can be affected.
 5. When asked to name the greatest obstacle they face in trying to protect themselves against STDs, people most often cite:

a) carelessness
b) ignorance
c) self-consciousness <-- correct answer

People of all ages cite embarrassment or self-consciousness as the greatest obstacle they face in trying to protect themselves against STDs. If you are one of those people who find such topics Unspeakable, click on this link to learn how to talk about safer sex and STDs.
 6. Experts now recommend that sexually active young people be immunized against what STD:

a) chlamydia
b) herpes
c) hepatitis B <-- correct answer

The Centers for Disease Control currently recommends that adolescents who have sex or inject drugs be vaccinated against hepatitis B. It's also part of the new standards for pediatric immunization, so it's important to make sure that your young children are immunized. The vaccine is given in the arm, in three doses. It's important to get all three shots, and advisable for teens to do so before they become sexually active and risk exposure to the disease. See Nothing But the Facts for more information about hepatitis B.

No vaccines are currently available for chlamydia or herpes.
 7. Which of the following STDs can be cured?

a) herpes
b) gonorrhea <-- correct answer
c) genital warts <-- your answer

Gonorrhea is usually easy to cure with antibiotics. Herpes and genital warts, while treatable, are chronic viral infections and are not curable. Proper management of herpes and genital warts, however, can help. If you've been infected with herpes or genital warts, you're not alone, and there is hope. Millions of people have been able to keep their symptoms under control. If you want to speak with someone about STDs, call the National STD Hotline at 800-227-8922, Monday-Friday, 8am-11pm ET. If you want to speak with someone about herpes, call the National Herpes Hotline at 919-361-8488, Monday-Friday, 8am-7pm ET.
 8. For women, the most common symptom of chlamydia and gonorrhea infection is:

a) vaginal discharge
b) sores and/or blisters in the genital region
c) no symptom <-- correct answer

It's estimated that 70 percent of women with chlamydia and 50 percent of women with gonorrhea experience no symptoms. This means that you can be infected and not even know it. See Sore Subjects to learn more about some STD symptoms that are recognizable. If you want to speak with someone about herpes, call the National Herpes Hotline at 1-800-361-8488, Monday-Friday, 8am-7pm ET.
 9. You may be at increased risk for HIV/AIDS if:

a) you have had many sex partners in the last 10 years <-- correct answer
b) you have given blood at a blood bank or blood collection center
c) you have eaten food prepared by a person infected with HIV

You can't get HIV/AIDs from giving blood or eating food prepared by a person infected with HIV. Having multiple sex partners, however, can increase the chance that you may be exposed to HIV, the virus that causes AIDS. To learn more about how HIV/AIDS is transmitted, check out Nothing But the Facts. If you want to speak with someone about HIV/AIDS, call the National AIDS Hotline at 800-342-AIDS, 7 days a week, 24 hours a day.
 10. The best form of protection against contracting STDs during sex is:

a) spermicides
b) condoms, used correctly all the time <-- correct answer
c) birth control pills

Condoms (male and female) are still the best form of protection for anal, oral, and vaginal sex. But even condoms cannot protect you against every STD. Condoms cannot always protect you against herpes, for example. Spermicides have been shown to kill some of the germs that cause STDs, so it is a good idea to use them with condoms for extra protection. The pill, Norplant, and Depo-Provera are only methods of birth control. They offer no protection against STDs. Got more questions? Take a look at FAQ.




The most common cause of puerperal endomyometritis is :
o        Prolonged ruptured of membranes [prom]

o        Puerperal sepsis accounts for significant postpartum maternal morbidity and mortality.

Cesarean delivery are risk factors for puerperal genital tract infection

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INTRAUTERINE GROWTH DISORDER:
COMBINATION OF STANDARD FETAL MESUREMENT :

2-3 TRIMESTER SONOGRAPHIC ASSESSEMENTS OF FETAL GROWTH WEIGHT = HC, BPD, AC, FL

HC = HEAD CIRCUMFERENCE

BPD= BIPARIETAL DIAMETER

AC : ABDOMINAL CIRCUMFERENCE

FL: FEMUR LENGHTH

ONE OF THE MOST EFFECTIVE TOOLS IN DIAG INTRAUTERINE GROWTH RETARDATION [IVGR] IS SONOGRAPHIC EVALUATION OF THE FETAL PARAMETERS.
TRANSCEREBELLAR DIAMTER [TCD] IS USED FOR ESTIMATING GESTATIONAL AGE BUT NOT FETAL WEIGHT

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IntraUterine Growth Retardation
Maldevelopment in utero may be due to a :

fault in the fertilised ovum,
a fault in the placenta which limits the supply of foods and oxygen to the fetus,
or to disease or malnutrition in the mother.
Certain of the first, and all of the second and third, types of maldevelopment retard growth and hence lead to small size at birth.

This smallness of size may be known only through weight. Though length would often bemore informative, , although accurate apparatus for measuring length now exists.

Standards for birth weight and length are available for each week of gestational age; the centiles are different for girls and boys and for the first born and later-born.

We are concerned here only with small-for-date babies, ie those who are below the centile limits for weight for their particular gestational age. Babies who are simply born early at the normal weight for that length of gestation seem mostly to catch up to a perfectly normal height. Small-for-date babies may be born at term, or may be born after a shorter gestational period.

Silver Russell Syndrome
The majority of small-for-date children, particularly those born at term, grow within the normal centiles, though they do not fulfil their genetic potential, and hence appear somewhat small for their parent's heights. Their average height centile seems to be about the 30th.

However, some fail to to catch up in this way. They remain short and lacking in subcutaneous fat and have a characteristic facial appearance.

The face as a whole is triangular, with large eyes and a small lower jaw; the forehead is large and prominent in relation to the face, and the ears are set low in the head and tend to stick out. The bridge of the nose is usually depressed and the mouth turned down at the corners. A proportion of these children have marked asymmetry of the limbs or body, one arm or leg being longer than the other, or one side of the face or chest more developed. Mental development is usually normal.

At present there is no effective treatment for these children who grow up normally in every way except for size.These children are healthy and active and should not be regarded as delicate. In middle childhood they put on some subcutaneous fat and their puberty occurs at a slightly earlier time but in the normal sequence. The syndrome hardly ever occurs twice in the same family, so the mother of such a child can be reassuredabout subsequent pregnancies. The cause of the disorder is unknown. The prognosis may be improved by the treatment given to low birthweight babies now a days, which consists of feeding them more intensively than before. This may also be important in the prevention of hypoglycaemia which is more common in these babies.


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INTRAUTERINE GROWTH RETARDATION (IUGII, Smcell~for-Gestational-Age 1SGA1 Pregnancy) ~ BASIC INFORMATION DESCRIPTION

The fetus is much smaller than expected for the length of the pregnancy.

IUGR occurs in 1 in l0 pregnancies.

FREQUENT SIGNS AND SYMPTOMS

 Usually no signs or symptoms occur. Diagnosis is based on prenatal physical examinations and ultrasound studies.

CAUSES Chromosome abnormalities and/or infections of the fetus are often the cause of IUGR In other cases, the placenta fails to provide adequate nutrients to the fetus. Most often, the placenta is normal, but is functioning abnormally.

Abnormal placenta anatomy, such as placenta previa or placental abruption, can result in IUGR.


RISK INCREASES WITH :

Multiple fetuses (twins or greater).
Poor maternal nutrition.
Maternal illness, such as:
cyanotic heart disease,
hypertension,
anemia,
diabetes mellitus with vascular involvement,
or sickle cell disease.
Smoking.
Fetal infections.
Maternal drug addiction or alcohol abuse.
Fetal congenital abnormalities;
chromosomal abnormalities.
Maternal low prepregnant weight and low weight gain with pregnancy.
Previous pregnancy with an intrauterine growth retardation baby.
Living at a high altitude.
Preventive risk

Avoidance of any of the risk factors that are within the control of the mother, such as:

smoking or alcohol abuse
. Genetic counseling prior to pregnancy.
Good medical care and management of any maternal chronic disorder listed in risk factors.
Good prenatal care. If pregnant, avoid people with infections.
EXPECTED OUTCOME

For the mother without an underlying condition, the outcome is equivalent to a mother who delivers an average-for-gestational-age (AGA) baby. A cesarean section delivery may be necessary in cases of fetal distress.

For the infant without anomalies (a deviation from what is considered normal), abnormalities or infection, the outlook is generally good for subsequent normal physical development and neurological outcome.

POSSIBIE COMPUCATIONS

Increased risk for fetal problems prior to, and at birth, such as lack of oxygen, low birth weight, prematurity, low blood sugar and temperature instabilities.

Higher risk exists for congenital defects.

Risk of SIDS (sudden infant death syndrome). Long-term, the child may develop physical or neurological handicaps. O

TREATMENT GENERAL MEASURES

Any substances being abused by the mother need to be discontinued (smoking, alcohol, drugs). Any maternal illness should be stabilized if possible. Ongoing testing will be done once or twice weekly to assess the condition of the fetus. Hospitalization may be required if outpatient steps are unsuccessful. Labor may need to be induced or a cesarean section performed if fetal compromise is diagnosed or it is determined that the optimal time for delivery has been reached (the point at which the baby will do as well outside as inside the uterus).

MEDICATION Low dose aspirin may be prescribed for some selected cases. ACTIVlrY Following diagnosis, complete bed rest is often recommended, while others may be on a limited activity routine. If bed rest is prescribed, lying on the left side helps pro mote blood flow and nutrition for the fetus. DIET If poor nutrition is a problem, a special diet will be prescribed. NOTIFY OUR OFFICE IF You are pregnant and have any concerns about the development of your baby. During treatment, any new signs or symptoms develop.


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Obstetrics: Intrauterine Growth Retardation (IUGR)
Peter P. Toth, M.D., Ph.D. and A. Jothivijayarani, M.D.
Department of Family Medicine
University of Iowa
Peer Review Status: Externally Peer Reviewed by Mosby


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Definition
IUGR is a diagnosis that the fetus weighs less than the tenth percentile for its gestational age.
Symmetric IUGR (intrinsic): normal head circumference-to-abdominal circumference ratio, caused by genetic disease and fetal infection with poor prognosis.
Asymmetric IUGR (extrinsic): increased HC/AC ratio, caused by placental insufficiency, good prognosis with appropriate treatment.
Risk Factors
Chronic maternal disease,
chronic maternal hypertension,
PIH,
diabetes,
cyanotic heart disease,
collagen vascular disease,
severe maternal anemia,
renal disease,
multifetal pregnancy.
Fetal genetic disorders or fetal malformations.
Intrauterine infections. Rubella, herpes, toxoplasmosis, syphilis, CMV.
Previous history of small-for-gestational-age baby, smoking, drug, or alcohol abuse.
Abnormalities of the placenta or placental blood flow.

Diagnosis
One should be suspicious when the fundal height does not exhibit the predicted 1 cm/week growth between 20 and 36 weeks of gestation.
A lag in fundal height by 4 cm warrants ultrasonographic evaluation. Serial ultrasonic scanning may confirm the diagnosis.


Management
The development of IUGR makes the pregnancy high risk.
Stillbirth,
oligohydramnios,
and intrapartum fetal acidosis are common antepartum complications.
Close antepartum surveillance is required, and the decision on when to deliver the infant is complex.

Neonatal complications include :

o        persistent fetal circulation,

o        meconium aspiration syndrome,

o        hypoxic ischemic encephalopathy,

o        hypoglycemia,

o        hypocalcemia,

o        hyperviscosity, and

o        defective temperature regulation.

These pregnancies should be managed by a perinatologist.



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What Are Growth Disorders?

o        Human Growth Hormone (HGH)
Deficiency

o        Cushing’s Syndrome (Cortisol, Stress,
Hormone Excess)

o        Hypothyroidism

o        Nutritional Short Stature

o        Intrauterine Growth Retardation ("IUGR")

o        Russell Silver Syndrome

o        Disproportionate Short Stature

o        Achondroplasia

What Are Growth Related Disorders?

o        Poor Nutrition and Systemic Diseases

o        Bone Disorders



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What Are Growth Disorders?

There are many causes of growth failure in children. Some are constitutional, some are genetic, and some are the result of hormonal disorders.

In some cases the growth disorder may be recognized at birth; in others, a parent may be concerned that the child is the shortest in the class, still wearing the same size clothing as last year, and growing less than two inches a year..

What is Human Growth Hormone (HGH) Deficiency?

HGH deficiency may occur at any time during infancy or childhood, with the most obvious sign being a noticeable slowing of growth.

The deficiency may be genetic is some families. Although these children may also possess signs of low blood sugar or obesity, they display average body proportions and (average intelligence. Through the use of injections of synthetic HGF over a period of several years, physicians can help these children deficient in HGH to achieve average height. .

What is Nutritional Short Stature?

Malnutrition on a constant basis prevents children from reaching their full growth potential. The body becomes weak and frail and usually shows signs that muscle or bone tissue is wasting. Malnutrition is the most common cause of growth failure around the world, primarily due to lack of protein and other basic nutrients ion the diet. A well balanced diet will help prevent or overcome this disorder.

What is Intrauterine Growth Retardation ("IUGR")?

A disorder which occurs while the baby is still in the mother's womb.

IUGR produces full-term babies unusually small in weight and/or length at birth. They are proportionately short statured.

What is Russell Silver Syndrome?

In this condition, short stature begins in the womb with the children typically developing asymmetry of their extremities, especially leg length discrepancy.

Cranio-facial features include:

small face and
relatively large head,
with the facial features ordered in a triangular configuration.
The corners of the mouth tend to be downturned.
The fifth fingers are usually very short and incurved, and there may be mild webbing of the soft tissue of the second and third toes.
During the first year of life there may be a tendency to episodes of low blood sugar (hypoglycemia).
Kidney malformations are frequent.

What is Disproportionate Short Stature?

Disproportionate short stature, commonly referred to as dwarfism, can manifest itself as short-limbed dwarfism or short-trunk dwarfism.
The growth retardation results primarily from impaired growth of bone and cartilage.
These types are usually not HGH deficient.

What is Achondroplasia?

The most common form of disproportionate growth retardation, achondroplasia is recognizable at birth and after the 24th week of gestation using ultrasound. Characteristics include:

A moderately enlarged head
Average height and size trunk
Short limbs
Underdevelopment of the mid-third of the face so that the nasal bridge is relatively low or flat
Short fingers with excessive separation of the fingertips, especially the third and fourth fingers


What Are Growth Related Disorders?
Most short children do not have a serious growth problem.
Many grow at a normal rate and reach an adult height that is about the same as their parents.
A child's rate of growth is an important clue to the presence or absence of a growth problem:
A child who is growing at a slower than normal rate may have a serious problem, regardless of his or her height.
There are many conditions and diseases that can cause poor growth and this page give facts about several of them.
1.       Poor Nutrition and Systemic Diseases
. Nutritional deficiencies will cause poor growth eventually - a balanced diet with adequate calories and protein is essential for growth.

There are a number of intestinal disorders which may lead to poor absorption of food.

Failure to absorb nutrients and energy from food then leads to growth failure.

Children with these conditions may have complaints that involve the stomach or intestines (bowels) and may have bowel movements that are unusual in pattern, appearance and odor. Treatment of these conditions often involves a special diet. Normal growth usually resumes after the condition has been treated.

Diseases of the kidneys, lungs and heart may lead to growth failure as a result of inadequate intake of nutrients or buildup of waste products and undesirable substances in the body. Children with diabetes, or "high sugar," may grow slowly, particularly when their blood sugar is not kept near the normal range.

Any disease that is severe, untreated or poorly controlled can have an adverse effect on growth. Severe stress or emotional trauma can also cause growth failure.

2.       Bone Disorders
One form of extreme short stature is caused by abnormal formation and growth of cartilage and bone.

Children with a skeletal dysplasia, or chondrodystrophy, are short and have abnormal body proportions; intelligence is normal.

Some chondrodystrophies are inherited, others are not.

The underlying causes of most of these skeletal dysplasias are not known

The chances of parent shaving a second child with the same problem cannot be estimated until the specific type of skeletal dysplasia is identified from physical examination and bone x-rays.


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Terbutaline : increased heart rate and possible arrhythmias

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IN TERM OF SERUM CONCENTRATION , THE MAJOR POST MENOPAUSAL STEROID HORMONE AND PITUITARY TROPIC HORMONE ARE : ESTRONE AND FSH

--------------------------------------------------------------------------------


COMPARE WITH COW'S MILK HUMAN BREAST MILK CONTAIN SIGNIFICANTLY GREATER AMOUNT OF VIT C -SAME AMOUNT OF WATER + SOLIDS

 COW'S MILK
 HUMAN MILK
VIT C
 +
 +++++
PROTEIN
 +++++
 +
WATER+SOLIDES
 +++++
 +++++
VIT K
 +++++
 +
IRON
 +
 +[BETTER ABSORB]


COW'S MILK HUMAN MILK

PROTEIN VITC

VIT K IRON BETTER ABSORBED


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                                                                                                                antepartum bleeding

PLACENTA PREVIA
 ABRUPTIO PLACENTAE
 OTHER THIRD TRIMESTER
TOTAL PP : COMPLETELY COVER INTERNAL OS
PARTIAL PP: PARTIALLY
MARGINAL PP: MARGIN
LOW LYING PP: NEAR INTERNAL OS
FINGER CAN PALP THE EDGE OF THE PLACENTA THROUGH THE CERVIX.
 PLACENTA PREMATURELY SEPARATES FROM THE UTERUS BEFORE DELIVRY OF THE FETUS
 A: OBSTECTRICAL::

b: non obstectrical
















--------------------------------------------------------------------------------

 ETIOLOGY:

1/MATERNAL FACTORS

MULTIPARITY: 80%
AGE OVER 35
NO PRIOR HISTORY
2/FACTORS RELATED TO ABNORMAL PLACENTATION

DEFECTIVE VASCULARIZATION OF THE DECIDUAL
SCARRING OF THE ENDOMETRIUM
VESSELS CHANGES AT THE PLACENTA SITE
INCREASED SURFACE AREA OF PLACENTAL IMPLANTATION
ERYTHROBLASTOSIS
ALTERED BLOOD SUPPLY TO THE ENDOTRIUM
***MYOMECTOMY

***CESAREAN

***HYSTERECTOMY



CLINICAL PRESENTATION

1/ PAINLESS VAGINAL BLEEDING

2/ MATERNAL BLOOD LOSS AND FETAL MORBIDITY


1/ PAINLESS VAGINAL BLEEDING:

3RD TRIMESTER
OCCUR DURING REST - ACTIVITY-SUDDENLY
AFTER TRAUMA
AFTER COITUS
AFTER PELVIC EXAMINATION


EARLY IN THE 3RD TRIMESTER WHEN THE LOWER UTERINE SEGMENT BEGINS TO CHANGE CAUSING THE CERVIX TO EFFACE AND DILATE




DIAG:

EXAM:

MALPOSITION OF THE FETUS [BREECH OR TRANSVERSE LIE]
MULTIPLE GESTATION
ADVANCE MATERNAL AGE

INDIRECT DIAG:

ULTRASOUND

SCANING

AMNIOGRAPHY

DEFINITIVE DIAG:

FINGER THROUGH THE CERVIX

DELIVERY BY CSECTION




COMPLICATION:

SHEEHAN'S SYNDROME

ACUTE TUBULAR NECROSIS

SEVERE POST PARTUM HEMORRHAGE

PLACENTA ACCRETA
 HEMORRHAGE INVOLVED INCLUDE:
***EXTERNAL HEMORRHAGES:

PERIPHERAL DETACHMENT OF THE PLACENTA AND MEMBRANE
ESCAPE OF BLOOD THROUGH THE CERVIX
EXTERNAL BLEEDING

***CONCEALED HEMORRHAGE LESS FREQUENCY

BLEEDING BETWEEN PLACENTA AND UTERUS
BLOOD TRAPPE BEHIND THE PLACENTA AND DOES NOT ESCAPE




ETIOLOGY:

SPONTANEOUS RUPTURE OF BLOOD VESSELS AT THE PLACENTAL BED
INABILITY OF THE UTERUS TO CONTRACT AND THUS CLOSE OFF TORN VESSELS
FORMATION OF THE RETROPLACENTAL CLOT.

MATERNAL HYPERTENSION 50%

LESS FREQUENT:

TRAUMA
SUDDEN DECOMPRESSION OF THE UTERUS
RUPTURE MEMBRANE IN THE HYDRAMNIOS
TWIN GESTATION

PERIPHERAL DETACHMENT LESS SEVERE THAN CENTRAL DETACHMENT.



DIAG:

SIGNS AND SYMPTOMS HIGH INDEX OF SUSPICION
FETAL MONITORING
THE CONTRACTION MONITOR MAY SHOWED COUPLED CONTRACTIONS [WITH NO RETURN OF UTERINE RELAXATION TO BASELINE RESTING TONE] AND INCREASED FREQUENCY OF CONTRACTION.
PREMATURE UTERINE CONTRACTION THAT CANNOT BE CONTROLLED WITH TOCOLYTIC AGENTS SUGGEST A SMALL OR CHRONIC ABRUPTION
THE DEMONSTRATION OF A RETROPLACENTAL CLOT BY ULTRASOUND SCAN MAY HELP IN MAKING THE DIAG OF P.A.

CLOTTING STUDY MAY REVEAL:

THROMBOCYTOPENIA
HYPOFIBRINOGENEMIA
FIBRIN SPLIT PRODUCTS

MANAGEMENT:

CAN DVLP : CIVD
HYPOVOLEMIA

IMMEDIATE DELIVERY IS NOT NECESSARY IF THE FETUS IS ALIVE AND NOT DISTRESSED

CESAREAN INDICATED WHENEVER THE MONITOR DETECTS DISTRESS OR MATERNAL HEMORRHAGE.


RAPID DELIVERY IS NECESSARY IF THE FETUS IS A LIVE AND DISTRESSED


VAGINAL DELIVERY IS THE PREFFERED METHOD IF THE FETUS IS DEAD.
 a: obstectrical:

RUPTURE UTERUS
RUPTURE VASAPREVIA
***BLOODY SHOW: ADMIXTURE OF MUCUS ASSOCIATED WITH LABOR




***RUPTURE VASA PRAVIA: FETUS CAN BLEED TO DEATH

PAINLESS
VAGINAL BLEEDING [NO UTERUS CONTRACTION]
CAUSE: ***RUPTURE VASA PRAEVIA
***RUPTURE PLACENTAL ==> FETAL LOOSE BLOOD.
DIAG : FETAL [NUCLEATED ] RED BLOOD CELL SCAN BE IDENTIFIED BY OBTAINING A GLASS SMEAR OF THE BLLOD AND STAINING IT WITH WRIGHT’S STAIN
***RUPTURE UTERUS:

WHEN A WELL CONTRACTED UTERUS SHOWS EXCESSIVE BLOOD LOSS AFTER REMOVAL OF THE PLACENTA.
  COMPLICATION:

HEMORRHAGIC SHOCK
CONSUMPTION COAGULOPATHY
RENAL FAILURE: ACUTE TUBULAR NECROSIS
RENAL CORTICAL NECROSIS: RARE
COUVELAIRE UTERUS
 B/ NON OBSTECTRICAL :

LOCAL FACTORS:

1.    VAGINAL

2.    CERVIX


1.    VAGINAL:

***VAGINAL LACERATION

***CONDYLOMA ACUMINATUM

2 . CERVIX

***EROSION ,

***POLYPS, CONDYLOMA ACUMINATUM

***CARCINOMA OF THE CERVIX .



ABRUPTIO PLACENTA

CLINICAL FEATURES
 MILD
 MODERATE
 SEVERE
PLACENTAL BLEEDING


PLACENTA SURFACE


ABDOMINAL PAIN


UTERINE TONICITY


FETAL DISTRESS


MATERNAL COAGULOPATHY
 <500


<1/4


LOWER DISCONFORT


INCOMPLETE RELAXATION


NO DISTRESS


ALTERED COAGULATION PROFILE
 500-1000 ML


1/4 - 1/2


CONTINUOUS TENDERNESS


SUSTAINED FIRM CONTRACTION


DISTRESS


POSSIBLE EARLY CONSUMPTION COAGULOPATHY
 >500 OR CONCEALING


>1/2


KNIFE LIKE TEARING


BOARD LIKE UNRELAXED


SEVERE DISTRESS OR DEMISE


AHOCK

OLIGURIA -CONSUMPTION COAGULOPATHY



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                  DYSFUNCTIONAL UTERINE BLEEDING:               .DUB      


DEF: EXCESSIVE UTERINE BLEEDING WITH NO DEMONSTRABLE ORGANIC CAUSE.

CAUSE :

ABNORMALITIES OF ENDOCRINE ORIGIN
MOST OFTEN ASSOCIATED WITH ANOVULATION
OCCASIONALLY ASSOCIATED WITH OVULATORY CYCLES THAT HAVE SHORT OR INADEQUATE FOLLICULAR OR LUTEAL PHASES.

***INTERMENTRUAL BLEEDING

***MENOMETRORRAGHIA

***MENORRHAGIA =HYPERMENORRHEA

***METORRHAGIA

***POLYMENORRHEA

***OLIGOMENORRHEA


ETIOLOGY OF DUB:

+++ANOVULATION CYCLE

+++OVULATORY CYCLES:          *** MIDCYCLE SPOTTING

                              ***FREQUENT MENSES

                              ***LUTEAL PHASE DEFICIENCY

                              ***PROLONGED CORPUS LUTEUM ACTIVITY

1/ANOVULATION CYCLES:

OCCURS IN THE ABSCENCE OF CYCLE HORMONALES CHANGES THAT DETERMINE THE MENSTRUAL CYCLE.

90% IS ANOVULATORY IN NATURE.


2/ OVULATORY CYCLES :


A/ MIDCYCLE SPOTTING:

o        SCANTY[LITTLE] INTERMENTRUAL DISCHARGE

o        DECREASE IN ESTROGEN AT MIDCYCLE ,FOLLOWING OVULATION.



B/FREQUENT MENSES:

o        =POLYMENORRHEA

ASSOCIATED WITH A SHORT FOLLICULAR PHASE



C/ LUTEAL PHASE DEFICIENCY:

o        ASSOCIATED WITH PREMENSTRUAL SPOTTING [STIGMA]

o        RESULT WHEN THE LUTEAL PHASE IS SHORTENED BY PREMATURELY DECREASED PROGESTERONE LEVELS.

D/ PROLONGED CORPUS LUTEUM ACTIVITY.

IS THE RESULT OF PERSISTENT PROGESTERONE PRODUCTION IN THE ABSCENCE OF PREGANCY

RESULTING IN PROLONGED CYCLES OR PROTRACTED [PROLONGED] MENSTRUAL BLEEDING


INTERMENSTRUAL BLEEDING

IS BLEEDING THAT OCCURS BETWEEN REGULAR MENSTRUAL PERIODS AND VARIES IN AMOUNT

MENOMETRORRHAGIA

IS PROLONGED UTERINE BLEEDING THAT OCCURS AT IRREGULAR INTERVALS.

MENORRHAGIA =HYPERMENORRHEA

IS PROLONGED [EXCEEDING 7 DAYS] AND EXCESSIVE [GREATER THAN 80 ML ] UTERINE BLEEDING THAT OCCUR AT REGULAR INTERVAL.

METRORRHAGIA

IS UTERINE BLEEDING THAT OCCUR AT IRREGULAR BUT FREQUENT INTERVALS -THE DURATION OF THE BLEEDING IS OFTEN PROLONGED

POLYMENORRHEA

IS UTERINE BLEEDING THAT OCCURS AT REGULAR INTERVALS LESS THAN 21 DAYS APART

OLIGOMENORRHEA

IS INFREQUENT UTERINE BLEEDING THAT OCCURS MORE THAN 40 DAYS APART



--------------------------------------------------------------------------------


PHYSIOLOGY OF DUB

1/ ANOVULATORY BLEEDING:

OSTROGEN WITHDRAWAL

OSTROGEN BREAKTHROUGH [NEWTHING] [ORIGINATION] BLEEDING.

THE ANOVULATORY PATIENT MUST DEPEND [RELY] ON ENDOGENOUS ESTROGEN TO CURE [HEAL] OR REHABILATE THE ENDOMETRIUM.


1/ THE HEALING IS TEMPORARY


2/ QUIKLY AS THE ENDOMETRIUM REBUILDS,TISSUE FRAGILITY AND BREAKDOWN RECUR AT OTHER ENDOMETRIAL SITES


B/ BLEEDING PATTERN:

B1/HEAVY BLEEDING:

DUE TO HIGH SUSTAINED LEVELS OF ESTROGEN AND ACCOMPANIES:

      +++POLYCYSTIC OVARIAN DISEASE

      +++OBESITY

      +++IMMATURITY OF THE HYPOTHALAMIC-PITUITARY OVARIAN AXIS

      +++LATE ANOVULATION


B2/ PROLONGED AND EXCESSIVE FLOW :

DEGRADATION OF THE ENDOTRIUM



MANAGEMENT OF DUB

A/ DIAG:

1/ENDOMETRIAL SAMPLING

      +++ENDOMETRIAL BIOPSY

      +++ENDOMETRIAL ASPIRATION

      +++DILATION AND CURETTAGE [D AND C]

2/HYSTEROSCOPY ,OR DIRECT VISUALIZATION OF THE ENDOMETRIAL CAVITY

3/BLOOD STUDIES

      +++HCG

      +++PLATELET COUNT AND FUNCTION TESTS TO DETERMINE THE       PRESENCE OF VON WILLERBRAND DISEASE OR THROMBOPENIA .

      +++COMPLETE BLOOD COUNT [PRESENCE OF LEUKEMIA]

ABNORMAL UTERINE BLEEDING :DIFFERENTIAL DIAG

REPRODUCTIVE TRACT PATHOLOGY
ENDOMETRITIS
ENDOMETRIAL POLYPS
uterine LEIMYOMA
PREGNANCY:  +++THREATENED ABORTION
       +++ECTOPIC PREGNANCY

      +++HYDATIDIFORM MOLE

ENDOMETRIAL HYPERPLASIA
ENDOMETRIAL CARCINOMA
CERVICAL NEOPLASIA
MEDICATION:
ESTROGEN ADMINISTRATION
ESTROGEN CONTAINING VAGINAL CREAM
COMBINATION ORAL CONTRACEPTIVES
ASPIRIN
TRAUMA:
FOREIGN BODY
INTRAUTERINE DEVICE [IUD]
OVULATORY DYSFUNCTION:
ANOVULATION
LUTEAL PHASE DEFICIENCY
ENDOCRINE GLAND DYSFUNCTION:
HYPOTHYROIDISM
HYPERTHYROIDISM
PITUITARY ADENOMA
SYSTEMIC DISEASE:
HEMATOLOGIC DISORDERS
+++VON WILLEBRAND'S DISEASE

+++THROMBOCYTOPENIA


CIRRHOSIS


THERAPEUTIC WEAPONS:

      +++ESTROGENS

      +++PROGESTINS

      +++COMBINATION OF AN ESTROGEN AND PROGESTIN

      +++NONSTEROIDAL ANTI-INFLAMMATORY DRUGS [ NSAIDs]



B/ ESTROGENS:

1/BLEEDING RESPONDS TO ESTROGEN THERAPY [RAPID GROWTH OF ENDOMETRIAL TISSUE OCCURS OVER THE DENUDED AND UNFINISHED [RAW] EPITHELIAL SURFACES.


2/ USING CONJUGATED ESTROGEN [10 MG/DAY IN DIVIDED DOSES] CONTROLS MOST ACUTE BLEEDING IN 24 HOURS.

-THE CONJUGATED ESTROGEN IS CONTINUED AT THE SAME DOSE AND A PROGESTIN [MEDROXYPROGESTERONE] IS ADDED AT 10MG/DAY .

-BOTH HORMONES ARE THEN CONTINUED FOR ANOTHER 7-10 DAYS.


3/PARENTERAL ESTROGENS:

IS EFFECTIVE IN TREATING ACUTE PROFUSE DUB.

-20MG OF CONJUGATED ESTROGEN IV EVERY 4-6 HOURS

BLEEDING STOPS IN 12 HOURS

-A PROGESTIN MUST BE STARTED AT THE SAME TIME.


4/COMBINATION OF AN ESTROGEN AND A PROGESTIN [ORAL CONTRACEPTIVES]

-STOP DUB

TRT CONTINUED FOR AT LEAST 1 WEEK AFTER THE BLEEDING STOPS

-ORAL CONTRACEPTIVES ARE LESS EFFECTIVE IN CONTROLLING BLEEDING THAN HIGH DOSES OF CONJUGATED ESTROGEN .

      ***THE COMBINATION OF ESTROGEN AND PROGESTIN DOES NOT AFFORD AS RAPID AN ENDOMETRIAL GROWTH PATTERN AS ESTROGEN ALONE .

      ***THE PROGESTIN DECREASES THE SYNTHESIS OF ESTROGEN RECEPTORS ,THUS DECREASING THE GROWTH PROMOTTING ACTION OF ESTROGEN ON THE FRAGMENTED ,BLEEDING ENDOMETRIUM .


5/ NON STEROIDAL ANTI INFLAMMATORY DRUGS [ NSAIDs]

- INHIBIT PROSTAGLANDIN SYNTHESIS

-PROSTAGLANDIN ACTION:  +++THROMBOXANE: PLATELET PROAGGREGATING

            +++PROSTACYCLIN: ANTIAGGREGATING VASODILATOR.

-THE CONCENTRATION OF PROSTAGANDINS:

      ***INCREASE PROGRESSIVILY DURING THE MENSTRUAL CYCLE

      ***PROSTAGLANDIN SYNTHETASE INHIBITORS DECREASE MENTRUAL    BLOOD LOSS.

-NSAIDs ALTERING THE BALANCE BETWEEN THROMBOXANE AND PROSTACYCLIN.

-IDEAL PHARMACOLOGIC=BLOCK SYNTHESIS OF JUST PROSTACYCLIN WITHOUT DECREASING THROMBOXAN FORMATION .

NSAIDs ARE PRIMARILY EFFECTIVE IN REDUCING MENSTRUAL BLOOD LOSS IN WOMEN WHO OVULATE.



--------------------------------------------------------------------------------


***DYSFUNCTIONAL UTERINE BLEEDING IS FREQUENTLY ASSOCIATED WITH :

      +++ANOVULATION


***THE ABNORMAL PATTERN OF BLEEDING THAT APPEARS IN CONJUNCTION WITH A SHORT FOLLICULAR PHASE IS CALLED :

      +++POLYMENORRHEA


***WHICH DIAG MIGHT BE ASSOCIATED WITH DYSFUNCTIONAL UTERINE BLEEDING:

      +++POLYCYSTIC OVARIAN DISEASE


***A 15 YEARS OLD GIRL IS BROUGHT TO THE PHYSICIAN'S OFFICE BY HER MOTHER BECAUSE SHE THINKS THAT HER DAUGHTER IS HAVING ABNORMAL BLEEDING .

THE PATIENT HAD HER FIRST MENSES 18 MONTHS PRIOR TO THE OFFICE VISIT.

WHICH O OF THE FOLLOWING CHARACTERIZES BLEEDING IN YOUNG WOMEN OF THIS AGE?

      +++ANOVULATORY BLEEDING


***WHICH TERM BEST DESCRIBES MENSES WITH A 100ML BLOOD LOSS EVERY 35 DAYS?

      +++MENORRHAGIA


***FUNCTIONS OF PROGESTINS INCLUDE ALL OF THE FOLLOWING:

      +++TREATING ENDOMETRIAL HYPERPLASIA

      +++DIMINISHING THE EFFECT OF ESTROGEN ON TARGET CELLS

      +++SUPPORTING AND ORGANIZING THE ENDOMETRIUM

      +++PROVIDING ANTIMITOTIC ACTIVITY.

EXCEPT:

+++ENHANCING ESTROGEN RECEPTOR REPLENISHMENT IN THE CELL




--------------------------------------------------------------------------------

THE POST PARTUM INVERTED UTERUS IS ONE OF THE EMERGENCY OBSTECTRICAL, DEATH CAN OCCUR QUICKLY BECAUSE OF BOTH BLOOD LOSS AND NEUROGENIC SHOCK.

GENERAL ANESTHESIA IS USED

ENFLURANE , LIKE HALOTHANE PRODUCES SIGNIFICANT UTERUS RELAXATION.


ANESTHETIC:PAINFUL LIKE LABOR WITHOUTCERVICAL CHANGE :INTRAMUSCULAR MORPHINE

PUDENDAL BLOCK:SPONTANEOUS DELIVERY AND EPISIOTOMY

             NOT ADEQUATE FOR A FORCEPS DELIVERY


SEXUAL AMBIGUITY MAY BE SEEN IN : MIXED GONADAL DYSGENESIS


DUB: IMMATURE HYPOPITUITARY AXIS

HETEROSEXUAL PRECOCIOUS PUBERTY: 21-HYDROXYLASE DEFECT


LH:STIMULATES ANDROGENE SECRETION

FSH: STIMULTES AROMATASE ACTIVITY


CAUSE OF PELVIC INFLAMATORY DISEASE:      ***CROHN'S DISEASE
                                          ***APPENDICITIS

                                          ***SARCOIDOSIS

                                          ***SHISTOSOMIASIS

      EXCEPT: SYPHILIS


THE FOLLOWING CONDITIONS HAVE BEEN IMPLICATED IN THE PATHOGENESIS OF ENDOMETRIOSIS:

                  ***COELOMIC METAPLASIA

                  ***RETROGRADE MENSTRUATION

                  ***IMMUNOLOGIC DEFICIENCY

                  ***LYMPHATIC SPREAD OF ENDOMETRIAL FRAGMENTS


HIGH ESTROGEN LEVELS IN PREGNANCY PREDISPOSE TO CHOLELITHIASIS


AN ABNORMAL FINDING IN A NEW BORN GIRL WOULD BE : AN INCREASED CORD BLOOD IGM LEVEL

NORMAL FINDING IN A NEW BORN GIRL WOULD BE :

HB OF 18G/DL
VAGINAL BLEEDING
GYNECOMASTIA
TOTAL BILIRUBINE OF 2mg/dl

CHEMICAL CONJUNCTIVITIS IS MOST LIKELY RESPONSIBLE FOR CONJUNCTIVAL IRRITATION IN A NEW BORN 24H AFTER AN UNEVENTFUL DELIVERY.
GONOCOCCAL OPHTALMIA è 2-3DAYS AFTER BIRTHè 21 DAYS IF PROPHYLAXIS IS GIVEN

CHLAMYDIAL CONJUNCTIVITIS IS THE MOST COMMON INFECTIONS 5-23 DAYS AFTER BIRTH

STAPHYLOCOCCUS IS THE LESS COMMON.



--------------------------------------------------------------------------------


DIFFERENTIAL DIAG OF VAGINAL INFECTIONS

DIAG CRITERIA
 NORMAL
 BACTERIAL VAGINOSIS
 TRICHOMONAS VAGINITIS
 CANDIDA VULVOVAGINITIS
VAGINAL PH
 3.8-4.2
 >4.5
 4.5
 <4.5
DISCHARGE
 WHITE , THIN, FLOCCULENT
 THIN WHITE GRAY
 YELLOW GREEN FROTHY
 WHITE, CURDY

"COTTAGE CHEESE"
AMINE ODOR "WHIFF TEST"
 ABSCENT
 FISHY
 FISHY
 ABSCENT
MICROSCOPIC
 LACTOBACILLI, EPITHELIAL CELLS
 CLUE CELLS. ADHERENT COCCI

NO WBC'S
 TRICHOMONADS

WBC>10/hpf
 BUDDING YEAST,HYPHAE.PSEUDOHYPHAE.



--------------------------------------------------------------------------------


GENITAL WARTS ARE CAUSED BY A VIRUS: HUMAN PAPILLOMA VIRUS [HPV] GENITAL TYPE.
INFECTION WITH HPV IS SPREAD BY SEXUAL[VAGINAL, ANAL, ORAL SEX] CONTACT OR FROM MOTHER TO BABY AT THE TIME OF DELIVERY
HPVè CAULIFLOWER LIKE CLUSTERS ON THE GENITALS [6-WEEKS TO 8 MONTHS AFTER CONTAMINATION]
TRT: FREEZING BY LIQUID NITROGEN
LASER THERAPY
ELECTRICAL HEAT


--------------------------------------------------------------------------------


SEXUALLY TRANSMITTED DISEASE



CLASSIC:

***GONORREHEA

***SYPHILIS

***CHANCROID

***LYMPHOGRANULOMA VENEREUM

***GRANULOMA INGUINALE.

[***AIDS]



BACTERIAL STD'S:

***NEISSERIA GONORRHOEAE

***HEMOPHILUS DUCREYI

***CALYMMATO BACTERIUM GRANULOMATIS

***GARDNERELLA VAGINALIS

_

1/ NEISSERIA GONORRHEAE:

GRAM NEGATIVE DIPLOCOCCUS

MOST COMMONLY REPORTED COMMUNICABLE DISEASE

HUMAN NATURAL HOST

PREDILECTION FOR COLUMNAR EPITHELIUM .

GROWS : CERVIX [MOST FREQUENT IN WOMEN], URETHRA, MOUTH, RECTUM.

GONORRHEA CAN BE PASSED FROM AN INFECTED WOMEN TO HER NEW BORN DURING DELIVRY.

WHEN INFECTION IN CHILDREN : SEXUAL ABUSE

IT CAUSE : WOMEN +++CERVICITIS

+++URETHRETIS

+++PELVIC INFLAMMATORY DISEASE [PID]

+++ACUTE PHARYNGITIS IN WOMEN


MEN +++URETHRITIS.

+++PROSTATITIS.

+++EPIDIDYMITIS.


EPIDEMIOLOGY: EPIDEMIC LEVELS

15-29 YEARS OLD

RISK FACTOR: ***YOUNG AGE

***MULTIPLE SEXUAL PARTNERS

***FAILURE TO USE BARRIER CONTRACEPTION


CLINICAL PRESENTATION: ***INCUBATION 3-5 DAYS

***40-60% OF WOMEN WITH GONORRHEA DVLP ONSET AT THE END OF

MENSTRUATION [PARTICULARLY WITH GONOCOCCAL PID]



***SYMPTOMS: -PURULENT CERVICAL DISCHARGE AS OCCURS IN ACUTE CERVITIS

-LOWER ABDOMEN PAIN

-ANOREXIA


-FEVER AS IS CHARACTERISTIC OF ACUTE PID.



DIAG: +++GRAM STAIN OF CERVICAL SECRETION [DETECTING DIPLOCOCCI OR POLYMORPHISM POLYNUCLEAR CELLS]

+++THAYER -MARTIN CULTURE MEDIUM

+++GONOZYME TEST [IMMUNOASSAY DETECTING GONOCOCCAL ANTIGENS]

COEXISTING CHLAMYDIAL INFECTION CAN OCCUR 45% OF PATIENTS


TRT: CONSIDER : +++SINGLE DOSE EFFICACITY

+++COEXISTING CHLAMYDIAL INFECTION


TRT: +++CEFTRIAXONE 200MG IM + DOXYCLYCLINE 100 ORALLY X 2/DAY -7DAYS.

+++NON PENICILLIN -RESISTANT GONORRHEA, AMOXICILLIN 3G ORALLY DAILY + PROBENICID 1G DAILY FOLLOWED BY DOXYCICLINE ORAL 100 MG TWICE DAILY.

+++IN RESISTANT INFECTIONS OR PENICILLASE -PRODUCING N-GONORRHEA,SPECTINOMYCIN 2G IM FOLLOWED BY DOXYCICLINE 2 DAILY FOR 7 DAYS.

FOLLOW UP CULTURE IN 4-7 DAYS SHOULD BE OBTAINED .

+++PATIENTS WITH ACUTE PID --->HOSPITALIZATION AND BROAD SPECTRUM ANTIBIOTICS.


_

2/ H.DUCREYI [CHANCROID]:

`ULCERATIVE GENITAL DISEASE

NONMOTOLE,GRAM NEGATIVE ROD

CHARACTERISTIC : CHAINING APPARENCE ON GRAM STAIN.


EPIDEMIOLOGY: ***RARE IN USA

***IN USA SEEN MOST COMONLY IN YOUNG SEXUAL ACTIVE MEN WHO VISIT PROSTITUTES.

***TRAUMA FACILITATE ENTRY INTO MUCOSAL VULVAR TISSUES IN WOMEN

***INCUBATION TIMES 3-5 DAYS.


CLINIC: ***LESION IS A SOFT SORE

***OR CHANCRE WITH A SUPERFICIAL ,NECROTIC ULCER BASE SURROUNDER BY A RED HALO.

***THE LESION IS TENDER ,50% OF THE CASE IS ACCOMPANIED BY INFLAMMATORY INGUINAL ADENOPATHY [BUBO].


DIAG : ***GRAM'S STAIN OF EXUDATE FROM THE CHANCRE

***GRAM'S STAIN OF THE ASPIRATE OF THE BUBO


TRT: ***10 DAYS OF ORAL SULFONAMIDES OR TETRACYCLINE.


_3/C GRANULOMATIS:

GRAM NEGATIVE ROD

GRANULOMATOUS AND ULCERATIVE LESIONS OF THE LOWER GENITAL TRACT .


EPIDEMIOLOGY : ***RARE IN USA

***INTESTINAL RESERVOIR FOR C.GRANULOMATIS

***INCUBATION TIME 1 MONTH


CLINIC: 1/ INITIAL LESION: INDOLENT ,IRREGULAR ULCER WITH A PINK TO BEEFY RED BASE


2/ SECONDARY PHASE: BEEFY RED EXUBERANT GRANULATION TISSUE WITH SCAR FORMATION .

INGUINAL SWELLING AND SUPPURATIVE ABSCESS MAY OCCUR SECONDARY TO GRANULOMATOUS TISSUE FORMATION.


3/ ADVANCED LESIONS: HYPERTROPHIC

FISTULAS OF THE ADJACENT STRUCTURES OF THE VAGINA ,BLADDER,AND RECTUM MAY OCCUR .

HEMATOGENOUS SPREAD TO DISTANT SITES.


DIAG: ***GRAM'S STAIN OF THE LESION REVEALS PATHOGNOMONIC CELLS.

THE MONONUCLEAR CELLS WITH INTRACYTOPLASMIC INCLUSION CYSTS CONTAIN ING THE PLEOMORPHIC ROD LIKE ORGANISM =DONOVAN'S BODIES.

*** TISSUE BIOPSIES: DEMONTRATE DONOVAN'S BODIES ON WRIGHT'S OR GIEMSA STAINS

TRT: ***TETRACYCLINE 500 MG ORALY 4 TIMES PER DAY FOR 3 WEEKS .


***IN ADVANCE CASES : VULVAR AND PELVIC RECONSTRUCTIVE SURGERY





 Chlamydial Infection
Chlamydial ("kla-mid-ee-uhl") infection is the leading sexually transmitted disease (STD) in the United States today, with an estimated 4 million new cases occurring each year.

When diagnosed, chlamydia can be easily treated and cured. Up to 40% of women with untreated chlamydia will develop Pelvic inflammatory disease (PID), a serious complication of chlamydial infection, Undiagnosed PID caused by chlamydia is common. Of those with PID, 20% will become infertile; 18% will experience debilitating, chronic pelvic pain; and 9% will have a life-threatening tubal pregnancy.

Chlamydial infection is caused by a bacterium, Chlamydia trachomatis, and is transmitted during vaginal or anal sexual contact with an infected partner. A pregnant woman may pass the infection to her newborn during delivery, with subsequent neonatal eye infection or pneumonia.

Chlamydia is also common among young men. Untreated chlamydia in men typically causes urethral infection, but may also result in complications such as swollen and tender testicles.

Symptoms
Men and women with chlamydial infections may experience abnormal genital discharge or pain during urination. These early symptoms of chlamydial infection may be absent or very mild. If symptoms occur, they usually appear within 1 to 3 weeks after exposure. One of every two infected women and one of every four infected men may have no symptoms whatsoever. As a result, the disease is often not diagnosed until complications develop.

In women, chlamydial infections can result in PID; in men, these infections may lead to pain or swelling in the scrotal area, which is a sign of epididymitis, an inflammation of a part of the male reproductive system located near the testicles. Left untreated, this condition, like PID in women, can result in infertility.

Chlamydial bacteria can cause proctitis (inflamed rectum) and conjunctivitis (inflammation of the lining of the eye). The bacteria have also been found in the throat as a result of oral sexual contact with an infected partner. A particular strain of chlamydia causes an uncommon STD called lymphogranuloma venereum (LGV), which is characterized by prominent swelling and inflammation of the lymph nodes in the groin. Complications may follow if LGV is not treated.

Diagnosis
Chlamydial infection is easily confused with gonorrhea because the symptoms of both diseases are similar, and they often occur together. Until recently, the only way to diagnose chlamydial infection was to take a sample of secretions from a patient's genital area and attempt to grow the organism in specialized tissue culture in the laboratory. Although still considered the most definitive test, this method is expensive and technically difficult, and test results are not available for up to 3 days.

Scientists have developed several rapid tests for diagnosing chlamydial infection that use sophisticated techniques and a dye to detect bacterial proteins. Although these tests are slightly less accurate, they are less expensive, more rapid, and can be performed during a routine checkup.

Treatment
A 7-day course of antibiotics such as tetracycline or doxycycline is the recommended treatment for chlamydial infection. Other antibiotics are effective, however, and can be used if tetracycline cannot be taken. For example, pregnant women should not take tetracycline, but rather can be treated with erythromycin. Penicillin, which is often used for treating some other STDs, is not effective against chlamydial infections. New medications are being developed that should greatly simplify treatment and help control the spread of chlamydia in the population.

It is very important that a person with chlamydial infection take all of the prescribed medication, even after symptoms disappear. To be sure that the infection is cured, a follow-up visit to the doctor or clinic 1 to 2 weeks after finishing the medication may be necessary. All sex partners of a person with chlamydial infection should be evaluated and treated to prevent re-infection and further spread of the disease.

Pelvic Inflammatory Disease
Each year up to 1 million women in the United States develop PID, a serious infection of the reproductive organs. As many as half of all cases of PID may be due to chlamydial infection, and many of these occur without symptoms. PID can result in scarring of the fallopian tubes, which can block the tubes and prevent fertilization from taking place. An estimated 100,000 women each year become infertile as a result of PID.

In other cases, scarring may interfere with the passage of the fertilized egg to the uterus during pregnancy. When this happens, the egg may implant in the fallopian tube. This is called ectopic or tubal pregnancy. This very serious condition results in the loss of the fetus and is a major cause of maternal death in the United States.

Effects of Chlamydial Infection in Newborns
A baby who is exposed to chlamydial bacteria in the birth canal during delivery may develop conjunctivitis (eye infection) or pneumonia. Symptoms of conjunctivitis, which include discharge and swollen eyelids, usually develop within the first 10 days of life. Symptoms of pneumonia, including a progressively worsening cough and congestion, most often develop within 3 to 6 weeks after birth. Both conditions can be successfully treated with antibiotics. However, because of these risks to the newborn, many doctors now recommend routine testing of all pregnant women for chlamydial infection.

Prevention
Because chlamydial infection often occurs without symptoms, people who are infected may unknowingly pass the bacteria to their sex partners. Many doctors recommend that all persons who have more than one sex partner, especially women under 25 years of age, be tested for chlamydial infection regularly, even in the absence of symptoms. Using condoms (rubbers) or diaphragms during sexual intercourse may help reduce the transmission of chlamydial bacteria. In addition, recent research has shown that women infected with chlamydia have a 3 - 5 fold increased risk of acquiring HIV, if exposed.
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Lymphogranuloma Venereum


Clinical description
Infection with L1, L2, or, L3 serovars of Chlamydia trachomatis may result in a disease characterized by genital lesions, suppurative regional lymphadenopathy, or hemorrhagic proctitis. The infection is usually sexually transmitted.

Laboratory criteria for diagnosis
Isolation of C. trachomatis, serotype L1, L2, or L3, from clinical specimen, or
Demonstration of inclusion bodies by immunofluorescence in leukocytes of an inguinal lymph node (bubo) aspirate, or
Positive microimmunofluorescent serologic test for a lymphogranuloma venereum strain of C. trachomatis (in a clinically compatible case)
Case classification
Probable: a clinically compatible case with one or more tender fluctuant inguinal lymph nodes or characteristic proctogenital lesions with supportive laboratory findings of a single C. trachomatis complement fixation (CF) titer of greater than 64

Confirmed: a case that is laboratory confirmed


--------------------------------------------------------------------------------

 Gonorrhea

In 1995, 392,848 cases of gonorrhea in the United States were reported to the U.S. Centers for Disease Control and Prevention (CDC). The Institute of Medicine, however, estimates that 800,000 cases of gonorrhea occur annually in the United States. The annual cost of gonorrhea and its complications is estimated at close to $1.1 billion.

Gonorrhea is caused by a bacterium, Neisseria gonorrhoeae, that grows and multiplies quickly in moist, warm areas of the body including the reproductive tract, the oral cavity, and the rectum. Although in women the cervix usually is the initial site of infection, the disease can spread to and infect the uterus (womb) and fallopian tubes, resulting in pelvic inflammatory disease (PID). This can cause infertility and ectopic (tubal) pregnancy.

The disease is most commonly spread during sexual intercourse – vaginal, oral, and anal. Gonorrhea of the rectum can occur in people who practice anal intercourse and also may occur in women due to spread of the infection from the vaginal area.

Gonorrhea can be passed from an infected woman to her newborn infant during delivery, causing eye infections in the baby. When the infection occurs in the genital tract, mouth, or rectum of a child, it is due most commonly to sexual abuse.

Symptoms

The early symptoms of gonorrhea often are mild, and many women who are infected have no symptoms of the disease. If symptoms of gonorrhea develop, they usually appear within two to 10 days after sexual contact with an infected partner, although a small percentage of patients may be infected for several months without showing symptoms. The initial symptoms in women include a painful or burning sensation when urinating and/or vaginal discharge that is yellow or bloody. More advanced symptoms, which indicate progression to PID, include abdominal pain, bleeding between menstrual periods, vomiting, or fever. Men are more often symptomatic than women. They usually have a discharge from the penis and a burning sensation during urination that may be severe. Symptoms of rectal infection include discharge, anal itching, and sometimes painful bowel movements.

Diagnosis

Three techniques, gram stain, detection of bacterial genes or nucleic acid (DNA), and culture, are generally used to diagnose gonorrhea. Many doctors prefer to use more than one test to increase the chance of an accurate diagnosis. The gram stain is quite accurate for men but is not very sensitive for women. Only one in two women with gonorrhea have a positive gram stain. The test involves placing a smear of the discharge from the penis or the cervix (the opening to the uterus) on a slide and staining the smear with a dye. The slide is examined under a microscope for the presence of the bacteria. A doctor usually can give test results to the patient at the time of an office or clinic visit. More often, urine or cervical swabs are used for a new test that detects the genes of the bacteria. These tests are as accurate as culture and are used widely.

The culture test involves placing a sample of the discharge onto a culture plate and incubating it up to two days to allow the bacteria to multiply. The sensitivity of this test depends on the site from which the sample is taken. Cervical samples detect infection approximately 90 percent of the time. The doctor also can take a throat culture to detect pharyngeal gonorrhea.

Treatment

Because penicillin-resistant cases of gonorrhea are common, other antibiotics are used to treat most patients with gonococcal infections. One of the most effective medicines to treat patients is ceftriaxone, which the doctor can inject in a single dose. Other effective antibiotics that a patient can take by mouth include a single dose of cefixime, ciprofloxacin, or ofloxacin. Pregnant women and patients younger than 18 years old should not take ciprofloxacin or ofloxacin.

Gonorrhea can occur together with chlamydial infection, another common sexually transmitted disease (STD). Therefore, doctors usually prescribe a combination of antibiotics, such as ceftriaxone and doxycycline or azithromycin. Single-dose oral therapy is available. All sexual partners of a person with gonorrhea should be tested and treated if infected whether or not they have symptoms of infection.

Complications

The most common consequence of untreated gonorrhea is PID, a serious infection of the female reproductive organs that occurs in an estimated 1 million American women each year. Gonococcal PID often appears immediately after the menstrual period. PID can scar or damage cells lining the fallopian tubes, resulting in infertility in as many as 10 percent of women affected. If the tube is only partially scarred, proper passage of the fertilized egg into the uterus is prevented. If this happens, the egg may implant in the tube; this is called ectopic or tubal pregnancy and is life-threatening if not detected early. Rarely, untreated gonorrhea can spread to the blood or the joints.

An infected pregnant woman may give the infection to her infant as the baby passes through the birth canal during delivery. A doctor can prevent infection of the eye, called ophthalmia neonatorum, by applying silver nitrate or other medications to the baby’s eyes immediately after birth. Because of the risks from gonococcal infection to both mother and child, doctors recommend that a pregnant woman have at least one test for gonorrhea.

Gonorrhea also increases the risk of HIV infection (HIV, human immunodeficiency virus, causes AIDS), so prevention and early treatment of gonorrhea is critically important.

Prevention

By using male condoms correctly and consistently during sexual activity, sexually active people can reduce their risk of gonorrhea and its complications.

Research

Scientists supported by the National Institute of Allergy and Infectious Diseases (NIAID) are continuing to learn more about the organism that causes gonorrhea and are working on better methods to prevent, diagnose, and treat it. The dramatic rise of antibiotic-resistant strains of the gonococcus underscores the need for a means of preventing gonorrhea. Scientists have developed a laboratory method to detect these resistant strains, which helps the physician select an appropriate treatment.

An effective vaccine against gonorrhea remains a key research priority for NIAID-supported scientists. Determining the sequence of the bacterial genome is expected to aid scientists in identifying new vaccine candidates.


NIAID, a component of the National Institutes of Health, supports research on AIDS, tuberculosis and other infectious diseases as well as allergies and immunology.

Prepared by:
Office of Communications and Public Liaison
National Institute of Allergy and Infectious Diseases
National Institutes of Health
Bethesda, MD 20892

Public Health Service
U.S. Department of Health and Human Services
June 1998


GONORRHEA (Neisseria gonorrhea)
Clap, Drip

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Incidence = 1.5 million cases per year There are about 1 million cases of pelvic inflammatory disease (PID) per year and 1/4 of these suffer serious long-term sequelae. cost per case = $677 total cost = $1,015,970,000


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Clinical Disease
urethritis
epididymitis
pharyngitis
vulvovaginitis
pelvic inflammatory disease (PID)
arthritis/dermatitis syndrome
DGI
ophthalmia neonatorum
keratitis/corneal gonorrhea


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Treatment
1. urogenital, rectal, pharyngeal:
ofloxacin 400 mg x 1 dose
cefixine 400 mg po x 1 dose
ceftriaxone 125 mg IM x 1 dose
Spectinomycin 2 gm IM x 1 dose
children:
erythromycin cefriaxone 125 mg IM x 1 dose or Spectinomycin 40 mg/kg IM x 1 dose
2. conjunctivitis: ceftiaxone 1 gm IM x 1 dose
3. Neonates (ophthalmia,infants born to infected mothers): Cefriaxone, 25-50 mg/kg/day IV or IM x 1 dose
4. PID:
ceftiaxone 250 mg IM x 1 dose + doxycycline 100 mg BIB for 14 days
ofloxacin 400 mg BID for 14 days + metronidazole 500 mg BIB for 14 days or clindamycin 450 mg QID for 14 days


Gonorrhea
What is Gonorrhea?
Gonorrhea, commonly called the "clap", is a sexually transmitted infection caused by bacteria. It is the most common reportable sexually transmitted infection in the United States.

How is it Spread?
Gonorrhea is spread by direct person to person contact. It is almost always transmitted through sexual contact. Gonorrhea can occur in the reproductive organs, urethra, rectum and throat. The most common sites are the urethra in males and the genital tract in females. It is also possible for pregnant women to pass the bacteria to their infant during birth.

How Do I Know If I Am Infected?
Because symptoms are not always present, you may be infected with gonorrhea and not know it. You can be tested for gonorrhea at Student Health Services. To test for gonorrhea, the physician will use a cotton swab to collect cells from your genitals.

What Are The Symptoms?
If present, symptoms appear within 2 to 14 days. Fifty percent of persons with gonorrhea may show no symptoms. Men are more likely than women to show signs of infection.

Gonorrhea in Men:

Painful urination
Creamy or green, pus-like penile discharge
Testicular pain
Gonorrhea in Women:

Creamy or green, pus-like vaginal discharge
Painful urination
Bleeding between periods
Excessive bleeding during menstrual period
Painful intercourse
Lower abdominal pain
Signs of Rectal infection:

Itching
Creamy, pus-like discharge
Rectal bleeding
Pain
Constipation
Are There Any Long Term Complications?
When treated early, there are no long term consequences of gonorrhea. Serious complications can result, however, when left untreated.

Long term complications in men may include:

Epididymitis - an inflammation of the testicles that can cause sterility
Long term complications in women include:

Pelvic Inflammatory Disease - an ascending infection that spreads from the vagina and cervix to the uterus and fallopian tubes. PID can lead to sterility.
Abscesses
Ectopic pregnancy - a pregnancy outside of the uterus
Perihepatitis - an infection around the liver
Sterility
Gonorrhea can be transmitted to newborns.
Approximately 2% of persons with untreated gonorrhea may develop Disseminated Gonococcal Infection (DGI). This is characterized by fever, skin lesions and arthritis type pain.

How Is Gonorrhea Treated?
Gonorrhea can be treated with antibiotics. It is important that all of the antibiotics are taken as prescribed, and that the infected person refrain from sexual intercourse during treatment. Proper hand washing is essential. The bacteria can be transferred to the eyes.

All sex partners should be informed to seek treatment. Because gonorrhea can be silent, they may not show symptoms until long term consequences have occurred.

How Can I Protect Myself?
Abstinence from both genital and oral sex is the only way to be 100% sure that you are protected from gonorrhea and other sexually transmitted infections.

If you are sexually active, you can lower your risk by following these guidelines:

Use condoms. Although condoms do not provide perfect protection, they do provide the best protection available. Condoms should be used for vaginal, anal, and oral intercourse.
Form a monogamous relationship in which both you and your partner are faithful to each other at all times. Do not engage in sexual intimacy until both of you have been tested.
Limit your number of partners. Your risk of acquiring gonorrhea and other STD's increases as your number of partners increases.
Regular check-ups. STD testing should be part of your regular exam. Do not wait for symptoms to appear. You should see your health care provider regularly if you or your partner have other sexual contacts.
DO NOT BECOME SEXUALLY INTIMATE WHEN DRINKING ALCOHOL OR USING OTHER DRUGS. Drugs reduce your ability to make sensible decisions.

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Gonorrhea


Clinical description
A sexually transmitted infection commonly manifested by urethritis, cervicitis, or salpingitis. Infection may be asymptomatic.

Laboratory criteria for diagnosis
Isolation of Neisseria gonorrhoeae from a clinical specimen, or
Observation of gram-negative intracellular diplococci in a urethral smear obtained from a man
Case classification
Probable: demonstration of gram-negative intracellular diplococci in an endocervical smear obtained from a woman, or a written (morbidity) report of gonorrhea submitted by a physician

Confirmed: a case that is laboratory confirmed

 .
Sexually Transmitted Diseases
An Introduction To Sexually Transmitted Diseases
August 1992

Sexually transmitted diseases (STDs), once called venereal diseases, are among the most common infectious diseases in the United States today. More than 20 STDs have now been identified, and they affect more than 13 million men and women in this country each year. The annual comprehensive cost of STDs in the United States is estimated to be well in excess of $5 billion.

Understanding the basic facts about STDs--the ways in which they are spread, their common symptoms, and how they can be treated--is the first step toward prevention. The National Institute of Allergy and Infectious Diseases (NIAID), a part of the National Institutes of Health, has prepared a series of fact sheets about STDs to provide sexually active people with some of this important information. Research investigators supported by NIAID are looking for better methods of diagnosis and more effective treatments, as well as for vaccines that will one day ensure that STDs, like many other infectious diseases, no longer pose serious threats to health. What are some of these basic facts? It is important to understand at least five key points about all STDs in this country today:
1.        STDs affect men and women of all backgrounds and economic levels. They are most prevalent among teenagers and young adults. Nearly two-thirds of all STDs occur in people younger than 25 years of age.
2.        The incidence of STDs is rising, in part because in the last few decades, young people have become sexually active earlier yet are marrying later. In addition, divorce is more common. The net result is that sexually active people today are more likely to have multiple sex partners during their lives and are potentially at risk for developing STDs.
3.        Many STDs initially cause no symptoms, particularly in women. When symptoms develop, they may be confused with those of other diseases not transmitted through sexual contact. However, even when an STD causes no symptoms, a person who is infected may be able to pass the disease on to a sex partner. That is why many doctors recommend periodic testing for people who have more than one sex partner.
4.        Health problems caused by STDs tend to be more severe and more frequent for women than for men, in part because the frequency of asymptomatic infection means that many women do not seek care until serious problems have developed.

Some STDs can spread into the uterus (womb) and fallopian tubes to cause pelvic inflammatory disease (PID), which in turn is a major cause of both infertility and ectopic (tubal) pregnancy. The latter can be fatal.
STDs in women may also be associated with cervical cancer. One STD, human papillomavirus infection (HPV), can result in genital warts, but can also lead to cervical and other genital cancers; the relationship between other STDs and cervical cancer is not yet clear.
STDs can be passed from a mother to her baby before or during birth; some of these infections of the newborn can be cured easily, but others may cause a baby to be permanently disabled or even die.
5.        When diagnosed and treated early, almost all STDs can be treated effectively. Some organisms, such as certain forms of gonococci, have become resistant to the drugs used to treat them and now require newer types of antibiotics. The most serious STD for which no cure now exists is acquired immunodeficiency syndrome (AIDS), a fatal viral infection of the immune system. Experts believe that having STDs other than AIDS increases one's risk for becoming infected with the AIDS virus.
Acquired Immunodeficiency Syndrome
AIDS was first reported in the United States in 1981. It is caused by the human immunodeficiency virus (HIV), a virus that destroys the body's ability to fight off infection. An estimated 1 million people are currently infected in the U.S., including more than 2000 infants, most of whom contracted the disease from their mothers. People who have AIDS are very susceptible to many life-threatening diseases, called opportunistic infections, and to certain forms of cancer.
Transmission of the virus primarily occurs during sexual activity and by sharing of needles used to inject intravenous drugs.
If you have questions about AIDS, you can call the U.S. Public Health Service confidential toll-free hotline number: 1-800-342-2437.
Chlamydial Infections
These infections are now the most common of all STDs, with an estimated 4 million new cases occurring each year. In both men and women, chlamydial infection may cause an abnormal genital discharge and burning with urination. In women, untreated chlamydial infection may lead to PID, one of the most common causes of infertility in women and of ectopic pregnancy. However, many people with chlamydial infection have few or no symptoms of infection. Once diagnosed, chlamydial infections are treatable with an antibiotic drug.
Genital Herpes
Genital herpes affects an estimated 30 million Americans. Approximately 500,000 new cases of this incurable infection develop annually. Herpes infections are caused by herpes simplex virus (HSV). The major symptoms of herpes infection are painful blisters or open sores in the genital area. These may be preceded by a tingling or burning sensation in the legs, buttocks, or genital region. The herpes sores usually disappear within 2 to 3 weeks, but the virus remains in the body and the lesions may recur from time to time. Severe or frequently recurrent genital herpes is now treated with acyclovir, an antiviral drug available by prescription; it helps control the symptoms but does not eliminate the herpes virus from the body. Women who acquire genital herpes during pregnancy can transmit the virus to their babies. Untreated HSV infection in newborns can result in mental retardation and death.

Genital Warts

Genital warts (also called venereal warts, or condylomata acuminata) are caused by a virus related to the virus that causes common skin warts. Genital warts usually first appear as small, hard, painless bumps in the vaginal area, on the penis, or around the anus; if untreated, they may grow and develop a fleshy, cauliflower-like appearance. Genital warts infect 500,000 Americans each year. Scientists believe that the virus responsible for genital warts also may cause several types of genital cancer. Genital warts are treated with a topical drug (applied to the skin), by freezing, or if they recur, with injections of a type of interferon. If the warts are very large, they can be removed by surgery.

Gonorrhea

Approximately 1-1/2 million cases of gonorrhea occur each year in this country. The most common symptoms of gonorrhea are a discharge from the vagina or penis and painful or difficult urination. The most common and serious complications occur in women, and as with chlamydial infections, these complications include PID, ectopic pregnancy, and infertility. Historically, penicillin has been used to treat gonorrhea, but several penicillin-resistant forms of the bacteria have recently appeared. Other antibiotics or combinations of drugs must be used to treat these resistant strains.

Syphilis

Syphilis has increased dramatically in recent years, with more than 130,000 cases reported in 1990. The first symptoms of syphilis may go undetected because they are very mild and disappear spontaneously. The initial symptom is a chancre, a painless open sore that usually appears on the penis or around or in the vagina. If untreated, syphilis may go on to more advanced stages, including a transient rash and, eventually, serious involvement of the heart and central nervous system. The full course of the disease can take years. Penicillin remains the drug most commonly used to treat syphilis.

Other diseases that may be sexually transmitted include trichomoniasis, bacterial vaginosis, cytomegalovirus infections, hepatitis B, scabies, and pubic lice.

STDs in pregnant women are associated with a number of adverse outcomes, including spontaneous abortion, prematurity and infection in the newborn. Low birth weight and prematurity appear to be associated with most acute STDs, including chlamydial infection and trichomoniasis. Congenital or perinatal infection (infection that occurs either during or before birth) occurs in 30-70 percent of infants born to acutely infected mothers and may include pneumonia, potentially blinding eye infections, and permanent neurological damage.

What Can You Do to Prevent STDs?

The best way to prevent STDs is to not have sexual intercourse. If you decide to be sexually active, there are things that you can do to reduce your risk of developing an STD.

Be direct and frank about asking a new sex partner whether he or she has an STD, has been exposed to one, or has any unexplained physical symptoms.
Learn to recognize the physical signs of STDs and inspect a sex partner's body, especially the genital area, for sores, rashes, or discharges.
Don't have sex if your partner has signs or symptoms of STDs. Urge him/her to get medical attention as soon as possible.
Use a condom (rubber) during sexual intercourse and learn to use it correctly. Diaphragms may also reduce the risk of transmission of some STDs. Although there is some laboratory evidence that spermicides can kill STD organisms, scientists are still evaluating the usefulness of spermicides in preventing STDs. Some studies have found that frequent use of spermicides (more than three times a week) may cause vaginal inflammation.
Anyone who is sexually active with someone other than a long-term monogamous partner should:
Have regular checkups for STDs even in the absence of symptoms. These tests can be done during a routine visit to the doctor's office.
Learn the common symptoms of STDs. Seek medical help immediately if any suspicious symptoms develop, even if they are mild.
Anyone diagnosed as having an STD should:
1.        Notify all recent sex partners and urge them to get a checkup.
2.        Follow the doctor's orders and complete the full course of medication prescribed. A follow-up test to ensure that the infection has been cured is often an important final step in treatment.
3.        Avoid all sexual activity while being treated for an STD.
Sometimes people are too embarrassed or frightened to ask for help or information. Most STDs are readily treated, and the earlier a person seeks treatment and warns sex partners about the disease, the less likely that the disease will do irreparable physical damage, be spread to others or, in the case of a woman, be passed on to a newborn baby.
Private doctors, local health departments, and STD and family planning clinics have information about STDs. In addition, the American Social Health Association (ASHA) provides free information and keeps lists of clinics and private doctors who provide treatment for people with STDs. ASHA has a national toll-free telephone number, 1-800-227-8922. Callers can get information from the ASHA hotline without leaving their names.
Research
STDs cause physical and emotional suffering to millions and are costly to individuals and to society as a whole. To help alleviate these burdens, NIAID conducts and supports many research projects designed to improve methods of prevention and to find better ways to diagnose and treat these diseases. NIAID also supports several large university-based STD research centers.
Within the past few years, NIAID-supported research has resulted in new tests to diagnose some STDs faster and more accurately. New drug treatments for STDs are under investigation by NIAID researchers. This is especially important because some STDs are becoming resistant to the standard drugs. In addition, vaccines are being developed or tested for effectiveness in preventing several STDs, including AIDS, chlamydia, genital herpes and gonorrhea.
It is up to each individual to learn more about STDs and then make choices about how to minimize the risk of acquiring these diseases and spreading them to others. Knowledge of STDs, as well as honesty and openness with sex partners and with one's doctor, can be very important in reducing the incidence and complications of sexually transmitted diseases.
Diseases That May Be Transmitted Sexually and the Organisms Responsible








Disease
 Organism(s)

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Acquired Immunodeficiency Syndrome (AIDS)
 Human immunodeficiency virus

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Bacterial vaginosis
 Bacteroides
Gardnerella vaginalis
Mobiluncus spp.
Mycoplasma hominis
Ureaplasma urealyticum

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Chancroid
 Haemophilus ducreyi

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Chlamydial infections
 Chlamydia trachomatis

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Cytomegalovirus infections
 Cytomegalovirus

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Enteric infections
Hepatitis A

Amebiasis
 Hepatitis A virus

Entamoeba histolytica (protozoan)
Giardia lamblia (protozoan)

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Genital herpes
 Herpes simplex virus

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Genital (venereal) warts
 Human papillomavirus

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Gonorrhea
 Neisseria gonorrhoeae

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Granuloma inguinale (donovanosis)
 Calymmatobacterium granulomatis

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Group B streptococcal infections
 Group B-hemolytic streptococcus

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Leukemia/Lymphoma/Myelopathy
 HTLV-I and II

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Lymphogranuloma Venereum
 Chlamydia trachomatis

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Molluscum contagiosum
 Molluscum contagiosum virus

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Pubic lice
 Phthirus pubis

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Scabies
 Sarcoptes scabiei

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Syphilis
 Treponema pallidum

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Trichomoniasis
 Trichomonas vaginalis

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Vaginal yeast infections
 Candida albicans

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Viral hepatitis
 Hepatitis A, B, C, D viruses




Pelvic Inflammatory Disease

Aside from AIDS, the most common and serious complication of sexually transmitted diseases (STDs) among women is pelvic inflammatory disease (PID), an infection of the upper genital tract. PID can affect the uterus, ovaries, fallopian tubes, or other related structures. Untreated, PID causes scarring and can lead to infertility, tubal pregnancy, chronic pelvic pain, and other serious consequences.

Each year in the United States, more than 1 million women experience an episode of acute PID, with the rate of infection highest among teenagers. More than 100,000 women become infertile each year as a result of PID, and a large proportion of the 70,000 ectopic (tubal) pregnancies occurring every year are due to the consequences of PID. In 1997 alone, an estimated $7 billion was spent on PID and its complications.

Cause

PID occurs when disease-causing organisms migrate upward from the urethra and cervix into the upper genital tract. Many different organisms can cause PID, but most cases are associated with gonorrhea and genital chlamydial infections, two very common STDs. Scientists have found that bacteria normally present in small numbers in the vagina and cervix also may play a role.

Investigators are learning more about how these organisms cause PID. The gonococcus, Neisseria gonorrhea, probably travels to the fallopian tubes, where it causes sloughing (casting out) of some cells and invades others. Researchers think it multiplies within and beneath these cells. The infection then may spread to other organs, resulting in more inflammation and scarring.

Chlamydia trachomatis and other bacteria may behave in a similar manner. Researchers do not know how other bacteria that normally inhabit the vagina (e.g., organisms such as Gardnerella vaginalis and Bacteroides) gain entrance into the upper genital tract. The cervical mucus plug and secretions may help prevent the spread of microorganisms to the upper genital tract, but it may be less effective during ovulation and menses. In addition, the gonococcus may gain access more easily during menses, if menstrual blood flows backward from the uterus into the fallopian tubes, carrying the organisms with it. This may explain why symptoms of PID caused by gonorrhea often begin immediately after menstruation as opposed to any other time during the menstrual cycle. It is noteworthy that the co-incidence of menses and chlamydial infection is not a prominent feature of chlamydial PID.

Symptoms

The major symptoms of PID are lower abdominal pain and abnormal vaginal discharge. Other symptoms such as fever, pain in the right upper abdomen, painful intercourse, and irregular menstrual bleeding can occur as well. PID, particularly when caused by chlamydial infection, may produce only minor symptoms or no symptoms at all, even though it can seriously damage the reproductive organs.

Risk Factors for PID

o        Women with STDs – especially gonorrhea and chlamydial infection – are at greater risk of developing PID; a prior episode of PID increases the risk of another episode because the body’s defenses are often damaged during the initial bout of upper genital tract infection.

o        Sexually active teenagers are more likely to develop PID than are older women.

o        The more sexual partners a woman has, the greater her risk of developing PID.

Recent data indicate that women who douche once or twice a month may be more likely to have PID than those who douche less than once a month. Douching may push bacteria into the upper genital tract. Douching also may ease discharge caused by an infection, so the woman delays seeking health care.

Diagnosis

PID can be difficult to diagnose. If symptoms such as lower abdominal pain are present, the doctor will perform a physical exam to determine the nature and location of the pain. The doctor also should check the patient for fever, abnormal vaginal or cervical discharge, and evidence of cervical chlamydial infection or gonorrhea. If the findings of this exam suggest that PID is likely, current guidelines advise doctors to begin treatment.

If more information is necessary, the doctor may order other tests, such as a sonogram, endometrial biopsy, or laparoscopy to distinguish between PID and other serious problems that may mimic PID. Laparoscopy is a surgical procedure in which a tiny, flexible tube with a lighted end is inserted through a small incision just below the navel. This procedure allows the doctor to view the internal abdominal and pelvic organs, as well as take specimens for cultures or microscopic studies, if necessary.

Treatment

Because culture of specimens from the upper genital tract are difficult to obtain and because multiple organisms may be responsible for an episode of PID, especially if it is not the first one, the doctor will prescribe at least two antibiotics that are effective against a wide range of infectious agents. The symptoms may go away before the infection is cured. Even if symptoms do go away, patients should finish taking all of the medicine. Patients should be re-evaluated by their physicians two to three days after treatment is begun to be sure the antibiotics are working to cure the infection.

About one-fourth of women with suspected PID must be hospitalized. The doctor may recommend this if the patient is severely ill; if she cannot take oral medication and needs intravenous antibiotics; if she is pregnant or is an adolescent; if the diagnosis is uncertain and may include an abdominal emergency such as appendicitis; or if she is infected with HIV (human immunodeficiency virus, the virus that causes AIDS).

Many women with PID have sex partners who have no symptoms, although their sex partners may be infected with organisms that can cause PID. Because of the risk of reinfection, however, sex partners should be treated even if they do not have symptoms.

Consequences of PID

Women with recurrent episodes of PID are more likely than women with a single episode to suffer scarring of the tubes that leads to infertility, tubal pregnancy, or chronic pelvic pain. Infertility occurs in approximately 20 percent of women who have had PID.

Most women with tubal infertility, however, never have had symptoms of PID. Organisms such as C. trachomatis can silently invade the fallopian tubes and cause scarring, which blocks the normal passage of eggs into the uterus.

A women who has had PID has a six-to-tenfold increased risk of tubal pregnancy, in which the egg can become fertilized but cannot pass into the uterus to grow. Instead, the egg usually attaches in the fallopian tube, which connects the ovary to the uterus. The fertilized egg cannot grow normally in the fallopian tube. This type of pregnancy is life-threatening to the mother, and almost always fatal to her fetus. It is the leading cause of pregnancy-related death in African-American women.

In addition, untreated PID can cause chronic pelvic pain and scarring in about 20 percent of patients. These conditions are difficult to treat but are sometimes improved with surgery.

Another complication of PID is the risk of repeated attacks of PID. As many as one-third of women who have had PID will have the disease at least one more time. With each episode of reinfection, the risk of infertility is increased.

Prevention

Women can play an active role in protecting themselves from PID by taking the following steps:

o        Signs of discharge with odor or bleeding between cycles could mean infection. Early treatment may prevent the development of PID.

o        If used correctly and consistently, male latex condoms will prevent transmission of gonorrhea and partially protect against chlamydial infection.

Research

Although much has been learned about the biology of the microbes that cause PID and the ways in which they damage the body, there is still much to learn. Scientists supported by the National Institute of Allergy and Infectious Diseases (NIAID) are studying the effects of antibiotics, hormones, and substances that boost the immune system. These studies may lead to insights about how to prevent infertility or other complications of PID. Topical microbicides and vaccines to prevent gonorrhea and chlamydial infection also are being developed. Clinical trials are in progress to test a suppository containing lactobacilli – the normal bacteria found in the vaginas of healthy women. These bacteria colonize the vagina and may be associated with reduced risk of gonorrhea and bacterial vaginosis, both of which can cause PID.

Rapid, inexpensive, easy-to-use diagnostic tests are being developed to detect chlamydial infection and gonorrhea. A recent study conducted by NIAID-funded researchers demonstrated that screening and treating women who unknowingly had chlamydial infection reduced cases of PID by more than 60 percent. Meanwhile, researchers continue to search for better ways to detect PID itself, particularly in women with "silent" or asymptomatic PID.


--------------------------------------------------------------------------------

NIAID, a component of the National Institutes of Health, supports research on AIDS, malaria, tuberculosis and other infectious diseases, as well as allergies and immunology.

Prepared by:
Office of Communications and Public Liaison
National Institute of Allergy and Infectious Diseases
National Institutes of Health
Bethesda, MD 20892

Public Health Service
U.S. Department of Health and Human Services
July 1998


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PELVIC INFLAMMATORY DISEASE - An inflammatory process that results from other pelvic diseases; may result from gonorrhea, chlamydia, ovarian cystic disease, or post-partum infections.


--------------------------------------------------------------------------------

Pelvic Inflammatory Disease (PID)

--------------------------------------------------------------------------------

WHAT IS PELVIC INFLAMMATORY DISEASE?

Pelvic inflammatory disease (PID) is an infection of the upper part of the female reproductive organs, especially the tubes "(salpingitis)". It is a result of sexually transmitted diseases (STDs) such as gonorrhea and chlamydia. These germs first infect the cervix but then go up to infect the uterus and tubes. Other bacteria from the vagina can then follow and make the infection worse. Sometimes PID is a complication of surgery to the uterus (such as an abortion) or the presence of an intrauterine device (IUD).


--------------------------------------------------------------------------------



WHO CAN GET PID?

Any woman who is sexually active may get PID. However, most cases are seen in women who are between the ages of 15 and 25.


--------------------------------------------------------------------------------



WHAT ARE THE SYMPTOMS OF PID?

This infection causes lower abdominal (pelvic) pain and pain during sex. It can also cause bleeding between periods or after sex. There is sometimes a yellow or greenish vaginal discharge that may have a foul odor. If the infection is severe, it also causes fever, chills, nausea and vomiting.


--------------------------------------------------------------------------------



WHAT ELSE CAN HAPPEN AS A RESULT OF PID?

Infections that are not treated or not completely treated can damage the tubes. The damage can block the tubes, making the woman unable to have babies in the future. It can also cause long-term pain. Some severe infections cause abscesses (pus pockets) on the ovaries. It may require surgery to drain the pus or to remove the organs.


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CAN A WOMAN GET PID MORE THAN ONCE?

Yes. Women may get PID after each STD. The more infections a woman gets, the higher her risk of not being able to have babies and/or having chronic pain.


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WHAT IS THE TREATMENT FOR PID?

If the infection is not too severe, antibiotics by mouth and by an injection (shot) can be given. However, if there is no relief within 48 hours, then the woman needs to go to a hospital to receive medicine by vein. Since most cases of PID are caused by STDs, the woman should avoid having sex while being treated. The partner should also be checked and treated for STD. If the partner is not treated, the woman may get PID again, especially if condoms are not used while having sex.


--------------------------------------------------------------------------------



WHAT SHOULD I DO IF I HAVE SYMPTOMS OF PID?

You should get medical care immediately. PID is a serious disease that requires immediate care. Furthermore, other serious conditions need to be ruled out. You should avoid having sex while you have symptoms since most cases of PID are caused by STDs.


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WHAT CAN BE DONE TO PREVENT PID?

Preventing STDs is the most important way to protect against PID. You should avoid sex with infected partners, and use protection like condoms every time you have sex. Try to limit your exposure to STDs. Unprotected sexual activity increases you chance of exposure and infection. If you have more than one partner or your partner has other sexual partners this may increase your chances of getting an STD if you think you may have come in contact with or may be infected with an STD, you should visit a local STD clinic, Family Planning clinic, hospital or doctor to get tested and treated before PID occurs. Your sex partner(s) also should get tested and treated.


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Ask NOAH About: Pelvic Inflammatory Disease (PID)
(Salpingitis)

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Erie County Department of Health
Bureau of Public Health Education and Information

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What Is Pelvic Inflammatory Disease (PID)?
How Do You Get Pelvic Inflammatory Disease (PID)?
How Common Is Pelvic Inflammatory Disease?
What Are Signs of Pelvic Inflammatory Disease?
What Is the Test for Pelvic Inflammatory Disease?
Is There a Cure for Pelvic Inflammatory Disease?
What Can Happen if PID Is Not Treated?
Can Pelvic Inflammatory Disease Be Prevented?


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What Is Pelvic Inflammatory Disease (PID)
Pelvic inflammatory disease, also called salpingitis, is the most common, serious complication of sexually transmitted disease (STDs). It is itself a bacterial infection which attacks a woman's reproductive system. As this infection spreads from the vagin a into the pelvic area it causes an inflammation of the womb, the ovaries, and the Fallopian tubes. Almost all cases of pelvic inflammatory disease (PID) are complications of untreated bacterial infections. PID is referred to as a sexually transmitted dis ease (STD) because the bacteria which result in PID are usually transmitted through sexual relations.


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How Do You Get Pelvic Inflammatory Disease (PID)?
You get PID from untreated bacterial infections within the vagina. These infections are often caused by sexually transmitted disease "organisms". Sometimes you get PID from having sexual or intimate bodily contact with another person who has gonorrhea. If this gonorrhea is not treated, one of the resulting complications is often pelvic inflammatory disease. Other times you get PID from untreated STDs such as chlamydia and other types of vaginitis. PlD is not always transmitted sexually; it may develop fro m other kinds of organisms in the gastrointestinal tract. The use of a birth control method called IUD (intrauterine device) may also lead to chronic PID. An IUD is a plastic device that is inserted into the uterus (womb) to prevent pregnancy.


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How Common Is Pelvic Inflammatory Disease?
Pelvic inflammatory disease is one of the most common STDs. Over one million women experience an episode of PID each year in the United States. This disease occurs most often among women under 25 years of age.


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What Are Signs of Pelvic Inflammatory Disease?
Once PID develops, some women may have painful stomach cramps, bleeding, odorous discharge, fever, chills, or an upset stomach. However, many women show no symptoms at all even though they may be seriously infected.


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What Is the Test for Pelvic Inflammatory Disease?
The doctor will perform a pelvic examination to determine if there are any visible problems. A sample of fluids from the vagina and cervix will also be taken for examination in a laboratory. Women who think they may have PID can be treated by their own do ctor or at any emergency health clinic. This testing and any resulting treatment is confidential. Women under the age of 18 may be examined without the consent of their parents.


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Is There a Cure for Pelvic Inflammatory Disease?
Yes. If treatment is begun promptly this disease can be cured with various combinations of antibiotic drugs. These drugs attack and destroy the bacteria which cause PID. Also any woman who using an IUD (intrauterine device) for birth control should have i t removed before treatment begins. Finally the woman's sex partner should also be examined and treated if necessary. Otherwise she may be repeatedly reinfected with this and/or related STDs.


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What Can Happen if PID Is Not Treated?
If it is not treated at all or if it is treated too late, pelvic inflammatory disease may worsen and cause a woman to become sterile (unable to have a child). PID is the major cause of sterility in young women and repeated episodes of PID increases and wo man's risk of becoming sterile. A woman that becomes pregnant after getting PID may develop an ectopic pregnancy (the embryo develops inside the Fallopian tube instead of the uterus) with internal bleeding which may seriously threaten her life. PID may al so result in abdominal pains for years if it is not treated.


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Can Pelvic Inflammatory Disease Be Prevented?
You can reduce your risk of PID by having sexual relations with only one person who also has sex only with you and is uninfected. You can also reduce your risk by using a contraceptive foam containing nonnoxonol-9 and by having your male partner use a con dom (rubber). Some studies indicate that the spermicide called nonnoxonol-9 may help to prevent some forms of STDs.

If you already had PID, don't use an intrauterine device (IUD) for birth control; this increases your risk of infection. Finally, if you have had PID in the past, even though you have been treated, report to your doctor/clinic immediately if you miss your menstrual period. You should do this because of your increased risk of ectopic pregnancy and its serious consequences.




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PELVIC MALIGNANCY


CERVICAL KC:

***CERVICAL TRANSFORMATION ZONE [TZ]

***INVASIVE CERVICAL KC *MICROINVASIVE CARCINOMA OF THE CERVIX

*INVASIVE CARCINOMA OF THE CERVIX



[RISK FACTORS:

***EARLY SEXUAL INTERCOURSE

***MULTIPLE SEXUAL PARTNERS

***HIGH PARITY

***YOUNG AGE OF FIRST PREGNANCY OR MARRIAGE

***LOW SOCIOECONOMIC STATUS

HUMAN PAPILLOMA VIRUS IS ASSOCIATED WITH CERVICAL NEOPLASIA

TRT CARCINOMA IN SITU [CERVICAL INTRAEPITHELIAL NEOPLASIA] CERVICAL CONIZATION

HYSTERECTOMY

CRYOTHERAPY

CO2 LASER

ELECTROCOAGULATION

SPREADS BY DIRECT LOCAL EXTENSION AND LYMPHATICS TO THE PERIAORTIC LYMPH NODES





ENDOMETRIAL KC:

***ENDOMETRIAL HYPERPLASIA *ADENOMATOUS HYPERPLASIA

*ATYPICAL ADENOMATOUS HYPERPLASIA

***ENDOMETRIAL CARCINOMA *ADENOCARCINOMA 60%

*ADENOACANTHOMA 22%

*SUBTYPE:

PAPILLARY SEROUS CARCINOMA

CLEAR CELL ADENOCARCINOMA

ADENOSQUAMOUS CARCINOMA




OVARIAN KC:

***EPITHELIAL TM 82% *SEROUS = SEROUS CYSTOADENOCARCINOMA

*MUCINOUS

*ENDOMETRIOID


***SEX CORD STROMAL NEOPLASMS *GRANULOSA THECA CELL TUMOR

*GRANULOSA CELL TM

*STERCOLI LEYDIG CELL TM:

ANDROBLASTOMA

ARRHENOBLASTOMA

*GERM CELL TM:

DYSGERMINOMA

ENDODERMAL SINUS TUMOR [PATHGOMONIC = SCHILLER DUVAL BODY]

EMBRYONAL CARCINOMA

CHORIOCARCINOMA

MALIGNANT TERATOMAS +++IMMATURE TERATOMA

+++MONODERMAL TUMORS

+++MATURE TERATOMA WITH MALIGNANT TRANSFORMATION

+++GONADOBLASTOMA


OVARIAN CANCER IS NUMBER 1 CAUSE OF GYNECOLOGIC CANCER DEATH

THE FIFTH MOST COMMON CANCER IN THE US FEMALE

RISK FACTORS = NULLIPARITY

FAMILY HISTORY

ENDOMETRIAL KC

SPEAD BY PERITONEAL SEEDING

TRT : SURGICAL DEBULKING FOLLOWED WITH CHEMOTHERAPY





VAGINAL KC: ***SQUAMOUS CELL CARCINOMA

***DIETHYLSTILBESTROL [DES] RELATED ADENO K


POSTMENOPAUSAL WOMEN

EXTENTION : INGUINAL LYMPH TO THE FEMORAL NODES THEN PELVIC NODES

TRT : RADIOTHERAPY

MELANOMA IS THE #2 CANCER OF THE VULVA- POOR PRGNOSTIC


VULVAR CARCINOMA: ***MICROINVASIVE CARCINOMA

***INVASIVE SQUAMOUS CARCINOMA



 ***ADENOMYOSIS: NORMAL ENDOMETRIAL GLAND ARE GROWING INTO THE MYOMETRIUM

                                 MULTIPAROUS WOMEN [35 YEARS OLD]

                                 DYSMENORRHEA AND MENORRHAGIA

                                 PHYSICAL EXAMINATION: ***FIXED -RETROVERTED UTERUS, WITH SCARRING AND TENDERNESS ALONG THE UTEROSACRAL LIGAMENTS.


***LEIOMYOMA IS THE MOST COMMON PELVIC TUMOR, THE MAJORITY ARE ASYMPTOMATIC AND THE UTERUS IS IRREGULAR IN SHAPE.



***IN AMENORRHEIC PATIENT WHO HAS HAD PITUITARY ABLATION FOR A CRANIOPHARYNGIOMA, THE RESULT IN AN OVULATORY CYCLE = HMG FOLLOWED BY HUMAN CHORIONIC GONADOTROPIN [HCG]


HYPOGONADOTROPIC AMENORRHEA OR SECONDARY AMENORRHEA ARE BOTH HYPOGONADROTROPIC AND HYPOESTROGENIC.

·         KALLMANN’S SYNDROME: IRREVERSIBLE DEFECT IN GONADOTROPIN SYNTHESIS AND AN OLFACTORY SENSORY DEFECT.

·         EMOTIONAL STRESS

·         NUTRITIONAL DEFICIENCY [ANOREXIA NERVOSA]

·         DRUGS:                ***BIRTH CONTROL PILLS

                                ***PHENOTHIAZINE

                                ***RESERPINE

                                ***GANGLIA BLOCKING AGENTS.

·         DISEASE OF THE PITUITARY :

                                ***TUMORS:      -CRANIOPHARYNGIOMAS

                                                                -CHROMOPHOBE ADENOMAS

                                                                -PROLACTIN PRODUCING ADENOMAS

                                ***ISCHEMIC AND NECROSIS OF THE PITUITARY GLAND SECONDARY TO OBSTECTRIC SHOCK [BLOOD LOSS].


***FOLLICLE STIMULATING HORMONE AND LH ARE ELABORATED BY :

                                                -BASOPHILLIC CELLS OF THE ADENOHYPOPHYSE [ANTERIOR PITUITARY].


***WOMEN WITH MILD TO MODERATE ENDOMETRIOSIS TRT EXCEPT: DEXAMETHASONE

TRT: DANAZOL - PROGESTINS - GNRH - CONSERVATIVE SURGERY


***DANAZOL

·         USED IN TRT OF ENDOMETRIOSIS AND FIBROCYSTIC BREAST DISEASE

·         WEAK PROGESTATIONAL AND ANDROGENIC AGENT.

·         DANAZOL = PROGESTIN

·         ACTION IN : CONTRACEPTION

·         DUB

·         ENDOMETRIOSIS

·         WITHDRAWAL BLEEDING

·         DOES NOT ALTER BASAL GONADOTROPIN LEVELS

·         ANTIESTROGENIC ACTION==> ENDOMETRIAL ATROPHY.


***EXERCISE AMENORRHEA IS ASSOCIATED WITH :

·         INCREASED BETA ENDORPHINS

·         INCREASE PROLACTIN

·         DECREASE GONADOTROPHINS

·         INCREASED BETA LIPOPROTEIN

·         ACTH INCREASE

·         INCREASE GROWTH HORMONE

·         SUPPRESSION OF THE PULSATILE SECRETION OF GnRH WITH A DECREASE IN GONADOTROPIN RELEASE.


***GONADOTROPINS ON THE OVARIAN FOLLICLE INCLUDE:

·         LH RECEPTORS ARE PRESENT ON THECA CELLS

·         THECA CELLS PRIMARILY PRODUCE ANDROSTENEDIONE AND TESTOSTERONE

·         GRANULOSA CELLS AROMATIZE ANDROSTENEDIONE AND TESTOSTERONE TO ESTRONE AND ESTRADIOL

·         FSH INDUCES THE APPEARENCE OF LH RECEPTORS ON GRANULOSA CELLS.


***EVALUATION INFERTILITY:

·         GONADOTROPIN EVALUATION: DAY 3 [CYCLE OF 28 DAYS

·         DETERMINATION OF SERUM PROGESTERONE LEVEL TO DOCUMENT OVULATION:DAY 21

·         POSTCOITAL TEST: DAY 14 [2-6 H AFTER COIT]

·         ENDOMETRIAL BIOPSY : 2 DAYS BEFORE MENTRUATION [DAY 26 FOR 28 DAYS CYCLE]

·         HYSTEROSALPINGOGRAM: DAY 8


*** ANEDOCYCLASE IS ACTIVATED BY LH

·         17 BETA HYDROXYLASE CONVERT ANDROSTENEDIONE TO TESTOSTERONE

·         5 ALPHA REDUCTASE CONVERT TESTOSTERONE TO DIHYDROTESTOSTERONE.

·         17 BETA HYDROXYLASE IS FOUND PRIMARILY IN THE TESTIS BUT ALSO IN IN ADRENAL GLAND. IT CONVERTS ANDROSTENEDIONE TO TESTOSTERONE .

·         20 HYDROXYLASE CATALYZES THE FIRST STEP IN THE PRODUCTION OF HORMONAL STEROIDS FROM CHOLESTEROL.

·          

***THE SMALLEST ANTEROPOSTERIOR DIAMETER OF THE PELVIC INLET IS CALLED:OBSTECTRIC CONJUGATE.

·         THE TRUE CONJUGATE IS MEASURED FROM THE TOP OF THE SYMPHYSIS TO THE SACRAL PROMONTORY.

·         THE INTERSPINOUS = TRANSVERSE MEASUREMENT OF THE MIDPLANE AND GENERALLY IS THE SMALLEST DIAMETER OF THE PELVIS.


***AN IM REGIMEN OF MAGNESIUM SULFATE CAN RESULT IN THERAPEUTIC LEVELS AS EFFECTIVELY AS CONTINOUS IV INFUSION.


***OSTEOGENIC SARCOMA: IS THE MOST COMMON PRIMARY MALIGNANT BONE TUMOR

SEEN IN ADOLESCENT AND YOUNG ADULT

INVOLVE DISTAL FEMUR OR THE PROXIMAL TIBIA


***USING THE PROGESTERONE CHALLENGE TEST IN A PATIENT WITH AMENORRHEA CAN :

o        INDICATE THAT THE PATIENT IS PRODUCING ESTROGEN.


***ENDOCRINOLOGICALLY ACTIVE OVARIAN TUMOR WITH PRECOCIOUS PUBERTY IN GIRLS: = GRANULOSA CELL TUMOR, WITH CALL EXNER BODIES

LOW MALIGNANCIES POTENTIAL BUT CAN PRODUCE ESTROGEN==> PRECOCIOUS PUBERTY.


***FIBROTHECOMAS CAN PRODUCE ESTROGENS FROM THE THECA LINE, BUT ARE LESS COMMON THAN A CELL TUMORS.



***BREECH PRESENTATION ARE USUALLY DELIVERED BY CESAREEN SECTION DUE TO HIGH RISK OF :

·         UMBILICAL CORD PROLAPSE

·         BIRTH ASPHYXIA

·         DYSTOCIA

·         FRANK BREECH IS THE ONLY BREECH PRESENTATION WHICH MAY BE DELIVERED VAGINALLY.


***THE GREAT MAJORITY OF POSTPARTUM HEMORRHAGES ARE DUE TO UTERINE ATONY.

TRT: DILUTE OXYTOCIN INFUSION

IF OXYTOCIN FAILS, USE ERGONOVINE.

THE SECOND MOST COMMON CAUSE OF POST PARTUM HEMORRHAGE IS GENITAL TRACT TRAUMA


***THE MOST COMMON CAUSE OF FEMALE INFERTILITY IS ENDOMETRIOSIS

SECOND CAUSE OF INFERTILITY = TUBAL OCCLUSION DUE TO PELVIC INFLAMMATORY DISEASE



***ASHERMAN SYNDROME:

·         AMENORRHEA ,HYPOMENORRHEA

·         OVULATION NONAFFECTED

·         DECREASED AMOUNT OF FUNCTIONAL ENDOMETRIUM

·         BEST STUDY DIAG= HYSTEROSALPINGOGRAM UNDER FLUOSCOPY

·         HYSTEROSCOPY WITH LYSIS OF ADHESIONS IS THE TRT OF CHOICE

·         PROPHYLACTIC ANTBTIC ARE A WISE PRECAUTION FOR SURGICAL TRT


CLINICALLY USEFUL HORMONE ANDROGENS PRODUCED IN THE OVARY OR ADRENAL GLAND = DHAS


***RELAXIN MODULATES THE FUNCTION OF THE CORPUS LUTEUM.


***SHORT LUTEAL PHASE IS DEFINED AS OVULATION WITH POOR PRODUCTION OF PROGESTERONE IN THE SECOND HALF OF THE CYCLE.


***higher risk dvlping endocarditis= CONGENITAL AORTIC STENOSIS

***NORMAL MARROW IRON STORES WOULD EXCLUDE A DIAG OF IRON DEFICIENCY.



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Third-Trimester Bleeding

Third-trimester bleeding occurs in 4% of all pregnancies. In 50% of cases, vaginal bleeding is secondary to placental abruption or placenta previa.

I.Clinical Evaluation of Late-pregnancy Bleeding

A.History of trauma or pain, and the amount and character of the bleeding are assessed.

B.Physical Examination

1.Vital signs and pulse pressure are measured. Hypotension and tachycardia are signs of serious hypovolemia.

2.Fetal heart rate pattern and uterine activity are assessed.

3.Ultrasound examination of the uterus, placenta, and fetus is completed.

4.Speculum and digital pelvic examination should not be done until placenta previa has been excluded.

C.Laboratory Evaluation

1.Hemoglobin and hematocrit.

2.INR, partial thromboplastin time, platelet count, fibrinogen level, and fibrin split products are obtained when placental abruption is suspected or if there has been significant hemorrhage.

3.A red-top tube of blood is used to perform a bedside clot test.

4.Blood type and cross-match.

5.Urinalysis for hematuria and proteinuria.

6.The Apt test is used to distinguish maternal or fetal source of bleeding. (Vaginal blood is mixed with an equal part 0.25% sodium hydroxide. Fetal blood remains red; maternal blood turns brown.)

7.Kleihauer-Betke test of maternal blood is used to quantify fetal to maternal hemorrhage.

II.Placental abruption (abruptio placentae) is defined as complete or partial placental separation from the decidua basalis after 20 weeks gestation.

A.Placental abruption occurs in 1 in 100 deliveries.

B.Factors Associated with Placental Abruption

1.Preeclampsia and hypertensive disorders

2.History of placental abruption

3.High multiparity

4.Increasing maternal age

5.Trauma

6.Cigarette smoking

7.Illicit drug use (especially cocaine)

8.Excessive alcohol consumption

9.Preterm premature rupture of the membranes

10.Rapid uterine decompression after delivery of the first fetus in a twin gestation or rupture of membranes with polyhydramnios

11.Uterine leiomyomas

C.Diagnosis of Placental Abruption

1.Abruption is characterized by vaginal bleeding, abdominal pain, uterine tenderness, and uterine contractions.

a.Vaginal bleeding is visible in 80%; bleeding is concealed in 20%.

b.Pain is usually of sudden onset, constant, and localized to the uterus and lower back.

c.Localized or generalized uterine tenderness and increased uterine tone are found with severe placental abruption.

d.An increase in uterine size may occur with placental abruption when the bleeding is concealed, and it may be detected by serial measurements of abdominal girth and fundal height.

e.Amniotic fluid may be bloody.

f.Fetal monitoring may detect distress.

g.Placental abruption may cause preterm labor.

2.Uterine contractions by tocodynamometry is the most sensitive indicator of abruption.

3.Laboratory Findings include proteinuria and a consumptive coagulopathy, characterized by decreased fibrinogen, prothrombin, factors V and VIII, and platelets. Fibrin split products are elevated.

4.Ultrasonography. The sensitivity of ultrasonography in detecting placental abruption is only 15%.

D.Management of Placental Abruption

1.Mild Placental Abruption

a.If maternal stability and reassuring fetal surveillance are assured and the fetus is immature, close expectant observation with fetal monitoring is justified.

b.Maternal hematologic parameters are monitored and abnormalities corrected.

c.Tocolysis with magnesium sulfate is initiated if the fetus is immature.

2.Moderate to Severe Placental Abruption

a.Shock is aggressively managed.

b.Coagulopathy

(1)Blood is transfused to replace blood loss.

(2)Clotting factors may be replaced using cryoprecipitate or fresh-frozen plasma. One unit of fresh-frozen plasma increases fibrinogen by 10 mg/dL. Cryoprecipitate contains 250 mg fibrinogen/unit; 4 gm (15-20 U) is an effective dose.

(3)Platelet transfusion is indicated if the platelet count is less than 50,000/mcL. One unit of platelets raises the platelet count 5000-10,000/mcL; 4 to 6 U is the smallest useful dose.

c.Oxygen should be administered and urine output monitored with a Foley catheter.

d.Vaginal delivery is expedited in all but the mildest cases once the mother has been stabilized. Amniotomy and oxytocin (Pitocin) augmentation may be used. Cesarean section is indicated for fetal distress, severe abruption, or failed trial of labor.

III.Placenta previa occurs when any part of the placenta implants in the lower uterine segment. It is associated with risk of serious maternal hemorrhage.

A.Placenta previa occurs in 1 in 200 pregnancies. Ninety percent of placenta previas diagnosed in the second trimester resolve spontane ously.

B.Total placenta previa occurs when the internal cervical os is completely covered by placenta.

C.Partial placenta previa occurs when part of the cervical os is covered by placenta.

D.Marginal placenta previa occurs when the placental edge is located within 2 cm of the cervical os.

E.Clinical Evaluation

1.Placenta previa presents with a sudden onset of painless vaginal bleeding in the second or third trimester. The peak incidence occurs at 34 weeks. The initial bleeding usually resolves spontaneously and then recurs later in pregnancy.

2.One fourth of patients present with bleeding and uterine contractions.

F.Ultrasonography is accurate in diagnosing placenta previa.

G.Management of Placenta Previa

1.In a pregnancy >36 weeks with documented fetal lung maturity, the neonate should be immediately delivered by cesarean section.

2.Low vertical uterine incision is probably safer in patients with ananterior placenta. Incisions through the placenta should be avoided.

3.If severe hemorrhage jeopardizes the mother or fetus, cesarean section is indicated regardless of gestational age.

4.Expectant management is appropriate for immature fetuses if bleeding is not excessive, and maternal physical activity can be restricted, and intercourse and douching can be prohibited, and the hemoglobin can be maintained at >10 mg/dL.

5.Rh immunoglobulin is administered to Rh-negative-unsensitized patients.

6.Delivery is indicated once fetal lung maturity has been documented.

7.Tocolysis with magnesium sulfate may be used with caution.

IV.Cervical Bleeding

A.Cytologic sampling is necessary.

B.Bleeding can be controlled with cauterization or packing.

C.Bacterial and viral cultures are sometimes diagnostic.

V.Cervical Polyps

A.Bleeding is usually self-limited.

B.Trauma should be avoided.

C.Polypectomy may control bleeding and yield a histologic diagnosis.

VI.Bloody show is a frequent benign cause of late third trimester bleeding. It is characterized by blood-tinged mucus associated with cervical change.


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Postpartum Haemorrhage (PPH)
Introduction:
        Definition:
               Primary PPH : loss of > 500ml of PV bleed within 24 hrs after delivery
               Secondary PPH : loss of any amount between 24 hrs & 6 weeks after delivery
        Normal mechanisms that reduce incidence of PPH:
               Contraction & retraction of uterus
               Coagulation
               Active management of 3rd stage with syntometrine & controlled cord traction
Causes of primary PPH:
        Retained products of conception
        Uterine atony (eg. Multiple pregnancy, multiparity, polyhydramnios)
        Uterine rupture (eg. Inappropriate use of oxytoxics)
        Uterine inversion
        Trauma (eg instrumentation)
        Bleeding tendencies
Causes of secondary PPH:
        Retained POC
        Infections
Management of primary PPH:
        Mainly anticipatory in the following high risk groups:
               Multiple pregnancy
               Multiparity
               Malpresentations
               Polyhramnios
               Previous LSCS
               Previous multiple D&C
               Prolonged labour
               Instrumentation
        Intrapartum management
               Correct anaemia
               Augmentation with syntocinon to prevent prolonged labour
               Careful instrumentation
               Active management of 3rd stage
               Meticulous repair of episiotomy & lacerations
        When PPH presents:
               Call for help
               Assess need for resuscitation:
                       if need be, setup 2 wide bore IV lines in the upper limb & run fluids rapidly
                       group & cross match 6 units of blood
                       do FBC
                       do PT/PTT
                       monitor pulse, BP, urine output & CVP if severe
               Check if placenta is delivered?
                       If not, deliver placenta by controlled cord traction, if placenta not delivered
                       by 30 minutes, the diagnosis of retained POC is made & oxytocics ares
                       stopped & manual removal of placenta under GA is done & antibiotic cover. If
                       MRP fails, diagnosis of adherent placenta is made & curretting can be done,
                       failing which, methotrexate via cord or IV is used. The last resort is a
                       myoterectomy.
               If placenta is delivered check if delivered completely (examine placenta)
                       If incomplete cotyledons, treat as above for retained POC.
                       If placenta complete, treat as uterine atony.
                               Rub uterus
                               Start IV ergometrine 0.5mg (max 3 doses)
                               Start syntocinon infusion 30-60U at 30 dpm
                               If uterus still not contracted, treart as retained POC & proceed to
                               do curretting in OT under GA.
                               If no POC found, exclude trauma to birth canal
                                      do examination under anaesthesia
                                      with Sim’s speculum & sponge forceps & repair all tears
                       If still bleeding, exclude DIVC & perform exploratory laparotomy.
                               Exclude uterine rupture
                               Once excluded, & still bleeding,
                                      ligate uterine artery
                                      failing which, ligate internal iliac artery
                                      failing which do emergency subtotal hysterectomy.
Pregnancy induced hypertension (PIH)
Introduction:
        Definition: Hypertension developing in a normotensive woman after 20th
        week of pregnancy & usually subsiding after delivery.
        Hypertension is defined as one reading of DBP greater or equal to 110mmHg
        or 2 readings 4 or more hours apart of DBP greater or equal to 90mmHg.
        The different grades are:
               Mild       (DBP =    90 -99mmHg)
               Moderate  (DBP = 100-109 mmHg)
               Severe     (DBP = 110mmHg or greater)
        With the presence of proteinuria, grade is one higher.
        Eclampsia is diagnoses when fits are present.
        Proteinuria is defined as greater or equal to 300mg/day
Risk factors:
        Maternal factors:
               Maternal age <20 or >35
               Primigravida
               Past hisotry of PIH
               Co-existing diabetes, renal disease or chronic hypertension
                Thyroid disease
               Familly history of hypertension
        Fetal factors:
               Multiple pregnancy
               Molar pregnancy
               Hydrops
Management:
        Basic principle: in severe cass, termination of pregnancy is the only way to
        effectively manage the condition. Balance risk of prematurity & risk to mother.     
        Once diagnosis is made, admit all patients. Remember PIH is a condition with
        signs & not symptoms.
        Rest in bed
        Monitor mother:
               Clinical features of impending eclampsia
               4 hourly BP
               Maternal weight gain
               Blood investigaions: (weekly)
                       FBC
                       PT/PTT (?DIVC)
                       Urea/creatinine
                       Electrolytes
                       Uric acid (normal = 4.5 mg/dL)
               24hour urinary total protein (weekly)
        Fetal monitoring:
               Serial SFH
               Fetal movement charting
               CTG 2 times per week
               Weekly Biophysical profile
                       Fetal movements
                       Fetal respiratory movements
                       Fetal tone
                       CTG
                       Amniotic fluid index
        For MILD cases: (aim: DBP < 100mmHg)
               When DBP < 100mmHg & no proteinuria, discharge with weekly followup
                       Timing of delivery at 40 weeks
        For MODERATE cases: (aim: DBP < 95mmHg)
               Start oral methydopa 250mg qds
               If maximum of 2g/day reqached & BP still high,
               add second agent:
                       Hydralazine
                       or labetalol
               Timing of delivery at 38 weeks
        For SEVERE cases: (aim: DBP < 90mmHg)
               Start IV hydralazine 100mg in 1 unit of 5% Dextrose
                       Start at 10 dpm increase by 10 every 10 minutes
                       until maximum of 50 dpm
               If BP still high,
                       Give bolus hydralazine
               If BP still high or signs of impending eclampsia
                       add benzodiazepine
               If BP still high,
                       do emergency LSCS
                       else timing of delivery if all is well at 36 weeks    
Postpartum management:
        Monitor BP, urine output in labour ward for 6 hours
        Discharge when normotensive & no proteinuria
        Review in 6 weeks & advice early booking for next pregnancy.
        If BP still high refer to physician.


Antepartum haemorrhage (APH)
Introduction:
        Definition: PV bleeding between 28th week of gestation to delivery of baby
        (cf. Abortion = PV bleeding before 28th weeks)
Causes of APH:
        Placenta praevia
        Abruptio placentae
        Local causes:
               Genital tract infection,
               trauma,
               tumour,
               polyps,
               erosions
        Bleeding tendencies
        Idiopathic
Management of APH
        Admit all patients
        Assess patient's for need for resuscitation
               If need be, setup 2 wide bore IV lines in upper limb & start IV fluids
               Group & cross match 6 Units
               Do FBC
               Do PT/PTT (?coagulopathy)
               Monitor CVP, urine output, pulse, BP
        Once patient is stabilised, keep patient NBM
        take history:
               Painless APH is placenta praevia
               Painful APH is abruptio placentae
               Quantify blood loss
                       Amount
                       Signs of CVS compensation
               Has it happened before?
               Exclude local causes
                       Coitus
                       Trauma
               Confirm dates
        Perform physical examination:
               General examination
                       Pallor
                       CVS status
               Abdominal examination (basically to exclude abruptio placentae)
                       Signs of pregnancy
                       SFH
                       Is uterus hard?
                       Lie & presentation of fetus
                       Do PR (do not do speculum or VE)
                       (Speculum only when PP excluded)
               Exclude abruptio placentae:
                       If abruptio placentae, exclude & treat DIVC (FFP), pregnancy is not
                       conserved if threat to mother’s life. Otherwise mode of delivery decided
                       upon by CTG (?fetal distress or IUD), VE (assess cervical score),
                       ARM (?meconium stained liqour).
                       Aim for vaginal delivery unless there are indications for LSCS.
        Do U/S
               Exclude placenta praevia
                       If indeed PP, admit & grade type (PP major / minor) & if PP major, plan
                       elective LSCS after 37 completed weeks (meantime keep 6 units of blood
                       group & cross matched) If PP minor, can allow vaginal delivery in OT
                       standby for emergency LSCS.
        Monitoring (more for PP after stabilisation in the wards):
               Mother:
                       Hourly parameters
                       Monitor Hb & need for transfusion
                       Start Pad chart
                       Monitor maternal weight gain
               Fetus:
                       Serial SFH
                       Fetal movement chart (count to 10 chart)
                       CTG


Placenta praevia (PP)
Introduction:
        Definition: Low lying placenta in the lower segment of the uterus.
        Types of placenta previa:
               Type I: Placenta just encroaches into lower segment
               Type II: Placenta edge touches the Os but does not cover it
                       Type IIa: Anterior
                       Type Iib: Posterior
               Type III: Placenta covers Os but is eccentrically placed
               Type IV: Placenta centrally covers the Os
        Placenta praevia minor is Type I & IIa
        Placenta praevia major is Types Iib to IV
Predispositions:
        Multiple pregnancy
        Multiparity
        Previous LSCS
        Previous TOP
Management:
        Basic principle:
               AT ALL COSTS CONSERVE THE PREGNANCY IN THE
               ABSENCE OF THREAT TO MOTHER’S LIFE OR IUGR
        Admit all cases
        Assess need for resuscitation
               If need be:
                       setup 2 wide bore IV canula
                       run fluids rapidly
                       monitor CVP, urine output, vital signs
               Group & cross match (6 units)
               Baseline FBC
               Do PT/PTT
        When patient stable:
               Monitoring:
                       Hourly parameters
        Take history:
               Painless PV bleed after 28 weeks is APH due to PP
               Exclude leaking liquor, show, contractions
               Exclude IUGR
               Any diagnosis of low lying placenta earlier in pregnancy
        Do physical examination:
               Check vital signs
               Check pallor (?chronic bleeds)
               Abdomninal examination:
                       Multiple pregnancy
                       Head not engaged
                       Abnormal lie
               DO NOT DO SPECULUM OR VE
        Do U/S (diagnose PP major / minor & check old notes)
        Even if stable / PP minor, do not send home.
               Complete rest in bed
               Put mother on pad chart
               Monitor mother:
                       4 hourly parameters
                       Monitor Hb weekly
               Fetal monitoring:
                       Serial SFH
                       Start on fetal movement chart
                       CTG weekly
                       3-4 weekly U/S
        For PP minor, when she goes into early labour,
        perform examination under anaesthesia in OT
        if PP major excluded, proceed to induce labour
        For PP major, plan an elective LSCS at 37 completed weeks
        Intrapartum:
               Difficult LSCS
               May have to cut through placenta site
        Postpartum:
               Anticipate PPH




Spontaneous Abortion
Pamela Talley, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. DEFINITIONS

A. Threatened: mild cramps with bleeding. The cervix is long and closed. The uterus is appropriate for gestational age. Roughly 50% progress to inevitable abortion

B. Inevitable: persistent cramps and moderate bleeding. The cervical os is open. Fetal or placental tissue is found in the vagina, protruding through the os, or there is a history of passing tissue

C. Incomplete: as per inevitable abortion but with some retained products of conception in the uterus or cervical canal causing ongoing cramping and excessive bleeding

D. Complete: entire conceptus expelled with decreasing or ceasing of cramps and bleeding

E. Missed: products of conception retained 3 or more weeks after fetal death. Signs and symptoms of pregnancy abate, pregnancy test becomes negative. A brownish vaginal discharge (rarely frank bleeding) occurs. Cramping is rare. The uterus is soft and irregular. Ultrasound rules out live pregnancy

F. Septic: any of the above scenarios plus a temperature over 38<;dg> C without another source of fever may be septic abortion. Associated with IUD or instrumentation in attempted induced abortion

II. INCIDENCE AND ETIOLOGY

A. Fifteen percent to 25% of clinically recognized pregnancies, perhaps closer to 50% of all conceptions

B. Causes include a large proportion of fetal abnormalities incompatible with life (chromosomal and other), defective implantation, maternal infection, uterine and cervical anomalies

III. EVALUATION

A. History suggests pregnancy (missed period(s), nausea, vomiting, breast tenderness) followed by cramping and spotting or bleeding often with passage of tissue. All patients with bleeding sufficient to soak one pad per hour or symptoms of orthostasis (dizziness upon standing, faintness) need to be examined. Others may be followed closely by phone. Remember that patients must be seen within 48 hours for Rho-GAM if indicated

B. Examination: stability of vital signs, orthostasis, pelvic examination looking for an open or closed cervical os, tissue, other causes of vaginal bleeding (e.g., cervical eversion, polyp, infection, vaginal lesion, ectopic pregnancy). Size of the uterus. Check for fetal heart tones with Doppler if over 12 weeks

C. Laboratory tests

1. Pregnancy test positive in 75% of cases

2. CBC, blood type, and antibody screen in all patients for Rh status. Rho-GAM indicated for all Rh-negative, antibody-negative women

3. Ultrasound and/or pathologic examination of tissue if indicated

IV. TREATMENT

A. If orthostatic, treat with IV normal saline or lactated Ringer's solution. Consider transfusion if the hemoglobin content is less than 8 g/dL

B. Threatened abortion: bed rest if possible, use acetaminophen for discomfort, nothing in the vagina (no tampons, douches, intercourse); consider ultrasound of the gestational sac, for cardiac activity, or to rule out ectopic pregnancy. Positive cardiac activity is predictive of continued pregnancy in greater than 90%. Consider monitoring quantitative B-HCG for prognosis; a rise less than 66% in 48 hours is predictive of abortion or ectopic pregnancy

C. Incomplete or inevitable abortion

1. Hospitalize if hypovolemic, anemic, or advanced gestation over 12 weeks

2. Tissue visible in the os should be gently removed with ring forceps to allow contraction of the uterus, but minimize manipulation to decrease the risk of infection

3. Patients with incomplete abortion (tissue passed with continued bleeding) often require suction curettage or D&C.; Consider oxytocin drip as an alternative (20 IU in 1000 cc of crystalloid solution at 50 to 100 cc/hr). If unsuccessful, proceed with D&C;

D. Complete abortion: discharge home if vital signs are stable, hemoglobin is documented to be stable, and bleeding is decreased. Consider methylergonovine maleate (Methergine), 0.2 mg orally three times daily for 3 days, if the diagnosis is certain or after uterine evacuation

E. Missed abortion

1. Obtain a CBC with differential, platelet count, PT, PTT, and disseminated intravascular coagulation (DIC) panel if indicated

2. Hospitalize if there are signs of infection or DIC or if the fetus has been retained longer than 4 weeks

3. Prepare to perform D&C;

4. Outpatient management may be considered if retained less than 4 weeks, if weekly fibrinogen levels are obtained, and if the patient is monitored closely for DIC. Fibrinogen levels less than 150 mg/dL call for immediate evacuation of the uterus

F. Septic abortion

1. Obtain a CBC, UA, culture of discharge from the uterus, blood cultures, chest x-ray for a diagnosis of septic emboli, and abdominal x-ray studies for diagnosis of perforation of the uterus (free air) or a uterine foreign body. Electrolytes and arterial blood gases (ABGs)

2. Organisms include both anaerobes and aerobes (Bacteroides, Streptococcus, Enterobacter, Chlamydia, Clostridium)

3. Hospitalize, treat sepsis, D&C;, IV antibiotics

a. Doxycycline plus cefoxitin or imipenem or ticarcillin or

b. Clindamycin plus a third-generation cephalosporin or gentamicin

4. Discharge home on a regimen of oral doxycycline or clindamycin

V. LONG-TERM MANAGEMENT

A. Give Rho-GAM to Rh-negative women

B. Provide emotional support

C. The traditional but not well founded recommendation is to wait 3 months before attempting conception

D. Evaluate the couple for habitual abortion if the woman has had two or more successive spontaneous abortions. Obtain tissue for karyotyping if possible


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Antenatal Fetal Surveillance
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. OBSTETRIC ULTRASOUND

A. Indications

1. Determine the presence or absence of an intrauterine pregnancy

2. Determine the gestational age

3. Measure fetal growth and identify intrauterine growth retardation

4. Identify multiple-gestation pregnancies

5. Detect fetal anomalies (nearly 100% sensitive for the detection of NTD)

6. Detect oligohydramnios or polyhydramnios

7. Demonstrate placental abnormalities

8. Identify maternal uterine and pelvic anomalies

B. Timing: will depend on the indication for ultrasound. In general, the earlier in pregnancy, the better the estimated date of conception (EDC) can be predicted by sonography. Fetal anomalies may not become apparent until after 20 weeks. Amniotic fluid volume (AFV), fetal movement, tone, and breathing in conjunction with a nonstress test (NST) can be used to calculate the biophysical profile (BPP) score. This can be helpful in the decision to induce or follow postdate pregnancies, high-risk pregnancies, or diabetic pregnancies

II. AMNIOCENTESIS INDICATIONS

A. Done at 16 to 18 weeks' gestation to identify selected inherited disorders in the following populations

1. Pregnancies in women aged 35 or older

2. Previous pregnancy resulting in the birth of a child with a chromosomal abnormality

3. Down syndrome or other chromosome abnormality in either parent or a close family member

4. Mother being a carrier of any X-linked disease

5. Neural tube defect in either parent or a first-degree relative

6. Previous child born with a neural tube defect

7. Abnormal serum AFP level

8. Either parent being a carrier of a genetically transmitted metabolic disease

9. Pregnancy after three or more spontaneous abortions

B. Done during late pregnancy to determine fetal lung maturity based on phospholipids

1. Lecithin-to-sphingomyelin (L/S) ratio. If L/S is greater than 2.0, then there is a low risk of respiratory distress secondary to prematurity.

2. Phosphatidylglycerol (PG). PG first appears at 35 weeks' gestation and increases in concentration until 40 weeks. If present, it provides reassurance of fetal lung maturity

C. Detect isoimmunization

III. INDICATIONS FOR NONSTRESS TESTING/BIOPHYSICAL PROFILE

A. Hypertension

B. Diabetes mellitus

C. Multiple gestation

D. Suspected oligohydramnios/IUGR

E. Known placental abnormality

F. Maternal heart or renal disease

G. Hemoglobinopathy

H. Postdate pregnancies

I. Previous unexplained fetal demise

J. Maternal perceptions of decreased fetal movement

IV. NONSTRESS TEST

A. Equipment: external fetal heart rate (FHR) monitor and uterine contraction monitor

B. Indications: high-risk pregnancies as noted above. Timing should be the earliest point at which an intervention would be performed if a clearly abnormal result is obtained (generally 32 to 34 weeks)

C. Interpretations: a reassuring NST demonstrates three or more fetal movements accompanied by a fetal heart rate acceleration of 15 beats per minute or more lasting at least 15 seconds during a 20-minute period. Lack of fetal movement is unsatisfactory for testing. A repeat NST should then be performed after a meal. Lack of movement for short periods of time may be due to fetal sleep. However, absence of movement for prolonged periods of time may be ominous. The NST is abnormal when the criteria for a reassuring NST are not met or late or variable decelerations are present. A BPP is then indicated

V. BIOPHYSICAL PROFILE

A. Equipment: real-time ultrasonography and external FHR and uterine contraction monitor

B. Indications: same as for NST; may be used as early as 26 to 28 weeks' gestation

C. Interpretation: five parameters are examined (fetal breathing motions, movements, gross body movement, fetal tone, qualitative amniotic fluid volume, and fetal heart rate pattern). Each is given a score of 0 or 2. The total score ranges from 0 (ominous) to 10 (very reassuring)

D. Manage pregnancy according to the biophysical profile results (Table 8-2)

.


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 BREECH PRESENTATION:


OCCURS WHEN FETAL BUTTOCKS OR LOWER EXTREMITIES PRESENT INTO THE MATERNAL PELVIS.

FRANCK BREECH: THIGHS ARE FLEXED -LEG EXTENDED
COMPLETE BREECH : BOTH TIGHS AND KNEES FLEXED
INCOMPLETE BREECH : ONE OR BOTH THIGHS ARE EXTENDED AND ONE OR BOTH KNEES BELOW THE BUTTOCKS.
·         Breech Delivery
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. OVERVIEW

A. Incidence: 25% of all pregnancies less than 28 weeks' gestation, 3% to 4% of all pregnancies at or beyond 34 weeks' gestation

B. Etiology: low birth weight, placenta previa, uterine and fetal anomalies, contracted pelvis, and multiple fetuses all contribute to breech presentations

II. TYPES OF BREECH PRESENTATION

1. Frank: thighs/hips flexed, knees extended; 65% of cases are frank

2. Complete: thighs/hips flexed, one or both knees flexed; 10% of cases

3. Incomplete/footling: one or both thighs extended, one or both knees below the buttocks; 25% of cases

III. BREECH DELIVERY--BUTTOCKS, EXTREMITIES, AND SHOULDERS

Criteria for vaginal delivery of breech presentation

A. Frank breech presentation

B. Fetal weight 2500 to 3800 g

C. Fetal head flexed

D. Gestational age at or beyond 36 weeks

E. Adequate maternal pelvis

F. No other maternal or fetal indicator for cesarean section


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Contraception
Pamela Talley, M.D.
Peer Review Status: Externally Reviewed by Mosby


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(see Table 7-1 for methods of contraception)

I. ORAL CONTRACEPTIVES (OCs)

A. Effectiveness may be decreased by missing pills, some antibiotics and anticonvulsants. Progestin-only pills have a higher failure rate and are used primarily in smokers older than 35 and women with intolerance to or contraindications to estrogen use

1. Absolute contraindications include pregnancy, history of thromboembolic disease, history of breast cancer, estrogen-dependent neoplasms, cerebrovascular accident (CVA) or coronary artery disease, liver tumor, impaired liver function

2. Relative contraindications can include hypertension, smoking, severe headaches, diabetes, hyperlipidemia, active gallbladder disease, sickle cell anemia, active mononucleosis, major surgery within 1 month, long leg cast, 40 years of age or older with cardiovascular risk factors, undiagnosed abnormal vaginal bleeding

B. Safety: risk of adverse cardiovascular effects minimized with the use of low-estrogen (35 ug or less) pills (i.e., Ortho-novum 7/7/7). Primary risk is in older smokers. OC use may protect against endometrial and ovarian cancer, but data on possible increased risk of breast cancer are inconclusive

C. "Morning-after'': 4 tablets of Ovral, an OC containing 50 ug ethinyl estradiol, begun within 72 hours of intercourse can usually prevent pregnancy by causing shedding of the endometrium and preventing implantation of the fertilized ovum. Mifepristone (RU 486), 600 mg within 12 hours, is more effective with fewer side effects but is not yet available in the United States.

II. INTRAUTERINE DEVICES (IUDs)

A. Progestasert releases progesterone, leading to less menstrual blood loss and less dysmenorrhea. Replace annually

B. ParaGard copper T380A can be left in place 8 years

C. Contraindications include mucopurulent cervicitis, history of pelvic inflammatory disease (PID), or ectopic pregnancy. The risk of ectopic pregnancy is lower than in women using no contraceptives but higher than in those using oral contraceptives

III. SPERMICIDES

Those containing nonoxynol-9 destroy sperm cell walls and provide some protection against sexually transmitted disease (STDs)

IV. BARRIER DEVICES

Condoms, diaphragms, caps, sponges, and new female condoms all decrease the risk of STDs when used properly

V. PERIODIC ABSTINENCE

Abstinence during presumed fertile times requires long periods of abstinence with calender, temperature, cervical mucus, and symptothermal methods. Highest failure rates are in women with irregular menstrual cycles.

VI. MEDROXYPROGESTERONE ACETATE (DEPOPROVERA)

Recently Food and Drug Administration (FDA) approved at 150 mg intramuscularly (IM) every 3 months. Most women are amenorrheic after 1 year, with some irregular bleeding during that year. Long-term safety is unclear. Possible increased risk of breast cancer and osteoporosis.

VII. PROGESTIN IMPLANTS (NORPLANT)

Subcutaneous insertion of 6 Silastic capsules containing levonorgestrel for slow release provides contraception for 5 years. Removal is possible at any time. Long-term safety is unclear


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Diabetes in Pregnancy
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. GESTATIONAL DIABETES MELLITUS (GDM), (Class A Diabetes)

A. Definition: excessive carbohydrate intolerance during pregnancy in women who did not have diabetes mellitus previously. The incidence varies from 3% to 12%

B. Risk factors

1. Obesity

2. Maternal age over 25

3. Positive family history of diabetes

4. History of gestational diabetes, macrosomic infant, or stillbirth

5. Symptoms or signs of diabetes along with glucosuria

C. Evaluation

1. Glucose challenge test (GCT)

a. Timing: a GCT is frequently performed as a routine screen for GDM in all pregnancies at 24 to 28 weeks' gestation. It should be performed earlier if symptoms are present. Some sources recommend screening at the first prenatal visit if there are risk factors

b. Procedure: a blood glucose level is obtained 1 hour after a 50-g oral glucose load

c. Interpretation: a level of 140 mg/dL or greater is abnormal. Although values below 140 have a high negative predictive value, there are many false positives. A 3-hour fasting glucose tolerance test (GTT) should be done at 1 hour if the GCT is greater than 130 mg/dL

2. Glucose tolerance test

a. Timing: recommended for follow-up of an abnormal GCT

b. Procedure: the patient must eat a diet containing at least 150 g carbohydrate for 2 days. The patient has a serum glucose level obtained after an overnight fast and then ingests 100 g of glucose solution. Serum glucose levels are then obtained at 1, 2, and 3 hours

c. Interpretation (Table 8-3): if two or more of these readings are abnormal, the patient needs diabetic teaching, if blood sugar levels cannot be controlled with diet, the patient needs to receive insulin therapy

D. Potential morbidity

1. Infants born to diabetic mothers have five times the normal risk of respiratory distress syndrome

2. Macrosomia and associated birth trauma are related to maternal hyperglycemia

3. Increased incidence of neonatal hypoglycemia, hypocalcemia, and jaundice

4. The incidence of congenital anomalies is increased with first-trimester hyperglycemia

E. Management of gestational diabetes

1. Dietary adjustment is the mainstay of therapy

a. Caloric intake should be 30 to 35 kcal/kg/day. Intake should be reduced to 24 kcal/kg/day if the patient is obese

b. The patient should avoid cakes, candy, and other fast-acting carbohydrates

c. Dietary composition should be 50% to 60% carbohydrate, 20% to 25% protein, and 20% fat, with high fiber content

2. Obstetric surveillance

a. Early ultrasound for accurate gestational dating

b. Follow every 2 weeks until 36 weeks, then weekly

c. Accucheck four times daily (fasting and 1-hour postprandial)

d. Check fasting blood glucose level and review home monitoring each visit. If fasting glucose levels are greater than 105 (or postprandial values are 120 to 130), then the patient should be hospitalized to ensure adherence to diet

e. If the fasting glucose level remains 110 or greater, insulin therapy is indicated

f. Check for ketonuria daily to make sure that there has been adequate caloric consumption

g. If macrosomia is suspected, ultrasound examination is performed. If the estimated fetal weight is 4000 g or greater, a cesarean section is recommended at term. Amniocentesis is helpful in documenting fetal lung maturity before cesarean section since infants of diabetic mothers have delayed lung maturity when compared with infants of nondiabetic mothers of similar gestational ages

h. Antepartum NST is often initiated on a weekly basis at 34 to 35 weeks' gestation. If euglycemia can be documented, consider delaying monitoring until 38 weeks. After 40 weeks' gestation, fetal surveillance is initiated, and delivery is recommended if there is any evidence of fetal compromise

i. Gestational diabetics should have a 75-g oral GTT checked 6 weeks postpartum to rule out persistent carbohydrate intolerance. Counsel the patient that she has an approximate 35% risk of diabetes developing at some point in her life

II. PREEXISTING DIABETES MELLITUS

A. The incidence of major anomalies (cardiac, neural tube, genitourinary, gastrointestinal, and musculoskeletal) is several times higher than for the general population, especially if there is first-trimester hyperglycemia. Consider prepregnancy counseling in diabetics of childbearing age

B. Vascular disease in particular is associated with IUGR and a greater incidence of fetal demise

C. Ketoacidosis may carry a 50% fetal mortality rate

D. Management: the care of pregnant diabetic individuals is best managed by a coordinated team of specialized health care providers and is beyond the scope of this chapter


Dysmenorrhea
Pamela Talley, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. CHARACTERISTICS AND ETIOLOGY

A. Primary dysmenorrhea: menstrual pain with normal pelvic organs. Usual onset before age 20. Pain begins within a day of the onset of flow and lasts 24 to 72 hours. Increased prostaglandin activity from hormonal and psychological factors causes increased uterine contractility

B. Secondary dysmenorrhea: menstrual pain with pelvic pathology on examination or at laparoscopy. Usual onset after age 20, progressive with age, and less characteristically timed with menses. Causes include endometriosis, leiomyomas, endometrial cancer, IUD use, polyps, PID, cervical stenosis, ovarian cysts, imperforate hymen, uterine synechiae

II. EVALUATION

A. History including past menstrual history, family history, review of systems, level of debility, and psychological overlay

B. Examination including pelvic, rectovaginal examination for uterosacral nodules

C. Laboratory tests not usually necessary. If indicated by the history and physical examination, consider Papanicolaou cultures, wet mount, endometrial biopsy, ultrasound, laparoscopy

III. TREATMENT

A. Primary

1. Reassurance

2. Prostaglandin inhibitors (ibuprofen, 400 to 800 mg orally three times daily, naproxen, 500 mg orally twice daily) 3 days before expected menses through day 2 of flow. Reassess the need for medications in 1 year. Mefenamic acid, 500 mg three times daily, is another alternative

3. Consider combined OCPs if the above is inadequate. Reassess in 1 year

4. If the above is unsuccessful, consider organic pathology (possibly laparoscopy)

B. Secondary

1. Laparoscopy often indicated

2. Treat the underlying cause



Dyspareunia
Pamela Talley, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. OVERVIEW

Dyspareunia is defined as painful intercourse. It may have a psychological or organic origin. Even if the basic cause is organic, psychological factors may secondarily emerge and result in patterns of behavior that must be addressed as well as the organic cause of pain

II. TYPES OF DYSPAREUNIA

A. Superficial dyspareunia: pain is perceived at or near the introitus

B. Deep dyspareunia: pain is perceived deep in the vagina or lower part of the abdomen

C. Nonorganic dyspareunia

III. DIFFERENTIAL DIAGNOSIS

A. Superficial dyspareunia

1. Inflammatory disease of the vulva, vagina, bladder, e.g., vulvovaginitis, trigonitis, urethritis, Bartholinitis, vestibulitis; causes are fungal, bacterial, viral (herpes, condylomas), irritant (tight-fitting clothes)

2. Tender, contracted scars, e.g., following episiotomy, vaginal repair

3. Atrophic vaginitis or vulvar dystrophy in an older patient. Atrophic vaginitis also occurs with anorexia, breast-feeding, pelvic irradiation

4. Rigid hymen or developmental anomaly in a younger patient

5. Errors in sexual technique, e.g., too little foreplay leading to poor lubrication, overzealous clitoral stimulation

6. Medications that decrease lubrication, e.g., anticholinergics, antihistamines, diet pills

7. Foreign bodies, e.g., coital aids

8. Anal intercourse without sufficient lubrication

9. Vaginitis medicamentosa from contraceptive chemicals, feminine deodorant sprays, douches

10. Vaginismus

B. Deep dyspareunia

1. Endometriosis

2. Pelvic inflammatory disease

3. Ovarian cysts; pelvic surgery causing adhesions, scarring, and an ovary sutured to the vaginal cuff

4. Radiation therapy effects

5. Pelvic neoplasm

6. Retrodisplaced uterus causing an ovary displaced to the cul-de-sac

7. Uterine prolapse

8. Cervical lacerations or scars

9. Rectal pathology

10. Orthopedic problems

C. Psychological dyspareunia

1. Sexual, e.g., fear, disinterest, ignorance, anxiety involving the relationship (partner with sexual dysfunction, feelings of hostility)

2. Negative experience, e.g., rape, sexual abuse

IV. EVALUATION

A. History

1. Onset: first attempt at intercourse vs. recent onset suggesting recent change or a situational problem

2. Occurrence of pain: before penetration, on penetration, with deep penetration. Failure to localize pain suggests a psychological cause

3. Duration of pain: pain existing for several years may not resolve even after a medical condition is identified and corrected

4. Establish whether a tampon can be inserted; if so, mechanical obstruction is unlikely

5. History of surgery, PID, radiation

6. History regarding sexual fears, time spent on foreplay, feelings toward the partner

7. Interview the partner

B. Physical examination

1. Pelvic examination: look for signs of vulvovaginitis, atrophic vaginitis, narrowed introitus, cervicitis, congenital abnormalities. Observe for involuntary spasm on attempted examination. Palpate for a uterine mass, retroverted uterus, and tenderness of the uterus, adnexae, or upon movement of the cervix. Examine for loss of support, cystocele, rectocele

C. Laboratory examination

1. Papanicolaou smear

2. Wet preparation

3. CBC, ESR, cervical cultures if evidence of PID

4. Pelvic ultrasound if a mass is suspected

5. Referral for laparoscopy if endometriosis, adhesions, or an adnexal mass is suspected

V. TREATMENT

A. Organic diseases should be appropriately treated, e.g., infectious diseases (vaginitis, Bartholin's gland duct cyst, PID), atrophic vaginitis, endometriosis

B. Inadequate lubrication without organic pathology should be treated with reassurance and advice regarding prolonging foreplay and use of a water-soluble lubricant. Changing coital positions, guiding the penis for insertion, and oral-genital foreplay are other possible suggestions

C. Specific surgical procedures may be required (introital dyspareunia), e.g., excision of painful scars or nerve endings damaged by herpetic infection, hymenotomy, plastic surgery for congenital or surgically acquired disorders not amenable to progressive self-dilatation

D. Specific surgical procedures (deep dyspareunia), e.g., ventral suspension of the uterus or ovaries, hysterectomy, lysis of adhesions

E. Marital-sexual therapy if indicated, e.g., emphasis on communication skills, sensate focus exercises, relaxation, masturbatory techniques

F. Behavioral techniques, e.g., changes in coital position (avoidance of deep pain), Kegel's pelvic floor exercises, vaginal self-dilation

G. Blocking or deconditioning the spastic vaginal response of vaginismus

H. Patient education in all cases

Early Antepartum Hemorrhage
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. DEFINITION

Vaginal bleeding at less than 20 weeks' gestation

II. DIFFERENTIAL DIAGNOSIS

A. Benign vaginal or cervical lesions; a pregnant cervix is very vascular and friable. This diagnosis is made by speculum examination--bleeding will not be from the os

B. Abortion

1. Threatened abortion: the early symptoms of pregnancy may be present. Vaginal bleeding has occurred, with or without cramping. No history of passage of tissue or amnionic fluid is obtained. On examination, the patient is afebrile, the abdomen is soft and nontender. The uterus is appropriate for gestational age and nontender. The internal cervical os is closed

2. Inevitable abortion: symptoms are the same as for threatened abortion. Menstrual cramping is often present, and evidence of ruptured membranes may be noted. The internal os is dilated. (Do not confuse with an incompetent cervix, which is not associated with cramping and is potentially treatable.)

3. Incomplete abortion: cramping and bleeding have occurred, and the patient reports passage of tissue. (Blood clots may be mistaken for tissue.) Speculum examination reveals a dilated internal os and tissue present within the endocervical canal or vagina. Bleeding may be heavy

4. Complete abortion: cramping and bleeding have occurred and a history of passage of tissue has been obtained. On examination, the uterus is firm and smaller than one would expect for the gestational length of pregnancy

5. Septic abortion: consider if a temperature of 38 degrees C is present with symptoms and signs of abortion in any stage. Abdominal and uterine tenderness is present as well as purulent discharge and possibly evidence of shock

C. Ectopic pregnancy: vaginal bleeding occurs in 50% to 94% of patients with ectopic pregnancies. Pelvic pain is generally present. Abdominal tenderness is present in 97% of cases. Rebound tenderness may be present. The uterine size is suggestive of early pregnancy, and the cervix is typically tender on motion. An adnexal or cul-de-sac mass can be palpated in 40% of cases. The risk of ectopic pregnancy is increased if there is a history of tubal infection or surgery, endometriosis, or prior infertility problem or if pregnancy occurred while taking progestin-only birth control pills (BCOs) or with an intrauterine device (IUD). Serum progesterone levels may be used to differentiate intrauterine pregnancies from ectopic pregnancies and pregnancies destined to go to spontaneous abortion

D. Molar pregnancy: the placenta undergoes trophoblastic proliferation and typically resembles a cluster of grapes. Occurs more often in women younger than 20 or older than 40 years of age and almost always causes some degree of vaginal bleeding. Hydatidiform moles are associated with hyperemesis gravidarum and onset of preeclampsia before the third trimester. The uterus is larger than expected for gestational age in 50% of the cases. Ovarian enlargement may occur secondary to thecal lutein cysts. Ultrasonic findings typically show the "snow storm'' pattern

III. MANAGEMENT

Serum progesterone levels in conjunction with ultrasound may be used to differentiate intrauterine pregnancies from ectopic pregnancies and pregnancies destined to go on to spontaneous abortion. See Chapter 7.


Ectopic Pregnancy
Pamela Talley, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. GENERAL INFORMATION

A. Ectopic pregnancy is potentially life threatening and, although common, may be difficult to diagnose. It must be suspected in any woman with vaginal bleeding and lower abdominal pain

B. Ninety-eight percent of ectopic pregnancies are tubal rather than cervical or abdominal

C. Risk factors: previous ectopic pregnancy, current IUD use, prior tubal surgeries, history of PID, prior infertility

II. EVALUATION

A. Symptoms: abdominal pain (98%), amenorrhea (65%), vaginal bleeding (80%), with or without symptoms of early pregnancy, nausea, vomiting, syncope, dizziness, referred shoulder pain, tenesmus, low-grade fever

B. Examination: check vital signs for orthostatic changes, hemodynamic instability. Pelvic findings may be normal early on; 50% have an adnexal mass. The uterus may be enlarged secondary to deciduation or blood. Cervical motion tenderness may be found as well as a doughy cul-de-sac secondary to bleeding

C. Unstable patient: when an acute abdominal emergency and/or hemorrhagic shock is suspected, immediate culdocentesis will confirm hemoperitoneum (<;mt>5 cc nonclotting blood). When combined with a positive quick urine pregnancy test, a positive culdocentesis predicts ectopic pregnancy in over 99% of cases. Do not waste time getting a serum pregnancy test or ultrasound. Obtain immediate surgical consultation

D. Laboratory tests

1. Pregnancy test: the sensitivity of the assay must be known. Newer urine tests are more sensitive (50 to 200 mIU HCG/mL). The optimal test is quantitative B-HCG, which detects 15 to 50 mIU HCG/mL roughly at the time of expected menses or 7 days postimplantation

E. Ultrasound: the former "discriminatory zone'' is the range of serum B-HCG (6000 to 6500) above which an intrauterine pregnancy should be detectable by transabdominal ultrasound in 95% of cases. With the use of transvaginal ultrasound this is now lowered to about 1500 (although still center dependent) when an intrauterine sac ought to be visable and make ectopic pregnancy unlikely. Ultrasound findings may include the presence of a solid, cystic, or complex adnexal mass adjacent to a slightly enlarged uterus; absence of an intrauterine sac; and free fluid (blood) in the cul-de-sac. An adnexal mass is often not detectable until HCG is in the 3500 to 6500 range.

F. In a stable patient, if unable to exclude ectopic pregnancy by ultrasound, consider serial measurements of quantitative B-HCG to distinguish ectopic from early intrauterine pregnancy. If the HCG level does not rise by 66% in 48 hours, suspect ectopic pregnancy. Monitoring serum progesterone levels also can be helpful

III. TREATMENT

Surgical, although some centers are using methotrexate therapy in patients with early ectopic pregnancies

IV. FERTILITY IMPLICATIONS

An average of 30% are infertile following an ectopic pregnancy



Common Gynecologic Infections
Pamela Talley, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. VULVOVAGINITIS

A. Most common outpatient gynecologic complaint

B. Symptoms include discharge, pruritis, odor

C. Evaluation: history, examination, microscopic examination of secretions with saline and KOH (wet preparation), vaginal pH with nitrazine

D. Treatment: see Chapter 11 for further information on diagnosis and treatment

II. CERVICAL INFECTIONS

A. Spectrum of symptoms: asymptomatic, mucopurulent cervicitis; may have associated urethritis or infection of Bartholin's gland

B. see Chapter 11 for further information on diagnosis and treatment

III. SYPHILIS

Incidence increasing in the United States. see Chapter 11 for details on diagnosis and treatment

IV. PELVIC INFLAMMATORY DISEASE

A. General: includes a wide variety of infections, e.g., puerperal and postoperative infections, septic abortions, and salpingitis. The term is used interchangeably with acute salpingitis--sexually transmitted, ascending infection of the upper genital tract

B. Pathogenesis: ascending infection from the cervix to the fallopian tubes with initial mucosal damage often by Neisseria gonorrhoeae and secondary infection by other organisms including Chlamydia, Mycoplasma, Ureaplasma, and gram-negative enterics and anaerobes. Often polymicrobial

C. Predisposing factors: multiple sexual partners, nonbarrier contraceptive use especially IUD, transvaginal instrumentation of the cervix/uterus, recent menstrual period, history of PID

D. Diagnosis

1. Differential diagnosis includes appendicitis, ectopic pregnancy, septic abortion, pyelonephritis, inflammatory bowel disease, endometriosis, hemorrhagic corpus luteum, ovarian cyst, adenexal torsion

2. Obtain urinalysis (UA), complete blood count (CBC), pregnancy test, erythrocyte sedimentation rate (ESR), Gram stain of cervical discharge, and appropriate cultures--endocervix, rectum, urethra, blood, and peritoneal fluid as indicated

3. Criteria for diagnosis: all three of the following

a. Lower abdominal pain and tenderness with or without rebound

b. Cervical motion tenderness

c. Adnexal tenderness

plus one or more of the following:

d. Temperature higher than 38 Celcius

e. White blood cell (WBC) count greater than 10,500

f. Culdocentesis with WBCs and bacteria

g. Mass on bimanual examination or ultrasound

h. Elevated ESR

i. Endocervical Gram stain with gram-negative intracellular diplococci or positive rapid assay for Chlamydia

E. Treatment

1. Outpatient therapy

a. Ceftriaxone, 250 mg IM, or cefoxitin, 2 g IM, plus probenecid, 1 g orally. Ciprofloxacin, 500 mg orally, has been used as an alternative in allergic patients

b. Either of the above followed by doxycycline, 100 mg orally twice daily for 14 days Azithromycin, 1 g orally, is an alternative in poorly compliant patients

2. Inpatient therapy

a. Cefoxitin, 2 g intravenously (IV) every 6 hours, plus doxycycline, 100 mg IV every 12 hours, or cefotetan, 2 g IV every 12 hours, plus doxycycline, 100 mg IV every 12 hours until improvement. Either followed by doxycycline, 100 mg orally twice daily to complete 14 days

b. Alternative preferred in IUD-related infection, suspected abscess, or procedure-related infection: clindamycin, 900 mg IV every 8 hours, plus a gentamicin loading dose of 2 mg/kg IV followed by gentamicin, 1.5 mg/kg every 8 hours until improvement. Then doxycycline, 100 mg orally twice daily, or clindamycin, 450 mg orally four times daily to complete 14 days. The gentamicin dose needs to be adjusted in the presence of renal insufficiency

3. Criteria for hospital admission

a. Uncertain diagnosis

b. Suspected pelvic abscess

c. Concurrent pregnancy

d. Severity of illness precluding outpatient therapy

e. Inability to comply with outpatient treatment including necessary follow-up after 48 to 72 hours of therapy

f. Failure of outpatient therapy

F. Complications: infection rarely remains confined to the fallopian tubes, and peritonitis is common. Increased risk of ectopic pregnancy, infertility, rupture of a tubo-ovarian abscess, adnexal torsion, bowel obstruction secondary to adhesions, and septicemia


Intrauterine Growth Retardation (IUGR)
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. DEFINITION

IUGR is a diagnosis that the fetus weighs less than the 10th percentile for its gestational age

II. RISK FACTORS

A. Chronic maternal disease, chronic maternal hypertension, PIH, diabetes, cyanotic heart disease, collagen vascular disease, severe maternal anemia, renal disease

B. Fetal genetic disorders or fetal malformations

C. Intrauterine infections: rubella, herpes, toxoplasmosis, syphilis, CMV

D. Previous history of a small-for-gestational-age (SGA) baby, smoking, drug or alcohol abuse

E. Abnormalities of the placenta or placental blood flow

III. DIAGNOSIS

One should be suspicious when the fundal height does not exhibit the predicted 1-cm/wk growth between 20 and 36 weeks' gestation. Serial ultrasonic scanning may confirm the diagnosis

IV. MANAGEMENT

The development of IUGR makes the pregnancy high risk. Close antepartum surveillance is required, and the decision on when to deliver the infant is complicated. These pregnancies are typically handled by physicians experienced in high-risk obstetrics and neonatal care


Hepatitis Screening in Pregnancy
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. RECOMMENDED SCREENING

A. Women from high-risk populations and/or locations: Asia, Pacific islands, Alaska (Eskimo), American Indians; immigrants from the South Pacific, Caribbean, Haiti, Sub-Saharan Africa. Also consider immigrants from the Middle East, Eastern Europe, Central and South America

B. Women with histories of liver disease; contact with a hepatitis B carrier, dialysis patients, or the mentally retarded; rejection as a blood donor; blood transfusion; frequent occupational exposure to blood in medical-dental settings; multiple episodes of sexually transmitted diseases; percutaneous use of illicit drugs

II. HEPATITIS B VACCINATION OF INFANTS

A. Now recommended for all infants

B. Administer hepatitis B vaccine at birth, 1 month, and 6 months (Recombivax HB, 2.5 ug = 0.25 mL IM, or Engerix B, 10 ug = 0.5 mL)

C. If the mother is HBsAg-positive, give the newborn hepatitis immune globulin, 0.5 cc IM, within 12 hours after birth

D. Schedule for vaccines begun in the office (Table 8-1)

a-FETOPROTEIN (AFP)
I. OVERVIEW

The measurement of AFP in maternal serum between 15 and 18 weeks' gestation may be used as a screening test to detect fetal neural tube defects. To evaluate AFP levels one must take into account maternal weight, length of gestation, and gestational age. Women with abnormal values should be referred for ultrasound and amniocentesis. The test should be run by a laboratory familiar with AFP screening and with well-established reference ranges

II. DISORDERS ASSOCIATED WITH ELEVATED AFP LEVELS

A. Underestimated gestational age

B. Open neural tube defects (meningomyelocele, anencephaly)

C. Fetal nephrosis/cystic hygroma

D. Fetal gastrointestinal (GI) obstruction/omphalocele/gastroschisis

E. Prematurity/low birth weight

F. Abdominal pregnancy

G. Fetal demise

III. DISORDERS ASSOCIATED WITH LOW AFP LEVELS

A. Overestimated gestational age

B. Missed abortions

C. Molar pregnancies

D. Chromosomal abnormalities (including Down syndrome)

IV. TRISOMY 21

Low estriol, elevated HCG, and low AFP levels are associated with trisomy 21 (Down syndrome). Many laboratories now routinely assay for these three in maternal serum drawn at 15 to 18 weeks' gestation

V. PROJECTED OUTCOME

In the United States, the incidence of a neural tube defect (NTD) is roughly 1 per 1000 live births. In a study of 21,000 nondiabetic women, 249 women (1.2%) had abnormal AFP values. Of these women, 42% had normal infants and 15% had twins. The rest had NTD (8%), fetal death (16.5%), or other abnormalities. Thus, roughly 57% of women with abnormal AFP levels (who have normal infants) will be referred for further testing

VI. RISKS

Psychological stress, false positives, false reassurance, and potential fetal trauma secondary to amniocentesis


Induction of Labor
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. INDICATIONS AND CONTRAINDICATIONS

A. Indications for induction of labor: pregnancy-induced hypertension, premature rupture of membranes, chorioamnionitis, postdate pregnancy, isoimmunization, other evidence of hostile intrauterine environment, diabetes mellitus, other selected maternal diseases, fetal demise

B. Contraindications: placenta previa, cord presentation, floating presenting part, abnormal fetal position, active genital herpes, invasive cervical carcinoma, pelvic structural deformities, and prior classic uterine incision. Oxytocin stimulation would be relatively contraindicated in conditions that predispose to uterine rupture (high parity, advanced maternal age, fetopelvic disproportion, uterine overdistension, prior uterine scar)

II. RISKS

A. Amniotomy

1. Cord prolapse. Make sure that the presenting part is well applied to the cervix

2. Injury to a fetal part (unlikely with blunt instruments)

B. Oxytocin

1. Hyperstimulation

2. Uterine rupture

3. Water intoxication (hyponatremia may result if excessive oxytocin is administered with large volumes of nonelectrolyte-containing IV fluids)

C. Prostaglandin E2: hyperstimulation and uterine rupture

III. METHODS

A. Determine the indications for induction of labor by weighing the relative contraindications and risks

B. Assess the inducibility of the cervix by using the Bishop score (see Table 8-5)

C. Decide whether to use amniotomy alone or in conjunction with oxytocin. Amniotomy in the face of a high Bishop score often leads to successful induction of labor. Oxytocin is indicated in arrest disorders of active labor if inadequate uterine activity is the etiology rather than CPD. Oxytocin is also indicated for a prolonged latent phase in conjunction with complicating factors such as premature rupture of membranes or a postdate pregnancy. Oxytocin should not be used in CPD

D. Guidelines for amniotomy

1. The cervix should be dilated enough to allow the the membranes to be reached with an amniotomy hook

2. The fetus should be vertex (unless breech delivery is planned) with the presenting part well engaged and well applied to the cervix

3. The umbilical cord should not be palpable

4. Membranes are hooked, and a gentle tug should cause release of amnionic fluid

5. Assess fluid for the presence of meconium

6. Monitor fetal heart tones before and after the procedure

E. Guidelines for oxytocin administration

1. Close monitoring of the parturient and fetus is essential. Most hospitals have written protocols available

a. Place 10 units of oxytocin in 1000 cc of D5 1/2 NS or D5LR

b. Begin with a low dose of oxytocin: 0.5 to 2 mU/min (each milliliter of the above solution contains 10 mU)

c. Various protocols exist regarding the rate for increasing the dose and the maximum dose. If little uterine response is observed, the dose can be increased by 1 to 2 mU/min every 30 minutes. Most patients respond to rates of 20 mU/min or less. The faster the increase, the more likely the risk of hyperstimulation. The rate of administration is held steady when a good labor pattern (contractions every 2 to 3 minutes lasting 60 to 90 seconds with 50 to 60 mm Hg intrauterine pressure and a resting tone of 10 to 15 mm Hg) is achieved

d. Ideally you want 150 to 250 Montivideo units. Montivideo units = (number of contractions/10 minutes) <;ts> (average peak of contraction <;ms> average baseline of contraction)

2. If at any point the fetal heart rate indicates distress, the patient should be placed on her left side, oxygen administered, and oxytocin therapy discontinued. Reinstatement of oxytocin drip requires reassessment of the situation


Evaluation of Labor
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. HISTORY

A. Defining labor

1. Contractions: onset, frequency, duration, intensity

2. Membranes ruptured or intact

3. Fetal movement

B. Review the prenatal course

1. Accuracy of the estimated date of confinement (EDC)--usually 40 weeks after the last menstrual period (LMP). May be modified by other parameters in pregnancy such as an early ultrasound

2. Length of gestation: calculated by comparing the date of labor with the EDC, using the EDC as "40'' weeks

3. Ask about coexisting medical problems

4. Calculate the weight gain during pregnancy

5. Review laboratory data: blood type, Rho(D) immunoglobulin requirements, VDRL, rubella immunity, hematocrit

C. Review previous pregnancies: number, gestation, fetal size, duration of labor, complications

II. PHYSICAL EXAMINATION

A. General: vital signs, funduscopy, thyroid palpation, chest examination, examination of the extremities, brief neurologic examination

B. Obstetric abdominal examination

1. Assess fetal position

2. Fundal height

3. Estimation of fetal weight

4. Auscultation of fetal heart tones

C. Pelvic examination

1. Inspection

a. Look for herpetic lesions, condylomas, lacerations

b. Speculum examination may reveal pooling of vaginal fluid consistent with rupture of membranes. A nitrazine test or swab of vaginal fluid on a glass slide may be necessary to prove the presence of amniotic fluid in the vagina. The basic pH of this fluid will turn the nitrazine paper blue. Care must be taken to avoid the cervical mucus, which is also basic and may give a false positive test. If an air-dried sample of fluid reveals a "fern pattern,'' then the presence of amniotic fluid is confirmed

2. Palpation of the cervix

a. Dilation of the cervical os. Dilation may range from 0 to 10 cm

b. Effacement: the degree of thinning of the cervix. The cervix may range from 3 cm long (thick or zero percent effaced) to paper-thin (100% effaced)

3. Palpation of the presenting part

a. Identification: head, foot, buttock, other

b. Station: described as the relationship of the fetal presenting part to the level of the ischial spines in the maternal pelvis. Station may range from 3 to +3. Zero station occurs when the lowermost presenting part is palpable at the level of the ischial spines

c. Position: described as the orientation of the presenting part in regard to the maternal pelvis. Vertex presentation with the occiput positioned either to the right or left anteriorly is the most common


Late Antepartum Hemorrhage
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. DEFINITION

Vaginal bleeding that occurs after 20 weeks' gestation

II. DIFFERENTIAL DIAGNOSIS

A. Placenta previa

1. Incidence: occurs in 1 of 200 deliveries. The diagnosis of placenta previa is very common in the second trimester, but more than 95% of these do not have placenta previa at delivery

2. Classification: placenta previa may be marginal, partial, or total

3. Diagnosis: vaginal bleeding is typically bright red and painless. The blood loss is not massive but tends to recur and become heavier as the pregnancy progresses. Diagnosis may be aided by ultrasound. The advisability of a speculum examination is debatable. Digital examination is contraindicated other than in a double setup situation when delivery is desirable and can be rapidly accomplished by cesarean-section. Maternal risk factors include increasing age, multiparity, and prior uterine scar

B. Placental abruption

1. Incidence: placental abruption occurs in 10% of all deliveries. Severe abruption is rare

2. Classification

a. Mild: slight vaginal bleeding (less than100 cc), no FHR abnormalities present, and no evidence of shock or coagulopathy

b. Moderate: moderate vaginal bleeding (100 to 500 cc) and uterine hypersensitivity with or without elevated tone. Mild shock and fetal distress may be present.

c. Severe: extensive vaginal bleeding (<>500 cc), tetanic uterus, and moderate to profound maternal shock are present. Fetal demise and maternal coagulopathy are characteristic

3. Diagnosis: the diagnosis of placental abruption is clinical. Although vaginal bleeding is present in 80% of cases, it may be concealed in the remainder. Thus, the maternal hemodynamic situation may not be explained by observed blood loss. Pain and increased uterine tone are typically present. Risk factors include a prior history of abruption, maternal hypertension, cigarette or cocaine use, increasing maternal age, or multiparity. Abruption may be associated with preterm premature rupture of membranes, twin gestation following delivery of the first infant, and trauma

C. Uterine rupture: very rare. May mimic severe abruption. An abdominal film may show free intraperitoneal air or an abnormal fetal position. Hysterectomy is required

D. Other: vasa praevia (velamentous insertion of the cord), and cervical dilation with loss of the mucous plug may be confused with other causes of vaginal bleeding or cervical or vaginal lesions (polyps, condylomas)

III. LABORATORY EVALUATION

Laboratory evaluation should include a CBC, blood typing and crossmatching, coagulation studies, urinalysis, and ultrasound

IV. MANAGEMENT OF PLACENTA PREVIA AND PLACENTAL ABRUPTION

A. Placenta previa

1. If pregnancy is 37 weeks or greater or if fetal maturity has been documented, a cesarean section is indicated unless only a minimal degree of placenta previa is present

2. If bleeding is sufficient to jeopardize the mother or fetus despite transfusion, cesarean section may be indicated regardless of gestation

3. In a preterm gestation, expectant management is indicated. Most patients require inpatient observation. Physical activity is restricted. Nothing is allowed in the vagina, including examining fingers. The hematocrit is maintained at 30% or greater. Once 36 to 37 weeks' gestation is reached with fetal maturity demonstrated by amniocentesis, the patient is readied for elective double-setup examination

4. Remember that placenta accreta may complicate placenta previa in women with history of previous cesarean section. Hemorrhage can necessitate hysterectomy

B. Placental abruption

1. If placental abruption is mild and the fetus is immature, expectant management may be indicated, with fetal heart rate monitoring and serial laboratory/ultrasound examination. Occasionally a small separation occurs without further problem. These patients have no uterine symptoms. Observation is required, but if no fetal distress occurs in the next 2 days, the patient may be sent home

2. In all other cases, delivery is indicated. A vaginal delivery is preferred when fetal distress is not present or the fetus is no longer viable. A cesarean section is indicated if fetal distress is present. A cesarean section is also performed when there is a threat to the mother's life or a failed trial of labor

3. Shock must be treated with adequate replacement of blood loss. Fresh whole blood is preferable. While awaiting blood, colloid may be used (1 cc colloid, e.g., albumin, Plasmanate) for every cubic centimeter of estimated blood loss or 3 cc crystalloid (e.g., normal saline [NS] or lactated Ringer's solution [LR]) per every cubic centimeter of blood. Urine output must be maintained at 25 to 30 cc/hr. A central venous pressure line or Swan-Ganz catheter will assist in monitoring the hemodynamic status

4. Coagulopathy should be treated with fresh whole blood. Fresh frozen plasma (FFP) is used alternatively. One unit of FFP increases the fibrinogen concentration by 25 mg/dL. Platelet transfusion is required if the count is less than 50,000. Heparin is not used in disseminated intravascular coagulation (DIC) secondary to placental abruption


Lower UTI - Male
Cornell Peters, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. ETIOLOGY

Ascending infection from the urethra most common, hematogenous, lymphangitic spread or extension from an adjacent organ possible. Pathogens: E. coli (80%), Proteus, Enterobacter, Pseudomonas, Serratia, Streptococcus faecalis, and Staphylococcus species are the most common

II. LOCALIZATION OF LOWER UTI

Divided urine collection may help localize infection

A. First voided 10 mL represents urethral

B. Midstream collection represents bladder

C. Prostate represented by prostatic secretions from massage and first-voided 10 mL postmassage

III. BACTERIAL CYSTITIS

A. Signs/symptoms: frequency, urgency, dysuria, nocturia, suprapubic discomfort, hematuria, low back pain. Systemic symptoms are absent

B. Laboratory findings: UA shows pyuria, bacteriuria, no casts. C&S; reveal more than 10 3 colonies of bacteria

C. Treatment: Should always obtain C&S; in males. Treat 10 to 14 days, then obtain follow-up culture. Antibiotic choices are similar to female UTI--section IV C. Consider intravenous pyelography (IVP)/cystoscopy to rule out structural obstructions to outflow after the urine is sterile

IV. ACUTE BACTERIAL PROSTATITIS

A. Signs/symptoms. Systemic: fever, chills, malaise, low back pain; urinary: frequency, pain, urgency, varying degrees of retention. The prostate is very tender, boggy, and perhaps hot to touch (do not massage--risk of bacteremia)

B. Laboratory findings: leukocytosis, bacteriuria, hematuria, pyuria. C&S; required

C. Therapy

1. Hospitalization is necessary for IV antibiotics if sepsis is suspected. Start an aminoglycoside and ampicillin or ampicillin/sulbactam pending culture results

2. Avoid urethral catheterization

3. If hospitalization is unnecessary, TMP/SMX DS, twice daily for 4 to 6 weeks, ciprofloxacin, 500 mg twice daily for 4 to 6 weeks, or norfloxacin, 400 mg twice daily for 4 to 6 weeks, may be used. Minocycline or carbenicillin are also acceptable treatment

4. In young, sexually active men, treat for gonorrhea and chlamydial infection for 14 days

V. CHRONIC BACTERIAL PROSTATITIS

A.Signs/symptoms: Low back and perineal Discomfort, voiding symptoms similar to acute bacterial prostatitis but with a more insidious onset, no systemic signs, rarely painful ejaculation. Prostate examination is normal

B. Laboratory tests: UA and cultures should be done. Prostatic secretions reveal inflammatory cells; UA will show WBCs and bacteriuria if secondary cystitis is present

C. Treatment of choice is ciprofloxacin, 500 mg orally, or norfloxacin, 400 mg orally twice daily for 4 to 6 weeks. This yields about an 80% cure rate. TMP/SMX (2 tablets containing 80 mg TMP and 400 mg SMX or 1 DS) twice daily for 3 months cures about a third and improves symptoms in about three quarters. Failure of therapy may indicate the need for IV therapy. Chronic suppression with TMP/SMX at nighttime or a quinolone may be helpful

VI. NONBACTERIAL PROSTATITIS

A. Etiology: unknown. Chlamydial infection is suspected but not proved

B. Signs/symptoms: as for chronic bacterial prostatitis

C. Laboratory findings: prostatic secretions reveal inflammatory cells but no bacteria. No causative agent is found in any cultures. Consider immunofluorescent studies for chlamydia

D. Therapy: doxycycline, 100 mg twice daily, or erythromycin, 500 mg four times daily for 4 weeks, is recommended but often unsuccessful. Other measures include sitz baths, nonsteroidal antiinflammatory drugs (NSAIDs), prostatic massage (controversial), and reassurance

VII. PROSTATODYNIA

Prostate pain without prostatic infection or inflammation; formerly called prostatosis

A. Signs/symptoms: as for chronic bacterial prostatitis

B. Laboratory findings: absence of inflammatory cells or bacteria

C. Therapy: reassurance. Consider a-adrenergic blockers (Prazosin) if symptoms include hesitancy and slow stream. Consider psychiatric consultation

D. Other prostatic infections: TB, mycotic, viral, nonspecific granulomatous, allergic granulomatous, cryptococcal in patients with acquired immunodeficiency syndrome (AIDS)

VIII. EPIDIDYMITIS

A. Etiology

1. Sexually transmitted form associated with urethritis, commonly caused by Chlamydia and/or Neisseria gonorrhoeae

2. Nonsexually transmitted form associated with UTI or prostatitis, commonly caused by Enterobacter or Pseudomonas

3. Causes such as trauma, tuberculosis, chemical from urine reflux, or as a complication of transurethral prostatectomy (TURP) or systemic infection are less common

B. Signs/symptoms: similar to urethritis/prostatitis/cystitis. Epididymitis is painful, and tenderness may extend to the groin, lower abdominal area, and/or flank. Fever, urethral discharge, and reactive hydrocele are common

C. Laboratory findings: white count is elevated with a left shift. UA may show pyuria/bacteriuria. C&S; is indicated

D. Differential diagnosis: mumps orchitis, tumor, testicular abscess, torsion, and trauma must be considered

E. Therapy

1. General measures: bed rest, scrotal elevation and support, analgesics, ice (early), heat (late), and spermatic cord block with lidocaine may be used

2. Antibiotics: if younger than 35 years, treat for gonorrhea, then follow with treatment for nongonococcal urethritis (see Table 11-2). If older than 35 years, treat with TMP/SMX or fluoroquinolone. If severe disease, can consider amoxicillin/clavulanate, ampicillin/sulbactam, imipenem/cilastatin

3. NSAIDs are effective for the inflammatory component

IX. URETHRITIS

A. Gonococcal urethritis

1. Signs/symptoms: urethral discharge (yellow-brown), dysuria, pruritus, possibly meatal erythema

2. Laboratory findings: calginate swab of the urethra (at least 1 hour after the last voiding) inserted 2 to 3 cm for a Gram stain should show 4 WBCs per HPF. The presence of gram- negative intracellular diplococci is evidence of N. gonorrhoeae. Growth on Thayer-Martin media is proof of infection but may only be positive in 50%

3. Fifty percent have concurrent chlamydial infection

4. Therapy (see Table 11-2)

B. Nongonococcal urethritis

1. Etiology: most commonly (80%) due to Chlamydia trachomatis or Ureaplasma urealyticum. Other causes include Candida, herpes, and Trichomonas

2. Signs/symptoms: similar to gonococcal urethritis, although the discharge (if present) is often clear or whitish. Asymptomatic infection is common

3. Laboratory findings: Gram stain of urethral swabbing reveals more than 4 WBC per HPF but lacks gram-negative intracellular diplococci. C&S; is necessary, although it is often negative in an improperly collected specimen. Immunoassays for Chlamydia should be done

4. Therapy (see Table 11-2)

C. Postgonococcal urethritis: occurs in patients who are treated for gonococcal urethritis but remain symptomatic. This is usually due to concurrent Chlamydia infection and responds to appropriate treatment


OBSTETRICS AND GYNECOLOGY
Review Date:  May 1997

* Material contained herein may be graphic but is intended for clinical use only. *


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ABRUPTIO PLACENTAE
MANAGING PREMENSTRUAL SYMPTOMS
PREGNANCY (morning) SICKNESS: A COMMON BUT STILL CHALLENGING       MEDICAL PROBLEM
PRIMARY CARE TREATMENT OF FEMALE URINARY INCONTINENCE
VULVOVAGINITIS



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ABRUPTIO PLACENTAE
Origination Date: November, 1995
Review Date:  May, 1997

Carl V. Smith, M.D.
Professor and Interim Chairman
McGoogan Professor of OB/GYN
University of Nebraska Medical Center
Omaha, NE

Purpose - Abruptio placenta is an infrequent (.5-1%), but serious complication of pregnancy. It is critical to be able to recognize and treat the diffuse intravascular coagulation (DIC) complication of abruptio placenta.

Educational Objectives
At the conclusion of this CME internet activity, participants should be able:

To be aware of the incidence of abruption of the placenta
To identify possible causes of abruptio placentae
To be able to diagnose cases of abruptio placentae
To list laboratory studies used to monitor cases of abruption
To understand how different routes of delivery are used in abruptio placentae management
To understand the management of the common complication of disseminated intravascular coagulopathy
Incidence

Abruptio placentae, defined as the premature separation of a normally, implanted placenta, occurs with a frequency of 1/100 to 1/200 pregnancies. The perinatal mortality rate in this disorder is commonly held to be between 20% and 50%. In 1977, however, Naeye et al reported a markedly lower perinatal mortality of approximately 4/1000. Nonetheless, this figure represented 15% of all perinatal deaths in the Collaborative Perinatal Project.

Etiology

Although the etiology of placental abruption remains controversial, its pathophysiology is better understood. It is initiated by hemorrhage into the decidua basalis which ultimately splits the decidua. This decidual hematoma may remain within the decidua or may extravasate into the myometrium (producing the Couvelaire uterus), across the fetal membranes (staining the amniotic fluid a port wine color), or may dissect toward the cervix and manifest itself as vaginal bleeding. This expanding hematoma may lead to compression or obliteration of the intervillous space resulting in reduced fetal oxygenation. In addition, reduction of placental surface area occurs, which further compromises the fetus. Fetal death may also occur, especially with a 50% or greater reduction of surface area.

Factors associated with the development of abruption include hypertension, high parity, inferior vena caval compression, sudden uterine decompression, blunt maternal abdominal trauma, short umbilical cord, cocaine abuse, and prior history of placental abruption.

Perhaps the most common associated complication is maternal hypertension. Abdella et al found hypertensive disorders in 26.8% of 265 consecutive cases of placental abruption. In order of decreasing frequency, these disorders were eclampsia, chronic hypertension and preeclampsia. An associated 38% combined perinatal mortality was observed in the hypertensive group. Those patients without hypertension and with placental abruption were observed to have an 18.5% perinatal mortality rate.

A second feature of patients with abruption is a history of prior abruption. The risk of recurrence is variably stated to be between 5.5% and 16.6%. In patients with abruption severe enough to produce fetal death, a similar pregnancy outcome nay be anticipated in 7% of subsequent pregnancies.

Diagnosis

Clinically, patients with this disorder have painful vaginal bleeding. This "pain" may take the form of uterine contractions, uterine tetany, or localized uterine tenderness. Approximately 80% of patients have vaginal bleeding in late pregnancy. The hemodynamic consequences of this blood loss is commonly believed to be out of proportion to the blood loss. In actuality, the bleeding may not be all external. Large quantities of blood can be sequestered within the expanding decidual hematoma. The other 20% of patients may have "concealed hemorrhage" and uterine contractions. The diagnosis in this group of patient required a high index of suspicion. Reasons for lack of vaginal bleeding in the latter group include: (1) the margins of the placenta remained intact despite the retroplacental hemorrhage and (2) firm application of the fetal presenting part, precluding escape of blood or amniotic fluid.

Other clinical signs and symptoms include uterine hypertonus, fetal distress, fetal death and rarely, hypovolemic shock. In a recent review of patients with abruption, the incidence of these were 17%, 60%, and 18%, respectively. Clinical suspicion may also be aroused when progressive enlargement of the uterine fundus is noted or when port wine-colored amniotic fluid is obtained on amniotomy.

The presence of third trimester vaginal bleeding should prompt the clinician to consider other causes. Velamentous insertion of the umbilical vessels with vasa previa should also be considered. Treatment of the vaginal blood with 10% potassium hydroxide (the APT test) and the observation of cells resistant to discoloration should suggest the presence of fetal bleeding. Lastly, placenta previa may be similar to abruption and may usually be excluded by an ultrasonographic examination.

Management

Patients suspected of having an abruption should be treated in a labor and delivery area if possible. One or two large bore intravenous lines should be inserted. Fluid replacement with isotonic crystalloid solution should be instituted. In cases of massive hemorrhage, indwelling catheterization of the bladder is recommended. Similarly, the placement of a central venous line or a flow-directed pulmonary artery catheter (Swan-Ganz) may be of value in assessing the patient's intravascular volume. Frequent monitoring of the patient's vital signs is imperative.

Laboratory examination including the following should be obtained: complete blood count, platelet count, prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen level, and fibrin split products. The patient should be crossmatched for 2 to 4 units of blood (whole or packed red blood cells).

Fetal assessment with external fetal heart rate monitors should be instituted immediately. Close observation for signs of fetal distress may reveal bradycardia, tachycardia, and late decelerations.

If the patient is hemodynamically stable, ultrasonographic evaluation should be performed to rule out placenta previa and to establish the number, position, and viability of the fetus. On occasion, a large retroplacental sonolucency may suggest abruption. Cervical examination may then be done after the exclusion of placenta previa.

The management of patients with mild degrees of abruption is controversial. In the markedly preterm pregnancy and if the mother is hemodynamically stable and devoid of coagulopathy, conservative management may be appropriate. Administration of corticosteroids to enhance fetal pulmonary maturity and continuous direct fetal heart rate monitoring may be a consideration. However the vast majority of those patients should be evaluated for delivery.

Method of Delivery

Once the decision to deliver a patient with a suspected abruption has been made, the route of delivery is controversial. Those patients in whom profuse vaginal bleeding, fetal distress, progressive increase in size of the uterine fundus, and tetanic uterine contractions develop, benefit most from emergency cesarean sections. A progressive decrease in the fibrinogen level, signalling impending coagulopathy, also mandates immediate abdominal delivery unless vaginal delivery is imminent.

In the absence of the aforementioned complications, vaginal delivery may be appropriate. Direct fetal heart rate monitoring, serial studies of coagulation and blood count, and close monitoring of vital sings are mandatory if this route of delivery is chosen.

Immediate access to emergency cesarean delivery is also required. Such selective management in a recent series of 50 patients showed no significant mortality differences between vaginally and abdominally delivered infants.

Management of Coagulopathy

Disseminated intravascular coagulation (DIC) is not an uncommon finding in patients with abruptio placentas. Overall, its incidence is approximately 10%. Abruption severe enough to cause fetal death produces a greater likelihood of DIC. Pritchard and Brekken described a fibrinogen level below 150 mg/dl in 38% and below 100 mg/dl in 28% of these patients. The presumed etiology of the DIC is access of tissue thromboplastin to the maternal circulation with resultant activation of the coagulation cascade. Activation of the fibrinolytic system completes the process.

The most definite method of therapy is removal of the products of conception. Such therapy may rapidly reverse even the most severe coagulopathy. Significant hemorrhage is unlikely if the fibrinogen level is above 100 g/dl. In the event of levels below that level, replacement therapy may be necessary, especially prior to operative delivery. Replacement may be accomplished with fresh, whole blood and fresh frozen plasma. The use of cryoprecipitate or pooled fibrinogen is more specific therapy but carries an increased risk of hepatitis.

One unit of cryoprecipitate will raise the plasma fibrinogen level by approximately 10 mg/dl.

The use of anticoagulation with heparin and of fibrinolytics (epislon-amniocaproic acid) are rarely required. If unremitting coagulopathy persists, consultation with a hematologist is recommended prior to use of those agents.

Significant postpartum hemorrhage may develop in patient with abruption. The mechanism may either be due to coagulopathy or uterine atony. Circulating fibrin split products are themselves, potent anticoagulants and uterine relaxants. Therapy is, therefore, directed towards the replenishment of clotting factors and corrections of the uterine atony. Rarely, patients require uterine or hypogastric artery ligation or hysterectomy.

Examination of the placenta after delivery should be done. The presence of a clot densely adherent to the fetal membranes or placenta is usually considered confirmatory evidence.


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Managing Premenstrual Symptoms
Origination Date: November, 1995
Review Date : May 1997

John F. Steege, M.D.
Professor and Chief
Department of Obstetrics and Gynecology
University of North Carolina
Chapel Hill, NC

Purpose - Many mood disorders may vary with the physiologic changes taking place during a menstrual cycle, but they should not be mistaken for PMS. Physicians should understand that the diagnosis of PMS requires a prospective symptom calendar rather than just a one-time history and physical.

Educational Objectives
At the conclusion of this CME internet activity, participants should be able:

To be familiar with the presumed etiologies of PMS
To be able to diagnose cases of PMS
To determine what treatment should be instituted for PMS
Incidence

While many women may have some noticeable physical and/or emotional changes premenstrually, only about 4 to 6% experience changes severe enough to affect function or interpersonal relationships. Symptoms exist over a wide spectrum, so treatment measures should be used starting with the simplest and moving on to the more complex.

Etiology

It is very clear at this time that premenstrual emotional symptoms do not correlate with the physical changes. Physical problems with mastalgia, fluid retention and so forth are not directly linked to whatever processes cause premenstrual emotional changes. Therefore, you should not expect salt restriction, diuretic use, etc. to substantially improve emotional changes. It is also clear that premenstrual syndrome is not caused by abnormal ovarian function. Women with PMS have the same levels of estrogen and progesterone over the menstrual cycle as do women without PMS symptoms. More likely, the biochemical causes of PMS may involve some central changes in neurotransmitter function which are modulated by an otherwise hormonally normal menstrual cycle. Recent trials of progesterone have shown that it fails to significantly benefit women with PMS. The emphasis has therefore shifted away from manipulations of sex steroids to psychotropic drug use when non-pharmacologic methods fail.

Diagnosis

The first step is to establish the diagnosis. Most women complaining of premenstrual symptoms will retrospectively report that they are positive such a pattern exists. But prospective charting often shows that symptoms may not be so cyclic after all. You should ask the person concerned about PMS to keep a daily calendar of her most prominent symptoms for several cycles. For most clinical situations a simple personal calendar will do. To be labelled "PMS", such symptoms should start no earlier than ovulation and should end within a few days after the beginning of menstruation.

In general, the worse a person's symptoms, the more likely the symptoms are to be premenstrual worsening of an ongoing disorder. Such individuals usually have continuous anxiety and/or depressive symptoms that get worse premenstrually.

When charting shows continuous symptoms that get worse premenstrually, we feel you should first treat the continuous disorder. Usually these women have already tried and failed more conservative non-pharmacologic therapies.

Management

If symptoms are mild or moderate and truly premenstrual only, some relatively simple dietary and behavioral measures often help. Suggest modest salt restriction and a relatively well-balanced diet evenly spaced throughout the day. Caffeine and alcohol should be avoided, since the usual pharmacologic effects of both may be increased premenstrually in women with PMS. Regular physical exercise, particularly aerobic exercise, may be useful to reduce stress and as coping skill. Exercise may also have beneficial effects on the neuro-transmitter mechanisms involved in premenstrual symptoms.

Many claims have been made for nutritional and vitamin therapies. Pyridoxine (Vitamin B6) in mild doses of less than 100 mgs. daily may help, although the evidence is mixed. High doses of B6 have been shown to be severely neurotoxic. No other particular trace element or vitamin has been shown to help in any reasonable controlled trials.

Many individuals note certain days in their menstrual cycle when they feel more stressed out by ordinary daily activities. They might try to schedule particularly stressful tasks for times other than the premenstrual time.

The patient with more severe symptoms is tougher to treat. For those with mainly anxiety that lasts a week or less, alprazolam often helps. Three studies show that it works well for PMS. Often doses of 0.25 or 0.5 mgs. tid are sufficient. Habituation or chemical addiction to alprazolam is uncommon when it is used in this way. Other anxiolytics may be tried, but none has been shown to be effective in controlled trials. One uncontrolled clinical trial supports the use of buspirone, but so far controlled trials have not been performed.

For the woman with severe symptoms lasting 10 days to two weeks or who has significant follicular phase symptoms as well, continuous serotonergic anti-depressant medications are useful. Women with severe premenstrual depression frequently have had a previous acute depressive episode and have a family history of depression. Recent studies show that women with PMS have decreased imipramine binding site levels, with values similar to women with depression. Finally, a very promising result was obtained in a small controlled trial of fluoxetine. Further trials with long-term use will be necessary before the ultimate place for this drug is determined.

Summary

PMS of any significant severity never occurs in a vacuum. Relationship and family problems are often present which in and of themselves would benefit from psychological support and attention. Medical and mental health professionals should collaborate on treatment.

References

Lurie S, Borenstein R: The premenstrual syndrome. Obstet Gynecol Surv 45:220-228, 1990.

Rubinow DR, Roy-Byrne P: Premenstrual syndromes, overview from a methodologic perspective. Am J Psychiatry 141:163-172, 1984.

Stone AB, Pearlstein T, Brown W: Fluoxetine in the treatment of premenstrual syndrome. Psychopharmacol Bull 26:327-331, 1990.

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Pregnancy (morning) Sickness:
A common but still challenging medical problem
Origination Date:  May, 1997

Juliet Markham MD and Frederick R. Jelovsek MD
Department of Obstetrics and Gynecology
East Tennessee State University
Johnson City, Tennessee U.S.A.

Purpose - Pregnancy (morning) sickness is a common occurance in pregnancy but other possible causes of nausea should not be ignored. Treatment is somewhat difficult because of the goal of minimizing a pregnant woman's exposure to medications especially in early pregnancy when this problem usually presents.

Educational Objectives
At the conclusion of this CME internet activity, participants should be able:

To appreciate the high incidence of pregnancy sickness
To review the etiology of pregnancy sickness
To be able to identify when to look for diseases other than pregnancy sickness
To list treatments for pregnancy sickness
Summary
Incidence
The incidence of pregnancy/morning sickness is roughly 60-80% in American women. Symptoms usually appear between the 2nd and 12th week of pregnancy and subside 6-8 weeks later. It is usually self-limited and only 1 in 200-300 patients experience the severe dehydration and ketosis, which is known as hyperemesis gravidarum 1. Although traditionally referred to as morning sickness, pregnancy sickness may occur any time of day or night. About half of all affected mothers get waves of nausea but no vomiting, while in the other half, nausea leads to vomiting to a varying degree.

Interestingly, pregnancies complicated by nausea and vomiting often have a lower pregnancy loss outcome than those pregnancies without, but there may be a slightly higher incidence of birth defects whether or not antiemetic therapy is administered 2,4.

The cost factor of women staying home from work, out of school, etc. is difficult to assess. It is likely to be a significant impact in today's work force.

Etiology

The cause of pregnancy sickness is not yet fully understood. Relaxation of the smooth muscle of the upper gastrointestinal tract due to the influence of progesterone may play a role. Previously, the nausea was thought to be related to human chorionic gonadotropin (HCG) since patients with twins or molar pregnancies have a high incidence of hyperemesis gravidarum and those conditions are characterized by high HCG levels. Direct intravenous injection of HCG does not reproduce nausea however, and the degree of nausea is not related to HCG levels. In the pathophysiology of nausea and vomiting, the vomiting center is located in the reticular formation of the brain, near the sensory nucleus of the vagus nerve. Mechanical stimulation may take place here or afferent impulses of stomach/duodenal distension. It is a complex reflex that is not well understood. Nausea is accompanied by mainly parasympathetic stimulation such as increased perspiration, salivation, pallor, bradycardia and hypotension. Vomiting is reversed peristalsis, forcibly emptying the stomach. There are many associated metabolic states causing nausea and emesis such as renal failure, alkalosis, pregnancy, drug overdose/toxicity, migraine/tension headache disorders and labyrinthine disorders, to name only a few. Antiemetics act on the vomiting center in the CNS by inhibiting its reflex activity. Corticosteroids have been used as effective antiemetics, but the mechanism of action is unknown.

Diagnosis

Classic onset in early pregnancy and disappearance by the second trimester are hallmarks of diagnosis. No other symptoms such as diarrhea, bloody diarrhea or hematemesis are associated. There is no pain other than mild discomfort resulting from the act of vomiting. Nausea that persists beyond the 20th week of pregnancy, or nausea with vomiting that produces ketosis or electrolyte disturbance should not be attributed to pregnancy sickness. Gastric reflux which is common in late pregnancy is uncommon with pregnancy sickness.

Treatment

Diet modification is the mainstay treatment for pregnancy sickness. This includes eating small frequent snacks, avoiding fatty and spicy foods, avoiding foods or odors that trigger the nausea, minimizing fluids with meals, and frequent consumption of crackers or dry cereals. Each patient seems to have different olfactory triggers - "a radar nose of pregnancy". Thus it is important to customize the diet for each patient. One patient's symptoms may be reduced by consuming saltines and ginger ale while another finds relief by ingesting potato chips and lemonade 3.

Pyridoxine (vitamin B6) 10-30 mg/day is sometimes used now in place of the previously, frequently used Bendectin® which was taken off the market in 1983. Bendectin® was composed of pyridoxine 10 mg and an antihistamine, doxylamine succinate 10 mg. Both of these components are still available today but would have to be prescribed separately. When sickness is severe and borders on hyperemesis gravidarum, antiemetics such as promethazine (Phenergan®) 12.5-25 mg tid, trimethobenzamide (Tigan®) 250 mg tid, prochlorperazine (Compazine®) 5-25 mg qid, chlorpromazine (Thorazine®) 10-25 mg QID, meclizine (Antivert®) 12.5 bid and dimenhydrinate (Dramimine®) 50 mg qid are sometimes used.

The reasoning behind any drug therapy for pregnancy sickness is obscure. Histamine H1-receptor antagonists and dopamine receptor antagonists may be effective because circulating gonadotropins sensitize vomiting pathways involving dopamine and histamine H1- receptors 4.

Herbal medicines have been recommended as preventative treatment but there is not much scientific data available. Ginger has long been used in Europe and Asia as a digestive aid especially for nausea and vomiting. It is thought to act locally on the digestive system with no known side effects. Ginger is a spice and a food as well as an herbal medicine. It is consumed worldwide in large quantities, with no known adverse effects recorded in the literature. Ginger improves production and secretion of bile from the liver and gallbladder. It is noted for improving gastrointestinal motility. Ginger as treatment of hyperemesis gravidarum has been studied in Denmark in a double- blind crossover trial 5. That trial found ginger to be effective therapy at reducing the symptoms of nausea and vomiting. Therefore, ginger may be effective in the management of pregnancy sickness since the symptoms are the same but less severe.

Peppermint has also been advocated for nausea and vomiting however it is likely that it is more effective as an aromatherapy. We could not find that it has been scientifically tested but it should be safe to use. A drop of essential oil on a sugar cube which is sucked slowly until the cube is melted or a glass of water spiked with two drops of essential oil has been recommended 6 as a method of administration.

Summary

Because pregnancy sickness comes in waves, there are many different olfactory triggers and interpersonal situations can play a role, the treatment for each patient is difficult to standardize. Since there are no predominantly successful treatments and the disease is not often severe, it remains untreated and underappreciated by many health care providers.


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Primary Care Treatment of Female Urinary Incontinence
Origination Date: May 1997

Frederick R. Jelovsek, MD
Professor Obstetrics and Gynecology
East Tennessee State University, Johnson City, TN, USA
Jelovsek@xtn.net

Purpose - In most instances, the likely cause of urinary incontinence in a woman can be diagnosed accurately in the primary care office by a thorough history and physical exam. Simple medical and behavioral treatments can cure or improve symptoms in many cases so that referral is not needed.

Educational Objectives
At the conclusion of this CME internet activity, participants should be able:

To determine when urinary incontinence problem should be fully worked-up and treated
To determine when to order multichannel urodynamic studies
To list non-surgical treatment of urinary incontinence that is likely to be effective
To determine when surgical treatment should be strongly considered
To be able to alter medical therapies in order to minimize incontinence symptoms
Summary



History and Physical Findings

During a regular health maintenance check-up, or during a review of systems for a problem-based visit, each female who is past menopause should be asked about the presence of urinary loss or leakage. Many women admit to some urinary loss on rare occasions, such as with a severe cold or a very full bladder, or even a urinary tract infection. For most women, however, it is not a serious or regular problem. When the patient says that she wears a perineal pad or panty liner because of frequent urinary loss, or if she alters her work, leisure or social activities because of fear of urinary loss, then urinary leakage should be fully diagnosed and treated.

The incidence of urinary incontinence jumps after the menopause (Olsen et al). We think this is because of progressive loss of vascularity after menopause due to estrogen deficiency. The vascularity of the pelvis helps prevent relaxation of the genital tissues. After menopause, especially if no estrogen replacement therapy is given, these tissues progressively weaken. This weakening may result in descensus of the urethral vesicle neck to cause stress incontinence. Atrophic changes of the vaginal epithelium and urethral meatus are also felt to contribute to urge incontinence. Other medical conditions that can cause urge incontinence also increase after age 50.

After determining whether a clinically significant problem of urinary incontinence exists, history questions should be directed toward determining whether the patient has had any history of central nervous system or spinal cord or other neurological or neuromuscular problems. Cerebral vascular accidents, Parkinson's disease, and Alzheimer's disease among others can cause a detrusor dyssynergia, which is an asynchronus coordination between the relaxation of the internal urethral sphincter, external urethral sphincter and the contraction of the detrusor muscle. Patients with multiple sclerosis or spinal cord injuries may often have urge incontinence problems with hyperreflexic bladders. Patients with severe osteoarthritis with lower spinal cord (sacral) diseases can have neurogenic bladders also. Trauma to the coccyx should be asked about. Other important findings in the patient history would be any surgery on the genital or urinary tract or radiation therapy to the pelvis. Previous gynecologic or urological surgery to fix urinary incontinence can significantly alter normal anatomy or physiology and those patients usually should be referred to an incontinence specialist. Any suspicion of continuous incontinence may indicate fistula formation. Fistulae are usually related to surgery or radiation therapy, or a chronic inflammatory process such as regional enteritis, or diverticulitis. End stages of cancer of the abdominal or pelvic cavity can produce urinary tract fistulas in these cases.

Finally, patients who are cognitively impaired either by psychological disease, psychological medications or any other medical disease, may manifest a factitious or "pseudo" incontinence and actually do not lose urine involuntarily, but are not aware that they are initiating the urination process.

On physical exam, the patient's mental awareness and a screening neurological exam such as lower extremity reflexes and sensations should be checked. The presence of any large abdominal masses such as abdominal tumors, uterine fibroids or even pregnancy should be checked for since mass pressure on the bladder can give urinary symptoms may include urinary loss. The pelvic exam can help differentiate causes of urinary incontinence. External genitalia should be viewed for inflammatory changes due to constant urine soaking as well as any urethral meatus prolapse or diverticulitis. A rectal wink reflex is obtained by gently stroking the external anal sphincter on each side and should result in a contraction of the sphincter. It indicates an intact pudendal nerve. The Q-tip test is conducted by placing a sterile Q-tip with xylocaine gel on it into the urethral meatus, usually up to the internal sphincter but not through it. The patient is then asked to strain down or to cough. Since the urethra is always fixed distally to the inferior margin of the pubic symphysis, the end of the Q-tip that is visible outside the urethra will elevate if there is descensus of the urethral vesicle neck. A change of 30 degrees or more indicates significant descensus of the urethral-vesicle neck and is almost always present with stress urinary incontinence.

On speculum exam, one should check for any descensus of the cervix or the vaginal vault. Prolapse of the vault structures descending to or beyond the hymeneal ring, will need to be evaluated by gynecology before any surgical repair because other pelvic support defects usually accompany this problem. If the vaginal sidewalls collapse in toward the center on opening a bi-valve vaginal speculum, you may suspect a paravaginal defect. This means detachment of the vagina from the levator ani muscles of the pelvis. The pubovesical-cervical fascia covering the vagina anteriorly is support for the urethra and with either a unilateral or bilateral paravaginal defect, patients almost always have a genuine stress urinary incontinence.

On bimanual exam, unusual tenderness of the urethra or bladder should be checked for and palpation of the urethra to look for a diverticulum or Skene's gland swelling. The uterus should also be palpated again to make sure that there are no central masses that are exerting undo pressure upon the bladder.

When to order multichannel urodynamic studies

If patients complain of urgency symptoms, there is often, but not always, a component of urge incontinence. If it is possible to perform simple office cystometrics with a water manometer, that should be done to detect any uninhibited bladder contractions. Otherwise, a cystometrogram at the most convenient and cost- effective facility should be ordered. This can show if uninhibited bladder contractions (detrusor instability) are present. If the patient notes a history of any radiation therapy to the pelvis, especially treatment for carcinoma of the cervix or endometrial carcinoma, a urethral pressure profile should be ordered. This will help check for intrinsic urethral insufficiency in which the internal urethral sphincter is unable to maintain a sufficient amount of background urethral tone to prevent loss of urine.

If patients have a history of difficult urination in which they need to strain to overcome resistance, a uroflow study is helpful because it may pickup or suggest a detrusor sphincter dyssynergia or may indicate a degree of functional urethral obstruction due to cystocele or prolapse. If there is any history of a previous bladder suspension and hesitancy or difficulty passing urine is present, it may be that there is some urethral obstruction that would be present on uroflow and would indicate the need for cystoscopy.

Urodynamic studies should not be ordered if the patient has any symptoms of urinary tract infection. Urinary tract infection can simulate any incontinence picture from urge to stress to mixed incontinence. Urodynamic studies performed in the presence of infection have been shown to be very inaccurate.

What non-surgical treatment can be used in the office

The most common form of non-surgical therapy for urinary incontinence is behavioral modification and various pharmacologic agents. Behavioral modification includes pelvic floor exercises such as Kegel exercises, and timed voiding or double voiding, known as bladder retraining. In a study by Karram, et al, one group of 100 women were started on therapy after a minimal office evaluation that did not include invasive urodynamic testing. They were compared with 102 women who were also treated based on first having invasive urodynamic testing. Both groups showed almost 60-70% subjective improvement or cure with the non-surgical therapy. Those authors felt it was more cost effective to initiate non-surgical therapy (Kegel exercises and bladder retraining) prior to urodynamic testing in many patients.

Instruction should be given to the patient and at the time of pelvic exam, the physician should demonstrate to the patient which muscle it is that the patient should contract. This is usually accomplished by placing one or two fingers in the vagina and having the patient concentrate on tightening around those fingers so that the examiner can feel it. The muscle that should contract is the bulbocavernosus muscle that surrounds the opening of the vaginal behind the hymeneal ring. The compressor urethrae (membraneous urethral sphincter) is continuous with this muscle. Most patients will also contract the levator muscles (pubo- and illiococcygeus) which is acceptable. Later, the patient can put her own fingers in the vagina to make sure the correct muscle is begin contracted. Contraction of the buttocks (gluteus) or the abdominal muscles are not desirable and patients have to be taught how to perform a correct Kegel contraction.

While these isometric exercises contracting the perineal muscles can be effective, most patients who have a positive benefit from them say that it takes at least 3-6 months of exercising before they see significant improvement. They must be encouraged to continue the exercises and they should be checked periodically to make sure that they are contracting the correct muscles.

Another muscle strengthing therapy useful if stress incontinence is not severe is the use of vaginal cones. These are a graduated set of weighted tampons that the patient wears several times each day for about 10 minutes. When she is able to successfully carry out normal activities at one weight, she goes up to the next weighted tampon in the series.

Bladder retraining is usually performed in one of two ways: a single void or a double void technique. Patients with a high residual urine or very large capacity bladders are often placed on a double-timed voiding technique so that they initially empty their bladder. Then after a few minutes try to empty their bladder a second time. The principle behind the standard bladder retraining is to make the detrusor muscle of the bladder respond when the patient wants it to respond, rather than allowing it to contract on its own (involuntary) schedule. This is accomplished by instructing the patient to void every hour, on the hour, for one week. A timer such as a watch with a little beeper that goes off each hour, or for whatever time it is set, or a small kitchen timer should be used. If patients are left to their own clock- watching, they will rarely be able to keep to such a rigid schedule because of activities which distract them from voiding when they should. After a week of being able to void on the hour without accident, the patient increases the time to 1 1/2 hours for a week, then 2 hours, 2 1/2 hours and 3 hours. Usually it takes 1-2 months to get to this point.

The patient should not hold urine longer than three hours during the day. Patients with urge incontinence, stress incontinence or mixed incontinence can significantly benefit from bladder retraining. It is a very worthwhile program to initiate when patients are initially seen, but it takes persistence on the patient's part to benefit. It also takes persistence on the physician's part in order to encourage and instruct patients about bladder retraining.

Pharmacologic therapy can be directed toward blocking uninhibited bladder contractions (anticholinergic drugs) or alpha agonists that will stimulate the internal urethral sphinchter to contract. This provides increased resistance to urinary leakage with detrusor contractions or sudden increases in intraabdominal pressure.

Oxybutynin chloride (Ditropan®) is usually given 2.5 to 5 milligrams t.i.d. Imipramine, 10 milligrams b.i.d. is also effective and has less side effects than the sometimes used higher doses of 50-100mg. Local muscle relaxants such as hyoscyamine sulfate (Cystospaz®) may be used as well as calcium antagonists such as nifedipine or prostaglandin inhibitors such as indomethacin. The overall success rate of these pharmacologic therapies, however, is not much more than 45% in most prospective, randomized clinical trials (3). Overall, bladder retraining seems to be more effective than most of the pharmacological therapies. Alpha agonists such pseudoephedrine hydrochloride (Sudafed®) 60 milligrams tid and phenylpropanolomine (Entex L.A.®) can be used to increase urethral tone for either stress or urge incontinence.

Finally, estrogen therapy is another pharmacologic agent used and seems to thicken the urethral mucosa and engorge the blood vessels beneath. It is felt to improve stress incontinence in over 50% of patients. It is usually given as a vaginal cream (one applicator full every other day) or orally.

If patients have predominantly stress symptoms, there are some vaginal pessaries that may help restore the urethra to an intraabdominal position and give it support when intraabdominal straining takes place. Patients may have difficulty keeping the pessary in depending on what other anatomical relaxation problems they have. Many elderly patients are quite hesitant or afraid to put pessaries in and out of the vagina. But, when patients are able to use them, they can often be effective in decreasing the symptoms. It can keep them dry enough so that there is not tissue breakdown of the perineal skin.

When to consider surgical treatment

A significant prolapse of the uterus, or the vaginal vault if the patient has had a hysterectomy, is likely to require a surgical approach. In fact, when prolapse occurs and there is no incontinence, treatment of the prolapse using vaginal pessaries can actually unmask an occult incontinence. In this case, prolapse is fixed with the pessary, but the urethral-vesical neck is no longer obstructed by acute angulation of the bladder and the urethra. Stress incontinence then occurs if urethral support is poor. If there is a continuous incontinence, a fistula of either the bladder to the vagina, the ureter to the vagina, or the bladder to the uterus is suspected. These will require surgical repair and should be directly referred.

How to alter medical therapy in order to minimize incontinence symptoms

Any medication that has significant alpha-adrenergic blocking activity can cause or worsen stress urinary incontinence. It keeps the internal urethral sphincter from contracting. Antihypertensive agents that have alpha blocking activity such as Minipress®, can be changed to non-alpha blocking medications. Some beta blockers may also worsen urinary leakage. If the patient can be managed with a non-alpha and non-beta blocker, eg. a calcium channel agonist or ACE inhibitor, that can help decrease the patient's symptoms. Skeletal muscle relaxants, especially the benzodiazapines, such as Valium®, Zanax® and Klonopin®, can overrelax the external urethral sphincter which is often the last vestige of maintaining an intraurethral pressure higher than detrusor or abdominal pressure. If patients' anxiety symptoms can be managed with non-skeletal muscle relaxants, that can improve their urinary loss symptoms.

If the patient is on any medications that have anticholinergic effects, they may be at risk for bladder atony and overflow incontinence. Maximum bladder capacity should be determined by measuring the amount of urine voided when the patient feels the urge to void. If this volume is greater than 800 ccs, bladder atony should be suspected. These patients should be switched if possible, to any agents with less anticholinergic symptoms. In addition, timed double voiding may help reduce the problem.

Summary

Urinary incontinence symptoms should be screened for in all menopausal women . If you determine they have significant leakage affecting their daily life, further workup and treatment is indicated. As long as there are not existent neurological problems or a significant vaginal prolapse, most patients can undergo office treatment to improve their urinary symptoms. Behavioral therapy using Kegel exercises and bladder retraining are the hallmarks of that treatment. Also, altering medications which patients may be on for other reasons and which have an effect on voiding mechanisms, may help to significantly lessen incontinence symptoms. The primary care physician can effectively manage more than half of the cases of urinary incontinence if motivated to do so.



Diagnostic category
 Question to ask
stress
 Do you lose urine when you cough, sneeze. or laugh suddenly?
stress
 Do you lose urine when you stand up, sit down or bend over?
urge/ type III stress
 history of radiation treatment to pelvis
urge
 Do you get the urge to void and not get to the bathroom in time?
urge
 history of neurologic diseases/trauma/strokes
urge or overflow
 Do you lose urine suddenly without any warning or straining?
obstruction/ detrusor-sphincter dyssynergia
 Do you have difficulty voiding?
overflow
 Do you wet the bed at night and are unaware of it?
overflow/continuous
 history of previous surgery on urethra/bladder
overflow / obstruction
 Do you fail to empty your bladder completely?
continuous
 Do you stay wet all the time without any urge to void?
need cystoscopy
 Do you have frequent (>3 per year) urinary tract infections?
need cystoscopy
 Do you have blood in your urine?
need cystoscopy
 Do you have pain when you void?
need cystoscopy
 Do you urinate very frequently (>14 per 24 hours)?



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Diagnostic category
 Physical exam finding
stress
 demonstrable urine loss (immediate) with coughing
stress
 Q-tip decensus with straining (valsalva)
stress
 paravaginal defect(s)
urge
 demonstrable urine loss (one more seconds delay) with coughing
urge
 upper extremity tremors
urge/overflow
 abnormal/unequal lower extremity sensation or motor problems
overflow
 postvoid residual urine >100 cc's
overflow
 total bladder capacity >800 cc's
overflow
 bladder, uterus, or vaginal prolapse to or through hymeneal ring
pseudo/overflow
 cognitive impairment
occult
 demonstrable urine loss with replacement of prolapse to normal position


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Type
 Activity avoided due to urine leakage/loss
home
 vacuuming
 stretching to shelves
 lifting bags or boxes
 military training
work
 lifting
 pushing
 waitressing
leisure
 gardening
 walking/speed walking
 tennis/golf
 bowling
 aerobic exercises
social
 athletic event observation
 sexual relations


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 Pelvic support defect
enterocoele
 Name
rectocoele
 rectovaginal septum and rectum
cystocoele
 bladder, pubovesical cervical fascia and anterior vaginal wall
cystourethrocoele
 urethral descent along with bladder (not a urethral diverticula)
perineal descent
 perineum and external anal sphincter
rectal prolapse
 inversion of rectal ampula with straining


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Vulvovaginitis
Origination Date: November, 1995
Review Date:  May 1997

Subir Roy, M.D.
University of Southern California
School of Medicine and Women's Hospital
Los Angeles, California

Purpose - Vulvovaginitis is a frequently occurring problem for many women. It is important to correctly diagnose the most common causes so that treatment will be specific and lessen the incidence of chronic, recurrent cases of vulvovaginitis.

Educational Objectives
At the conclusion of this CME internet activity, participants should be able:

To understand the physiology of the vagina subject to change in infectious states
To be able to identify and treat trichomonas vaginitis
To be able to diagnose and treat vaginal candidiasis
To identify bacterial and other causes for vaginitis
Background

Vulvovaginitis, a common problem treated in office practice has many causes and is often transmitted by sexual contact. The cardinal symptom of vaginitis is an abnormal vaginal discharge. If the vulva is involved, the patient may also complain of pruritus, burning pain, dysuria, and dyspareunia. The cause of the symptoms is usually one or more micro-organisms. A vaginal discharge can also be physiologic when due to (1) mucus secretion from the endocervix at midcycle or (2) desquamation of epithelial cells premenstrually. Sometimes chemical irritation, an allergen, or a foreign body will produce an inflammatory reaction. Other factors that contribute to vulvovaginitis are poorly cornified vaginal epithelium, as seen in prepubertal girls and postmenopausal women, fecal contamination from the anus, sexual intercourse, chronic cervicitis, pregnancy, excessive local heat and moisture, broad spectrum antibiotic therapy sufficient to destroy the normal bacterial flora, and coexisting systemic disease, particularly diabetes.

The vagina is normally acidic (pH 3.8 to 4.2) because of the lactic acid produced by Doderlein's bacillus (Lactobacillus acidophilus). Cervical mucus, menstrual blood, overgrowth of other organisms of the vaginal flora, and progesterone all raise the vaginal pH and favor the growth of trichomonads and Gardnerella vaginalis (previously known as Corynebacterium vaginalis or Haemophilus vaginalis).

A patient history should include accounts of any previous vaginal infections and their treatment, as well as hygienic, contraceptive, and sexual practices. Microscopic examination of a wet smear will help to differentiate among infections due to fungi, trichomonads, and bacteria.

Trichomonas

Trichomoniasis of the urogenital tract is caused by the flagellated protozoan Trichomonas vaginalis, a sexually transmitted microorganism found in adults of either sex. A moderate rise in vaginal pH (greater than 4.5) favors its growth. Another factor encouraging trichmonal infection is local erosion resulting from chemical or mechanical trauma, neoplasms, or other forms of vaginal infection. Presumably there is no significant host immunity to Trichomonas.

Clinical Picture

Asymptomatic carrier - Approximately 15% of women in the reproductive years of life harbor T. vaginalis, but only one third of these women have symptoms and signs of local inflammation, probably because the organism is more virulent. Asymptomatic carriers identified by wet mount preparations at the time of routine gynecologic examination should be treated to prevent transmission of the disease and to minimize the possibility that an acute infection will eventually be established.

Active infection - Trichomoniasis usually produces a malodorous discharge that may be frothy, profuse, thick or thin, and green, yellow, gray or white in color. If the vulva is involved, there may be local pain, itching, dyspareunia, dysuria, or urinary frequency. Erythema and edema of the vulva and vagina and punctate subepithelial hemorrhages or strawberry marks on the vagina and cervix are sometimes observed.

Diagnosis - In 80% or more of cases, a wet smear prepared with warm saline and examined immediately will contain motile trichomonads. They are easily identified by their size, shape, and flagellate motion. Other cases may be identified by cytologic smear, though there is a considerable incidence of both false-positive and false-negative reports. Staining methods add little to diagnosis, and cultures are seldom needed.

Systemic treatment - The drug of choice is metronidazole (Flagyl®), and an adequate dose for most patients is 500 mg every 12 hours for 7 days ( a smaller amount than recommended by the manufacturer), 250 t.i.d. for 7 days, or 2 grams as a single oral dose. Topical metronidazole has not been found to be effective. The teratogenic potential of metronidazole is unknown, but probably safe. Many consider it prudent to withhold this drug during the first 17 weeks of pregnancy, while others feel it can be used in early pregnancy. The short-term cure rate with this regimen approaches 98% with a 10% side effect rate consisting chiefly of gastrointestinal complaints. Long-term cure rates depend on whether trichomoniasis is also eradicated from patients' sexual partners.

Topical treatment - A number of topical preparations are available, including suppositories, creams, and douches. Among these, betadine douche at bedtime for seven to ten days may be used. Although not particularly effective, betadine douche may be useful in controlling symptoms in patients with multiple sexual partners when the partners cannot be treated. Metronidazole gel (Metrogel®) vaginally may be used in early pregnancy although it is not a first line choice for treatment of trichomoniasis.

Therapy for sexual partners - Ideally, male sexual partners should be examined and treated if indicated. The diagnosis of trichomonads in the male is made on a wet mount of urethral discharge obtained spontaneously or after prostatic massage. As a compromise, a couple can be treated concurrently. The male should use a condom during therapy to reduce the risk of reinfection. An alternative for the male partner is to abstain from intercourse for a month (or use a condom) in expectation that the infection will clear spontaneously.

Resistant Disease - Continuing or recurrent symptoms may be a cue to a coexisting pathogen such as Candida, to recurrent infection from an untreated sexual partner, to drug resistance or poor drug absorption, or to local inactivation of the drug by vaginal bacteria. In the last case, oral metronidazole should be repeated in combination with intravaginal antibacterial therapy.

Candida

Vulvovaginitis due to Candida is usually caused by the species C. albicans, a dimorphic fungus that forms yeast like buds, pseudohypha, and hyphae. This ubiquitous organism is frequently found as a saprophyte on the skin and in the bowel, oropharynx, and vagina. When host defenses are impaired, it becomes a pathogen.

Factors that presumably predispose to candidal vulvovaginitis include: an excess of vaginal glucose, as occurs in pregnancy or diabetes; a reduction in vaginal bacterial flora, as occurs with the use of broad spectrum antibiotics; and an excess of local moisture, as occurs during hot, moist weather or with tightly fitting clothing.

Clinical Picture

Vulvitis - A candidal infection usually involves both the vulva and the vagina. The major vulva symptom is pruritus, which may be associated with dysuria, dyspareunia, and local pain. The skin is erythematous, slightly edematous, and often excoriated.

Vaginitis - A typical discharge is thick and whitish and resembles cream cheese or cottage cheese. The vaginal surface may be erythematous but often appears normal.

Diagnosis

Candidiasis that produces a typical cheesy discharge can be diagnosed on sight. Vaginal pH is usually less than 4.5. Other cases can be diagnosed by microscopic examination of a wet smear prepared by mixing a sample of the discharge with a few milliliters of normal saline to which several drops of 10% potassium hydroxide have been added. Candidal cells are oval or round and approximately the size of a red blood cell. Elongated buds and pseudomycelia may also be present. Still other cases will require a culture for confirmation. Either Sabouraud's or Nickerson's medium inoculated with cells from a cotton swab will show evidence of growth in two to three days.

Treatment

The vagina is first cleansed as thoroughly as possible to remove excess discharge before the start of treatment.
A topical antifungal agent is usually prescribed. Nystatin (Mycostatin®, Nilstat®) vaginal tablets, one in the morning and one at night for 14 days. Miconazole nitrate (Monistat® 7) cream, one applicator full intravaginally nightly for seven days. The suppository form (200 mg) is once a day for 3 days. Clotrimazole (Gyne-Lotrimin®, Mycelex-G®), one applicator full intravaginally nightly for 7 to 14 days, or one table intra-vaginally nightly for 7 days, or two tablets intravaginally nightly for 3 days. Clotrimazole (Mycelex-G®, 500 mg), one suppository at bedtime has been reported to be efficacious. Terazole® (terconazole, 80 mg) suppository intravaginally nightly for 3 days is very effective. Fluconazole (Diflucan®) 150 mg oral tablet one time dose is commonly used although resistances are starting to be reported.
Although messy and somewhat irritating, genitan violet solution (1%) aqueous is an effective adjuvant that can be applied at an office visit for chronic recurrent candidiasis.
Coexisting vulvitis is best treated by local application of a corticosteroid cream plus an antifungal agent - for example, Mycolog II® ointment - which has a higher pH than the vagina and does not burn when applied to the vulva.
Clothing that increases local heat and moisture, such as nylon underwear and tightly fitting garments, should be avoided.
Intercourse should be avoided during the first few days of treatment or until it is no longer painful.
Broad spectrum antibiotics (such as tetracycline for the treatment of acne) should be discontinued until the vulvovaginitis is eradicated.
Treatment Failure

Reexamine the patient carefully to be certain that symptoms are not due to the emergence of a coexisting pathogen such as Trichomonas.
Evaluate the possibility of reinfection from a candidal infection of the patient's sexual partner's penile skin.
Repeat treatment with a different agent or combined topical and oral medication.
Evaluate the possibility that the patient may have been misdiagnosed.

Bacterial Vaginosis (Gardnerella vaginalis)

When vulvovaginitis is due to neither Trichomonas nor Candida, the diagnosis is usually labeled "bacterial vaginosis". The most common form of bacterial vaginitis is a mixed infection. It is caused by Gardnerella vaginalis, a mobiluncus species, a bacteroides species and/or mycoplasma hominis in association with other anaerobic organisms. A superficial infection produces erythema, small punctate hemorrhages, and a homogeneous gray, malodorous discharge. The diagnosis can be suggested by finding "clue cells" - stratified squamous cells with a granular appearance due to a coating of organisms and/or a "fishy odor" when the KOH solution is added to the wet-drop, which liberates short-chain amines that are produced by the abundant anaerobic organisms. Vaginal pH is greater than 4.5.

Local treatment with Metrogel® cream (metronizadole 0.75%) twice a day for 5 days, or clindamycin (Cleocin®) vaginal cream (2%) each day for 7 days is 85% curative. Ampicillin 500 mg four times a day for five days may eradicate Gardnerella, but since it also kills Lactobacillus, the vaginal pH is raised, producing the environment that leads to reinfection. Metronidazole 500 mg orally twice daily for seven days is the treatment of choice. It eradicates G. vaginalis and other anaerobes while sparing the lactobacilli. Clindamycin (Cleocin®) orally, 150 mg tid for 5 days can also be used. If reinfection occurs, the patient's sexual partner should also be treated with metronidazole on the supposition that he is harboring the organism.

Colon Bacilli

A persisting vaginitis, particularly in children, can result from repeated contamination of the vulvar area by feces. Although any of the usual inhabitants of the lower bowel can be involved, Escherichia coli is most likely to be the offending organism. Teaching proper hygiene usually cures the infection. Acute vaginitis usually responds to a 4-5 days course of oral ampicillin.

Miscellaneous Bacteria

Many other bacteria are capable of causing vaginitis. Two examples are streptococci, which produce a thin, watery discharge, and staphylococci, which can occur in hospital personnel.

Herpes Simplex Virus

The most common venereal disease in women in many parts of the country is herpetic infection of the vagina and vulva. The disease is usually self limited but occasionally secondary bacterial inflammation must be treated. Acyclovir (Zovirax®) treatment can reduce the frequency of recurrence in chronic herpetic vulvitis but its efficacy is questionable in altering an acute herpetic breakout.

Condyloma Acuminatum

Condyloma acuminatum is due to a viral venereal infection (papilloma virus) that produces multiple small warts. These lesions are found most often n the vestibule but may also involve the labia, perianal skin, vagina and cervix. Large lesions tend to coalesce and become secondarily infected.

Treatment is tedious and protracted. For small lesions, the best established treatment is trichloracetic acid applied directly to the individual lesions. The surrounding skin should be protected against the irritating effects of this drug by a coating of petrolatum, and the residual acid should be washed away with soap and water one to two hours after application.

Therapy should be repeated at weekly intervals until all lesions are cleared. Any other coexisting infection, such as trichomoniasis, should be treated concurrently. Extensive lesions may require electrocautery, cryosurgery, laser therapy, surgical excision under anesthesia, or the local administration of 5-fluorouracil. The latter therapy should be reserved for a last-resort effort to eradicate the condition. A newer treatment, podofilox (Condylox®), can be applied by the patient at home for external lesions. It is applied b.i.d. for 3 days then withheld for 4 days. This one week cycle is repeated up to 4 times until warts disappear. In pregnancy, podophyllin and podofilox are contraindicated.

Chemicals and Allergens

Almost any agent that comes into contact with the vulva or vagina can cause erythema, irritation, ulceration, and/or discharge. The list includes soaps, douche materials, bubble bath, contraceptive preparations, powder, cloth, dyes, perfumed or colored toilet paper, and local medications. Treatment begins with elimination of as many of these items as possible, including a change from nylon to cotton underwear.

Cervicitis

If the primary source of a vaginal discharge is extensive cervicitis that manifests itself as ectropion (i.e. erythema, edema, and friable) and if yellow or green mucopurulent cervical secretions and greater than ten polymorphonuclear leukocytes per oil-immersion-field (x 1,000) with few bacteria are noted on gram stain (called "mucopus" by King Holmes) then Chlamydia trachomatis should be suggested and treated orally with doxycycline (100 mg b.i.d. for ten days), erythromycin (500 mg q.i.d. for ten days), sulfamethoxazole (1 gm b.i.d. for ten days), or azithromycin (Zithromax®, 1 gram orally times one dose). If antibiotic therapy proves unsuccessful, then cautery, cryosurgery, or laser therapy may be necessary once neoplastic disease has been ruled out.

Pediculosis

An infestation with Phthirius pubis will cause chronic vulvar irritation but can easily be missed unless a careful examination is made for this tiny louse. Lindane (Kwell®) lotion or shampoo is the treatment of choice. Also used is pemethrin cream 5% (Elimite®). Clothing and linen should be changed frequently. Repeat treatment in one week is commonly required, as is treatment of sexual partners.

Scabies

Scabies is due to the mite Sarcoptes scabiei, which produces small itchy subcutaneous burrows, papules, and vesicles along the writs, finger webs, and torso. Treatment is the same as for pediculosis.


Ovarian Masses
Pamela Talley, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. OVERVIEW

A. Adnexae are the potential spaces between the uterus and the lateral pelvic walls

B. Normal structures

1. Ovaries, usually 3 to 5 cm in length but influenced by hormones

2. Fallopian tubes normally cannot be felt

3. Ninety percent of adnexal masses involve the fallopian tubes and/or ovaries

II. EVALUATION

A. History

1. Ovarian neoplasms are often clinically silent except for nonspecific "pressure'' symptoms including urinary frequency, constipation, and pelvic heaviness

2. Very large tumors may cause abdominal swelling and may be confused with pregnancy

3. Pain may result from stretching of the ovarian capsule, torsion, rupture, or intracystic hemorrhage

4. Functional cysts may cause menstrual abnormalities

B. Physical examination

1. Benign tumors are characteristically unilateral, cystic, and mobile and do not cause ascites

2. Malignancies are usually solid, fixed, and nodular and may cause ascites

C. Diagnostic evaluation should include ultrasound. Other tests such as chest radiography, abdominal radiography, IVP, bowel radiography, and laparoscopy may be indicated

III. TREATMENT OF OVARIAN MASSES

A. Women of childbearing age with clinically benign ovarian cysts under 6 cm in diameter may be observed monthly. If a cyst persists or increases in size during the period of observation, proceed with evaluation and probably surgical excision. If the cyst persists but decreases in size, it may be observed through another cycle

B. Premenstrual and postmenopausal females are at high risk for malignancy. One should proceed to full evaluation without a period of observation. Early diagnosis is essential and usually necessitates surgical excision

C. Cysts greater than 10 cm in diameter are more likely to be malignant and require immediate evaluation and probable excision

D. Solid ovarian tumors (by ultrasound) are almost always malignant and demand immediate and aggressive evaluation and treatment. An exception to this is the rare luteoma of pregnancy


Abnormal Papanicolaou Smears
Pamela Talley, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. APPROACH BASED ON PAPANICOLAOU SMEAR (see Table 7-3)

A. Normal: repeat every year from age 18 to 65. If low risk, may change to every 3 years after two consecutive normal smears. After age 65 may discontinue after two consecutive normal smears

B. If no endocervical cells present, repeat in 1 year or sooner

C. Inflammatory/reactive/reparative changes/atypia: look for the causative agent on wet mount, and culture and treat. If no agent identified, treat with doxycycline, 100 mg twice daily for 7 days. Repeat the Papanicolaou smear in 3 months. If resolved, repeat in 6 months, then yearly. If abnormal at 3 months, perform colposcopy

D. Indications for colposcopy and directed biopsy: dysplasia (mild, moderate, severe), squamous cell carcinoma, adenocarcinoma, human papillomavirus (HPV) (cervical or external genitalia), persistent inflammation


Pediatric Gynecology
Pamela Talley, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. OVERVIEW

Gynecology of infancy and childhood is often neglected, primarily because problems are uncommon before the onset of puberty; however, when such problems arise, they must be appropriately evaluated. If child abuse is suspected, document the examination carefully and report to the appropriate authorities. Consultation with a specialist in pediatric gynecology may be helpful in cases with legal implications

II. COMMON DISORDERS OF INFANCY AND CHILDHOOD

A. Vulvovaginitis--most common complaint

1. Symptoms include soreness, pruritis, discharge, burning

2. Requires examination, microscopic examination of vaginal secretions, UA, and possible cultures. Recurrent/ refractory infections or foul-smelling, bloody discharge requires vaginoscopy to exclude a foreign body or tumor

3. Causes

a. Nonspecific polymicrobial infection secondary to poor hygiene or a foreign body

b. Primary infections, which include Candida, Gardnerella, Trichomonas, gonorrhea, syphillis, herpes, etc.

c. Neoplasms--rare

4. Treatment

a. Remove foreign bodies with warm saline irrigation or bayonet forceps. Take cultures and treat concurrent infection

b. Treat specific infections

1) Candida--see the section on common gynecologic infections in this chapter

2) Gardnerella/Trichomonas: metronidazole, 35 to 50 mg/kg/day up to 750 mg divided three times daily for 7 days

3) Gonorrhea: Ceftriaxone, 250 mg IM, or spectinomycin, 40 mg/kg IM

4) Urinary tract infection (UTI): amoxicillin, 20 to 40 mg/kg/day divided three times daily for 10 days if sensitive. Trimethoprim/sulfamethoxazole is an excellent alternative

5) Scabies/pediculosis pubis--see Chapter 10

c. Sitz baths

d. Educate on perineal hygiene

B. Pinworms (Enterobius vermicularis)

1. May cause vulvovaginitis, rectal itching common, frequently have vaginal pain

2. See Chapter 10, Pediatrics, for diagnosis and treatment

C. Diaper dermatitis (primary contact irritant dermatits)

1. Caused by irritants in urine producing a red, papulovesicular, shiny rash sparing skin folds; may fissure

2. Treat with frequent changes and allowing the skin to dry fully, good hygiene, and protection with zinc oxide or white petroleum. Treat secondary infections (Streptococcus Staphylococcus, Candida).

D. Labial adhesions

1. Related to low estrogen levels, poor hygiene, and vulvar irritation; usually asymptomatic. Symptomatic when interfering with urination and leading to dysuria and recurrent vulvar and vaginal infections

2. Treat with topical estrogen cream twice daily for 7 to 10 days

E. Neonatal vaginal bleeding: may occur at 3 to 5 days and represents withdrawal of placental estrogens. No treatment except reassurance of parents

F. Urethral prolapse

1. Prolapse of estrogen-dependent distal urethral mucosa and formation of a painful, friable mass at the vaginal orifice. A catheter passed through the center enters the bladder

2. Treat initially with topical estrogens and antibiotic creams. If urinary retention is present or the lesion is large and necrotic, surgical excision may be required

III. RARE BUT SERIOUS DISORDERS OF INFANCY/CHILDHOOD

A. Sarcoma botryoides (embryonal carcinoma of the vagina)

1. Manifested as a bloody vaginal discharge most commonly in very young girls (less than 3 years) with polypoid growth that may look like a cluster of grapes

2. Survival rare but improving with the use of combination chemotherapy and radical surgery

B. Ovarian tumors

1. Symptoms include pain, mass, and pressure; may cause vaginal bleeding if hormonally active

2. Requires complete evaluation by an experienced gynecologist


Pelvic Pain
Pamela Talley, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. DIAGNOSTIC APPROACH TO PELVIC PAIN

A. History

1. Pain: onset, location, duration, description, intensity, relationship to menses

2. Menstrual history: changes, last menstrual period (LMP), spotting, birth control, sexual activity, signs of pregnancy (nausea, breast tenderness, urinary frequency)

3. Systems: specific questions with the above differential diagnosis in mind (genitourinary [GU], gastrointestinal [GI], gynecologic systems). Evidence of hypovolemia

B. Physical examination

1. Abdomen: peritoneal signs, masses, tenderness, bowel sounds, rectal examination with guaiac, flank tenderness

2. Pelvic: complete vulvar and vaginal examination, cervix (dilation, tissue at os, lesions, tenderness to movement), uterine tenderness and size, adnexae (masses, tenderness, unilateral or bilateral)

C. Diagnostic aids

1. Blood tests: CBC with differential, ESR. Elevated with infections or inflammations, hemoglobin and hematocrit may be decreased with hemorrhage. Useful with repeat testing over time

2. Cultures: blood, cervical, urine, as indicated

3. Urinalysis: helpful to differentiate GU pathology. May still be negative if complete obstruction is present

4. Stool guaiac: points toward the GI tract if positive

5. Pregnancy test: must know the sensitivity of the test being used. A urine pregnancy test may miss very early ectopic pregnancies. Serum radioimmunoassay (RIA) is extremely sensitive and picks up virtually all pregnancies

6. Culdocentesis: positive with any intraperitoneal bleeding (e.g., ectopic pregnancy, bleeding corpus luteum cyst, ruptured liver adenoma, ruptured spleen, peptic ulcer)

7. Ultrasound: useful to distinguish intrauterine from extrauterine pregnancy, may also be abnormal in appendicitis, luteal cysts, PID, spontaneous abortion

8. Abdominal films: may show a ureteral stone, bowel obstruction

9. Radiologic studies: barium enema, intravenous pyelography (IVP), computed tomography (CT)

10. Laparoscopy: sometimes performed before laparotomy

II. MANAGEMENT (see Table 7-2)

A. Assess vital signs, stabilize if necessary

B. Order CBC with differential UA, urine or serum pregnancy test

C. Consider culdocentesis if the patient has unstable vital signs or peritoneal signs

D. If evidence of peritoneal irritation (surgical abdomen), intraperitoneal bleeding with signs or symptoms of pregnancy, or a positive pregnancy test, consult with obstetrics/gynecology. If hemorrhage is suspected (unstable vital signs), do not order more time-consuming tests (e.g., ultrasound) before surgical consultation

E. If findings are as in D but without signs or tests suggesting pregnancy, consult obstetrics/gynecology or general surgery

F. If the patient is stable and without signs of a surgical abdomen, consider further workup to determine the cause of pain as indicated by the history (e.g., cultures, ESR, ultrasound, barium enema, sigmoidoscopy, colonoscopy, IVP, abdominal flat plate)


Postdate Pregnancy
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. DEFINITIONS

A. Prolonged pregnancy: longer than 40 weeks

B. Postdate pregnancy: longer than 42 weeks' gestation

C. Postmature pregnancy: Longer than 42 weeks' gestation with evidence of placental dysfunction

II. ETIOLOGY

A. Most common: error in estimating the EDC

B. Risk factors: history of prolonged gestation (50% risk), older age, anencephaly, or fetal endocrinopathy

III. POTENTIAL MORBIDITY

A. Maternal

1. Birth trauma secondary to delivery of a macrosomic infant

2. Increased incidence of operative delivery, secondary infection, and/or hemorrhage

B. Neonatal: meconium aspiration, polycythemia, hyperbilirubinemia, hypoglycemia, and anoxic organ damage

Postpartum Hemorrhage
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. DEFINITION

Postpartum hemorrhage is most often defined as greater than 500-cc blood loss in the first 24 hours after delivery. However, blood loss after spontaneous vaginal delivery is frequently up to 600 cc and between 1 and 1.5 L after instrumental or operative delivery. Therefore, clinical experience is necessary to determine when bleeding is occurring too rapidly, at the wrong time, or is unresponsive to appropriate treatment. Blood loss will be less well tolerated if the patient has not had the normal expansion of blood volume during pregnancy, such as in cases of preeclampsia

II. DIAGNOSIS

A. Risk factors: multiparity (more than five babies), previous postpartum hemorrhage, manual removal of the placenta, placental abruption or previa, polyhydramnios, prolonged labor, precipitant labor, difficult forceps delivery, prolonged oxytocin administration, breech extraction

B. Etiology

1. Uterine atony accounts for most cases

2. Other causes include retained placenta, cervical or vaginal tear, coagulopathy

C. Physical examination

1. Vital signs (BP and pulse may underestimate the degree of blood loss)

2. The uterus should be palpated for evidence of atony, tenderness, or lack of involution

3. Vaginal examination may reveal evidence of laceration (generally bright red blood) or atony (darker blood). Bimanual examination may reveal a mass (suggesting a broad ligament or paravaginal hematoma)

4. A hematocrit is only helpful in comparison to the value before delivery. It will not adequately reflect acute blood loss

III. MANAGEMENT

A. Evaluate promptly once excessive bleeding is detected. Reliable IV access must be obtained with two large-bore IV catheters. Monitor vital signs and maintain circulatory status with fluids. If the patient shows evidence of symptomatic hypovolemia, blood should be sent for typing and crossmatching. A coagulation profile should also be obtained

B. Review the clinical course for a probable cause (see the predisposing factors listed above)

C. Perform bimanual examination in the recovery area/delivery room

1. If the uterus is found to be boggy, initiate stimulation with massage or oxytocin (40 units in 1,000 mL crystalloid--infuse at 200 mL/hr or 10 units oxytocin IM)

2. If placental fragments are detected within the uterus on exploration or on ultrasound, return to the delivery room for curettage

3. Laceration or hematoma should be repaired in the delivery room

D. If a cause is not identified or fails to respond to the above measures, notify obstetric physicians, anesthesia, and operating room personnel of the potential need for surgical intervention

E. Inform the patient of the problem and what measures are being taken to correct it. Get an appreciation of her desires regarding further childbearing and hysterectomy

F. If hemorrhage is unresponsive to the above measures, administration of prostaglandins should be considered. Prostaglandin E2 vaginal suppositories (Prostin E2 = 20 mg) have been used

G. If uterine bleeding persists, then surgery must be considered. Packing is a temporary measure that is rarely effective. Surgical alternatives include uterine artery and hypogastric artery ligation. Hysterectomy is the treatment of last resort when the patient desires future fertility but may be preferred if sterility is desired


Premature Rupture of Membranes (PROM)
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. DEFINITIONS

A. "Premature'' rupture of membranes occurs if there is a delay of greater than 1 hour until onset of labor

B. "Preterm premature'' rupture of membranes occurs before 37 weeks' gestation

II. DIAGNOSIS

A. History of fluid gush

B. Sterile speculum examination

1. Pooling of fluid in the vaginal vault

2. pH determination: amniotic fluid typically turns nitrazine paper blue. Contamination with vaginal/cervical mucus, blood, or urine may lead to false interpretation

3. Fern test: allow a sample of fluid to air-dry on a glass or slide. Examination of amniotic fluid under the microscope reveals a classic "fern'' pattern

C. Cervical digital examination is controversial. Increases the risk of amnionitis. Avoid if possible unless the patient is in labor and delivery is inevitable

III. MANAGEMENT

A. Term PROM: Most sources recommend induction and delivery within 24 to 36 hours after admission

B. Preterm PROM: fetal maturity must be considered. Manage conservatively until the fetus is mature unless chorioamnionitis or fetal distress develops or labor cannot be inhibited with tocolysis. Positive cervical cultures should be treated but do not necessitate induction without other signs of chorioamnionitis. Follow maternal and fetal vital signs, including temperature every 6 hours and daily white blood cell (WBC) count. Use of antibiotics for prophylaxis is under investigation

C. Amnionitis: signs include maternal or fetal tachycardia, maternal fever, uterine tenderness, foul cervical discharge, uterine contractions, leukocytosis, the presence of leukocytes or bacteria in amniotic fluid


Abnormal Vaginal Bleeding and Amenorrhea
Pamela Talley, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. TERMINOLOGY

A. Menorrhagia: heavy or prolonged bleeding

B. Metrorrhagia: intermenstrual bleeding, spotting or breakthrough

C. Polymenorrhea: menstrual interval less than 21 days

D. Oligomenorrhea: menstrual interval greater than 35 days

E. Amenorrhea: absence of menstrual bleeding

II. ETIOLOGY OF VAGINAL BLEEDING

A. Dysfunctional uterine bleeding: usually associated with anovulatory cycles and irregular sloughing of estrogen-stimulated endometrium. Represents abnormal hormonal regulation with tonic hormone levels rather than cyclical fluctuating gonadotropins and sex hormones. Common causes include puberty, climacteric, anorexia nervosa, polycystic ovarian disease, and obesity

B. Benign organic lesions: including chronic cervicitis, cervical polyps, endometrial polyps, leiomyomas, and chronic endometritis as well as a low-grade form associated with IUD use

C. Malignant lesions: including vaginal, uterine, cervical carcinomas; estrogen-producing ovarian neoplasms

D. Coagulopathies: most common is Von Willebrand's disease. Also consider leukemias, thrombocytopenias

E. Pregnancy-related bleeding: including ectopic pregnancy, threatened abortion, molar pregnancy, abruptio placentae, placenta previa

F. Miscellaneous: viral illnesses, hypothyroidism, liver disease, oral contraceptive breakthrough bleeding, ovulatory bleeding, etc.

III. EVALUATION

A. History including menstrual history, drug history, pregnancy, bleeding tendencies, contraceptive use (oral contraceptive pills [OCPs] or IUD)

B. Physical evaluation including pelvic examination noting hirsuitism, virilization, vagina/cervical lesions, uterine size and shape, and adnexal masses. Obtain Papanicolaou smear and consider endometrial biopsy

C. Initial laboratory tests include CBC with platelets, prothrombin time (PT), partial thromboplastin time (PTT), pregnancy test, and thyroxine (T4)/thyroid-stimulating hormone (TSH). Consider follicle-stimulating hormone (FSH)/leutinizing hormone (LH), prolactin level and androgens as indicated

IV. TREATMENT OF IRREGULAR BLEEDING

A. Adolescent: usually represents anovulatory bleeding

1. After exclusion of organic disease and pregnancy, treat with any combined progestin-estrogen OCP pack, 1 pill four times daily until gone (7 days). Expect cessation of flow in 12 to 24 hours. Heavy withdrawal flow with cramping will start 2 to 4 days after the pills are gone. On day 5 of withdrawal flow, begin daily low dose combination OCPs for at least 3 months and longer if continued contraception is indicated. If contraception is not needed, may use cyclic medroxyprogesterone acetate, 10 mg daily for 10 days each month. Reconsider the need for therapy in 1 year

2. Profuse bleeding (hemoglobin less than 10 g/dL, orthostatic) may require IV conjugated estrogens, 25 mg every 4 hours (maximum of three doses), followed by medroxyprogesterone acetate, 10 mg orally daily for 7 to 10 days, to initiate withdrawal bleeding. On day 5 of withdrawal begin low-dose OCPs as above

3. Special situations requiring estrogen alone include those patients with an atrophic endometrium. Patients fitting this category include those with prolonged bleeding, biopsy with scant tissue, and breakthrough bleeding on progestin-only pills, Norplant, or Depo-Provera. Therapy includes conjugated oral estrogen, 1.25mg daily for 7 to 10 days, followed by medroxyprogesterone acetate

B. Reproductively mature female: as above except repeated episodes of irregular bleeding should be treated with dilatation and curettage (D&C;) and hysteroscopy to evaluate for organic lesions, e.g., polyps, submucosal fibroids. Hysterectomy may be considered for recurrent bleeding if reproductive potential is not desired

C. Postmenopausal bleeding: always requires complete evaluation for carcinoma including endometrial biopsy, possible D&C.; Treat benign lesions if identified. Refer for definitive treatment of malignant lesions

V. AMENORRHEA IN REPRODUCTIVE-AGE MATURE FEMALES

A. History including menstrual and obstetric, weight loss/gain, drug use (phenothiazines), headaches/visual disturbances, hirsuitism, exercise

B. Examination including pelvic, noting hirsuitism, galactorrhea

C. Initial evaluation should include serum prolactin, TSH, and a progesterone challenge with medroxyprogesterone acetate, 10 mg/day for 5 days. Withdrawal bleeding within 7 days indicates that the ovaries are secreting estrogen

D. Treatment depends on the above results

1. Galactorrhea/hyperprolactinemia: the most common lesion is microadenoma of the pituitary, but rule out drug causes, hypothyroidism. May have headaches or visual symptoms. High-resolution CT of the sella turcica or magnetic resonance imaging (MRI) are the imaging studies of choice. Refer appropriately if abnormal, or if normal follow prolactin levels every 6 months and CT or MRI every 1 to 2 years. Can treat with bromocriptine to suppress prolactin and shrink adenomas

2. No galactorrhea and positive progestin challenge (expected withdrawal bleeding, normal prolactin)

a. Treat the underlying cause if identified, considering polycystic ovarian disease (PCOD; have elevated LH, normal or low FSH, possibly mildly elevated androgens) and ovarian/adrenal tumors if hirsute

b. Combined OCPs can be used. An alternative is the use of monthly or every-other-month medroxyprogesterone acetate, 10 mg daily for 10 days, to prevent endometrial hyperplasia

c. If fertility is desired, clomiphene citrate can be used in PCOD at 50 mg/day orally for 5 days; ovulation, 5 to 10 days after the last dose

3. No galactorrhea and a negative progestin challenge with a normal prolactin level

a. Determine the FSH concentration; consider Asherman's disease (uterine synechiae) if there is a history of D&C.; FSH levels greater than 40 mIU/mL indicate gonadal failure including menopause. FSH levels less than 40 mIU/mL suggest severe hypothalmic dysfunction

b. Treat hypoestrogenism to maintain bone density and prevent genital atrophy with combined OCPs or one of several hormone replacement regimens (see menopause)

c. If fertility is desired, refer for combined clomiphene/human menopausal gonadotropin therapy


RHScreening and Rho(D) Immunoglobulin
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. PROTOCOL FOR ROUTINE Rh SCREENING AND ADMINISTRATION OF Rho(D) IMMUNOGLOBULIN

A. Initial visit: draw blood for ABO group, Rh type, and antibody screening (indirect Coombs' test)

B. If the patient is Rh-negative, repeat the antibody screen at 26 weeks, and if no antibody is detected, give 300 ug Rho(D) immunoglobulin (1 vial = 300 ug) intramuscularly (IM). If antibody is detected, see III below

C. Following delivery: check the fetal ABO/Rh type. If the infant is Rh-positive, the mother receives 300 ug Rho(D) immunoglobulin IM within 72 hours of delivery

D. One vial suppresses immunity to approximately 30 mL whole blood (15 mL of Rh-positive packed red blood cells [RBCs])

II. ADDITIONAL Rho(D) IMMUNOGLOBULIN REQUIREMENTS

A. If at anytime during pregnancy fetal-maternal hemorrhage is suspected, a Kleinhauer-Betke test should be performed. If positive, 10 ug of Rho(D) immune globulin should be administered per milliliter of fetal blood calculated to have entered the maternal circulation

B. A 50-ug dose of Rho(D) immunoglobulin (1-vial microdose = 50 ug) is indicated for an Rh-negative woman after a first trimester terminated or miscarried pregnancy

C. A 300-ug dose of Rho(D) immunoglobulin is indicated for an Rh-negative woman who undergoes amniocentesis, who undergoes a spontaneous or induced abortion at or beyond 13 weeks' gestation, or who has an ectopic pregnancy (greater than13 weeks)

D. The Kleinhauer-Betke test should be performed postdelivery if a larger-than-usual fetal-maternal hemorrhage may have taken place such as with placental abruption. More than the standard 300-ug dose may be required (which protects only up to 15 mL of Rh-positive red cells)

III. ISOIMMUNIZATION

If the patient is Rh-negative and the antibody screen is positive before Rho(D) immunoglobulin administration, obtain an antibody titer and refer to a specialist. These infants are at risk for erythroblastosis fetalis


FEMALE GENITAL TRACT
Rosemary E. Zuna, M.D.
Department of Pathology
Cornell University Medical College

INFLAMMATION AND PELVIC INFLAMMATORY DISEASE
Lower Genital Tract
Frequently involve the vagina and cervix as well

A. Vulvovaginitis, cervicitis:
Common organisms:

Candida albicans 3773

Trichomonas vaginalis 3765

Syphilis 3333 3338

Granuloma inguinale

Lymphogranuloma venerum

Chancroid

Neisseria gonorrhea

Mycoplasma

Chlamydia

B. Bartholin's Cyst*
Cystic dilation of the duct of the Bartholin (vulvovaginal) gland, located bilaterally in the posterior aspect of the labium majus. Acute inflammation with swelling, fibrosis and reactive epithelial hyperplasia causes obstruction and dilatation. It is often preceded by an abscess. The organisms involved include gonococcus, staphylococcus and negative bacilli.

1. Gross Appearance

Swelling in the posterior aspect of the labium majus may be up to 5 cm. in diameter.

3323

2. Microscopic

a. Normally, the Bartholin's duct shows a transition from mucin-secreting epithelium at its origin to stratified squamous epithelium at the vulvar orifice.

b. An abscess is associated with a dense neutrophilic exudate and tissue necrosis. With healing, fibrosis may occur.

c. A Bartholin's cyst can be lined by stratified squamous epithelium or attenuated columnar epithelium.

C. Viral Infection
1. Herpes Simplex

779

Legend Cellular changes caused by herpes simplex infection includes large, multinucleated epithelial cells characterized by molded nuclei with a homogeneous ground glass appearance. Intranuclear viral inclusions can sometimes be seen.

3334

2. Human Papilloma Virus infections:

a. Gross

1. Condyloma acuminatum (venereal wart):

Papillary, exophytic cauliflower-lesions caused by human papilloma virus-induced proliferation of the squamous epithelium. The exophytic lesions of the lower genital tract are typically associated HPV types 6 and 11. Verrucous cauliflower-like nodules that may cluster on the mucosa of the vulva, perianal region, urethra, perineum, cervix and vagina.

2. Flat condyloma:

HPV associated squamous lesions that do not have the exophytic growth pattern of the condyloma acuminatum. Usually difficult to detect with the unaided eye. May be HPV type 6, 11, 16, 18, or other subtypes. Usual pattern for cervix.

b. Microscopic

1. Exophytic lesions show hyperplasia of the squamous epithelium. Characteristic perinuclear halo's (koilocytosis*) are usually present in the superficial cell layers. The nuclei in these cells are classically wrinkled, resembling raisins, bi- and trinucleated cells are common. There is little or no dysplasia in these lesions.

3769

Legend In situ hybridization of condyloma acuminatum. Black areas indicate viral containing nuclei.

3768

2. Flat lesions have similar epithelial changes. However, HPV 16-18 containing lesions are associated with maturation and nuclear abnormalities that have been identified as precancerous (dysplasia).

3772

Legend Moderate dysplasia of cervix presenting as a flat lesion with in situ hybridization identifying HPV 16-18 DNA within the nuclei (black stained area).

3770 3771

c. Clinical Aspects

1. Condyloma acuminata:

Condyloma acuminata are typically sexually transmitted. The lesions frequently regress spontaneously, but the process may persist with new lesions developing as older lesions regress. Poorly understood immune factors, presumably cell mediated, are involved in the persistence or regression of these lesions. Pregnancy, oral contraceptives and immunosuppressed status favor growth and persistence of these lesions. In some individuals the virus apparently persists in a subclinical state.

2. Cervical dysplasia:

a) Definition:

The morphologic precursor of squamous cell carcinoma of the cervix. Synonymous terms include "cervical intrepithelial neoplasia" (CIN) and "squamous intraepithelial lesion" (SIL). Most dysplastic lesions contain HPV DNA, usually HPV 16. HPV may represent a contributing factor to cervical carcingenesis. Similar lesion can be found in the vulva and vagina.

b) Microscopic Appearance:

9243 Figure 24-20

1. Delayed and/or disordered maturation of the squamous mucosa.

2. Alterations of DNA content resulting in abnormal nuclear size and shape.

774 774¥26320

Legend The marked maturation delay in this tissue can be identified by the presence of immature cells oriented perpendicular to the basement membrane (BM, blue dotted line) in the lower 2/3 of the epithelium (blue arrow). Mitotic figures can be seen at inappropriately high levels in the epithelium. Partial maturation is identified in the upper 1/3 by the cells that lie parallel to the BM (green arrow) and begin to acquire more cytoplasm. (The nuclei are widely spaced.) Compare with normal cervical epithelium (1774). Abnormal nuclear content is reflected in the increased nuclear size, as well as the variation in nuclear size and shape. This illustration presents severe dysplasia.

1774

Legend Normal cervical epithelium, transition.

c) Clinical Aspects

1. Asymptomatic; usually not visible to un aided eye. Usually detected by Pap smear screening in which cells are circumferentially scraped from the cervical transformation zone and smeared on a glass slide for microscopic analysis.

1409 1409¥26302

Legend This image depicts dysplastic cells in a Pap smear. Although the cells have the abundant, polygonal cytoplasm of mature squamous cells, the nuclei are enlarged. Several of the cells are bi-nucleated. The intermediate cell at the far right (arrow) indicates the normal nuclear size.

2. Although the cytologic and histologic features of dysplasia have been recognized for many years, the strong correlation of dysplasia with human papilloma virus (HPV)* was recognized only recently. Demographic studies have correlated cervical carcinoma with sexually transmitted disease and a transmissible agent. Risk for developing cervical cancer correlates with 1) early age of first intercourse (under age 20) and 2) multiple sexual partners.

3. Over 90% and possibly all of cervical dysplasias and carcinomas harbor intranuclear HPV DNA sequences, strongly implicating HPV as an etiologic agent.

4. Cervical carcinogenesis is an inefficient process that can span 20 or more years from the earliest dysplasia through the development of invasive disease. However, rare cases in younger women can evolve very rapidly. Approximately 50% of dysplasias spontaneously regress or remain constant without progression. Unfortunately, we cannot yet distinguish those that will progress and must treat all lesions.

Upper Genital Tract
Pelvic Inflammatory Disease* (PID)
A clinical syndrome consisting of a complex combination of signs and symptoms referable to an ascending inflammatory reaction, which involves to a variable extent the entire female genital tract.

A. Mucosal:
Gonorrhea* is the classical example of this pattern. Usually associated with sexually transmitted disease. Recently, the Chlamydia has been recognized as an important pathogen.

1. Organisms: N. Gonorrhea, anaerobes including bacterioides and anaerobic Streptococci, E. coli, Chlamydia trachomatis, Mycoplasma hominis, and Ureaplasma hominis.

2. Ascends along the mucosal surfaces following infection of the lower female genital tract such as Bartholin's gland, periurethral glands or endocervical glands.

3. Most important impact is on the fallopian tubes initially as salpingitis (inflammation of the fallopian tube) and later with fibrosis.

4. Pathogenesis of Gonorrheal Salpingitis*

a. Acute suppurative salpingitis: classically bilateral

1. Gonococci adhere to the surface of nonciliated tubal epithelial cells within 3 hours after exposure. This process is mediated through gonococcal pili, which are fibrillar proteins on the surface of the organism.

2. The bacteria penetrate the epithelial cells eventually causing cell lysis and sloughing.

3. The tissue response to this insult includes diapedesis of neutrophils from the capillaries with vascular engorgement and edema of the tubes.

4. Pus (neutrophilic exudate) accumulates within the tubal lumen and may leak through the fimbria into the peritoneal cavity including the ovarian surface.

b. The mucosal folds, fimbria and ovarian surface become matted and fused with fibrinous exudate causing fibrinous adhesions. (The fibrin is leaked from small vessels that were damaged by proteolytic enzymes released by the degranulating neutrophils).

c. The tubal lumen becomes distended by the accumulation of pus (pyosalpinx). With the fusion of the fimbria, the fallopian tubes resemble retort tubes. The adhesion of the tubal fimbria to the ovary results in tuboovarian abscesses, which are usually bilateral.

783 783¥26324

Legend In this specimen from a patient with pelvic inflammatory disease, tuboovarian complexes are present on both sides of the central uterus. On each side, the tube and ovary are indistinguishable, forming a single mass. This is due to adhesion formation.

3237

1. The patient is frequently ill with fever, leukocytosis and abdominal tenderness.

2. In late stages the gonococcus is rarely cultured from these lesions. Other organisms such as streptococci, Bacterioides or Staphylococcus may be present, suggesting secondary infection.

d. Resolution occurs by fibrosis. Fibroblasts grow into the fibrinous adhesions from the exposed connective tissue. These cells produce collagen, resulting in permanent fibrous adhesions*. The pyosalpinx evolves into a hydrosalpinx, a fluid filled, dilated sac-like fallopian tube.

782 782¥26323

Legend In hydrosalpinx only a rare attenuated mucosal fold is present extending into the lumen of a markedly dilated fallopian tube lumen.

e. Residual inflammation may persist resulting in chronic salpingitis.

781

Legend In chronic salpingitis the mucosal folds become thickened by the accumulation of inflammatory cells and the associated stromal reaction. Lymphocytes and plasma cells usually predominate, although esosinophils, neutrophils and histiocytes can also be seen.

5. Chlamydia trachomatis is increasingly recognized as a significant cause of a smoldering, chronic form of pelvic inflammatory disease that may be relatively asymptomatic.

6. Sequelae of chronic PID: Tubal fibrosis interferes with the function of the fallopian tube as oviduct. This results in:

a. Sterility: The tubal damage hampers the movement of sperm which interferes with fertilization.

b. Ectopic pregnancy*: This is the implantation of the fertilized ovum in an abnormal location. (This is usually the fallopian tube but rare implantation in the ovary and peritoneal cavity occur.) Hemorrhage into the tube associated with tubal pregnancy is the most common cause of hematosalpinx.

785

Legend This amputated fallopian tube ruptured under the stress of a tubal pregnancy. The fetus remains in situ (arrow). The thin muscular wall of the fallopian tube cannot withstand the expansion of a developing pregnancy. This clinical scenario represents a life threatening medical emergency for the woman.

786

Legend A dilated, dusky, reddish-blue fallopian tube remains attached to the uterus. The fallopian tube represents the hematosalpinx of an ectopic pregnancy.

B. Hematogenous:
Frequently associated with instrumentation of the uterus or complications of pregnancy. The inflammatory process evolves through vascular penetration rather than mucosal surfaces. Classically, this was known as puerperal sepsis or childbirth fever and is relatively uncommon today.

1. Organisms include Staphylococci, Streptococci, coliform bacteria and Clostridia.

C. Granulomatous
Rare today but classically associated with disseminated (miliary) tuberculosis.

3305 3304

ABNORMAL UTERINE BLEEDING
Dysfunctional Uterine Bleeding*
Abnormal bleeding in the absence of organic lesion of the endometrium or uterus.

Anovulatory cycle*
The most common cause of dysfunctional uterine bleeding. It is associated with failure to ovulate. A corpus luteum does not form and progesterone is not produced.

a. The underlying causes are varied. Anovulatory cycles are common in adolescence (menarche) and around the time of menopause.*

b. Failure to ovulate results in continued estrogen stimulation of the endometrium without the moderating effects of progesterone (i.e. unopposed estrogen stimulation). Histologically, this results in prolonged proliferative phase, without evidence of secretory change. The endometrium may show mild (cystic) hyperplasia.

c. Endometrial bleeding is associated with degeneration of the unruptured ovarian follicle, leading to fluctuation in estrogen levels. Endometrial bleeding is associated with decreased estrogen levels and occurs at irregular (non-cyclic) intervals.

d. Although considered normal at menarche and menopause, persistent anovulatory cycles are abnormal during the child bearing years. Chronic anovulation may result in:

1. infertility

2. endometrial hyperplasia

3. increased risk for endometrial carcinoma

e. Diagnosis is made on an endometrial biopsy performed during the second (secretory) half of the woman's cycle. The presence of proliferative endometrium rather than secretory allows a diagnosis of anovulation.

f. Causes of chronic anovulation are:

1. Frequently unexplained, likely due to subtle hormone imbalance.

2. A hormonally functional ovarian lesion such as granulosa theca cell tumor

3. Polycystic-ovary syndrome* (Stein-Leventhal*)

4. Endocrine disorder such as pituitary tumor

5. Generalized metabolic disturbance such as marked obesity, malnutrition.

Bleeding Secondary to Organic Disorders
Abnormal uterine bleeding may also be associated with morphologic lesions of the endometrium and uterus. These include:

a. Complications of pregnancy

1. Spontaneous abortion

2. Retained products of conception

3. Ectopic pregnancy

4. Gestational Trophoblastic disease

b. Leiomyomas*

Benign, smooth muscle tumors of the myometrium that occur in 20-40% of women of childbearing age; most common tumors of the uterus; true neoplasms rather than myometrial hyperplasia; estrogen probably promotes growth.

1. Gross Appearance

a) Pseudoencapsulated, tan-white, rubbery whorled nodules associated with the myometrium; vary from less than 1mm to 15cm or more; May undergo cystic degeneration, calcification torsion with necrosis and carneous (red) degeneration.

771

Legend Calcification is a dystrophic change that can occur in leiomyomas.

1768

Legend Carneous degeneration, myoma uteri.

1767

b) Frequently multiple

c) Location in myometrium influences the sequelae:

1) Intramural: most common; expand the uterine wall

2) Subserosal: peduculated masses protruding from the serosal surface; associated with an irregular uterine shape.

3345

3) Submucosal protrude into the endometrial cavity; commonly associated with abnormal bleeding.

1766

2. Microscopic Appearance

Interlacing fascicles of smooth muscle cells arranged in a whorled pattern. Varying amounts of fibrous connective tissue are also present.

1437

3. Clinical Significance

a. Abnormal bleeding especially with submucous tumors; The endometrium may atrophy over the surface of the leiomyomas resulting in an incomplete cleavage plane during menstruation;

b. Rare sarcomatous transformation. However, some authorities believe that leiomyomas rarely if ever transform to leiomyosarcoma. They postulate that leiomyosarcomas arise denovo from the myometrium.

3329

Legend While most of this lesion shows the typical whorled, firm, white appearance of benign leiomyoma, the tan area at the lower edge of this tumor is softer with a fish flesh consistency and focal necrosis. This is an area of leiomyosarcoma in what appeared to be an ordinary leiomyoma. This is an extremely rare occurence.

c. Endometritis*

Inflammation of the endometrium; Generally infectious in origin; Relatively uncommon.

1) Acute Endometritis:

Bacterial infection is usually associated with retained products of conception following delivery or spontaneous abortion. Causative agents typically include Group A hemolytic streptococci and Staphylococci.

2) Chronic endometritis:

The presence of plasma cells in the endometrial stroma. May be found associated with:

3281

Legend At low power, the endometrial stroma appears hypercellular with inflammatory cells spilling into the gland lumens.

3280 3280¥26309

Legend At high power, the additional cells in the stroma are identified as plasma cells, which are never normal in the endometrium.

1. Chronic pelvic inflammatory disease

2. Post partum (following delivery) or after incomplete abortion associated with retained products of conception.

3. Intrauterine contraceptive devices (IUD)

3278

Legend An intrauterine contraceptive device (Lippes loop) is in place in the uterus. Notice the attached string protruding through the cervix. Intended to monitor the location of the IUD and to allow for easy removal, this string can act as a conduit for microbes into the normally sterile endometrium.

1010

Legend Actinomyces infection is a recognized complication of long-term IUD usage. Enmeshed in inflammatory exudate is a tangle of the filamentous bacteria. The pink, club-shaped material arrayed at the edge of the bacterial aggregate is a proteinaceous deposit encasing the filamentous bacteria that is termed 'Splendore-Hoeppli phenomenon. Although frequently seen with Actinomyces, Splendore-Hoeppli is a non-specific finding.

4. Tuberculosis

451

Legend Granulomas with epithelioid histiocytes and multinucleated giant cells are present in the stroma of this endometrium. The necrosis that is typical of tuberculous granulomas is rarely seen in tuberculosis of the endometrium. A mixed chronic inflammatory exudate is also seen.

d. Endometrial Polyps

Masses composed of benign endometrial glands and stroma that project into the endometrial cavity; usually in perimenopausal women.

1. Gross Description

a) Single or multiple

484 484¥26318

Legend Multiple polyps.

b) 0.5 - 3.0 cm in diameter

c) Sessile or polypoid

2. Microscopic Description

3271 3271¥26307

Legend Endometrial polyp.

a) Functional glands and stroma

b) Disordered glands and stroma with features of cystic hyperplasia.

c) Stroma may show increased collagen. A prominent vascular core is typically seen.

3273

Legend Endometrial polyp with increased stromal collagen.

3. Clinical correlation

a) May be asymptomatic with no sequelae.

b) May cause abnormal bleeding because of:

1. Ulceration of the tip of the polyp

2. Torsion and ischemic infarction.

3. Prolapse through the cervix.

863

Legend A hemorrhagic mass is protruding through the cervix.

Upon sectioning the uterus, the mass is seen to be a polyp attached to the endometrium by a long stalk.

862

Legend This lesion illustrates an endometrial polyp that prolapsed through the cervix.

c) The major importance of polyps is the need to distinguish from carcinoma. Malignant change in a benign polyp is very rare.

e. Endometrial Hyperplasia*

Endometrial hyperplasia is an abnormal proliferation of endometrial tissue that is characterized by increased endometrial thickness grossly and abnormal glandular patterns histologically. It is associated with hyperestrogenic states and in severe cases with increased risk for developing endometrial carcinoma.

1. Gross Appearance

The endometrial cavity may be morphologically normal with only a smooth uniform surface and slight increase in endometrial thickness. Focal areas of increased thickness or cystic dilatation of glands may result in an irregular, lumpy appearance to the velvet-like, tan-gray endometrial surface.

2. Microscopic Appearance

The microscopic appearance is highly variable, reflecting a wide spectrum of epithelial complexity. The major histologic subtypes correlate with biologic potential.

These include:

a. Simple Hyperplasia (Cystic-Glandular)

867

Legend Cystically dilated glands lined by tall columnar epithelium are present enmeshed by abundant endometrial stroma. This is a typical pattern for cystic hyperplasia.

b. Complex Hyperplasia (Adenomatous Hyperplasia)

c. Atypical Hyperplasia (Adenomatous Hyperplasia with Atypia) [See Robbins, pp.1150-1]

901

Legend Endometrial currettage, atypical adenomatous hyperplasia.

3276

Legend Atypical adenomatous hyperplasia.

3. Clinical Aspects

a. Endometrial hyperplasia is relatively uncommon before the age of 40. When present in a younger woman it is usually associated with chronic anovulation or estrogen producing ovarian tumors, such as granulosa-theca cell tumors. Hyperplasia in young women usually fall into the simple and adenomatous categories and have a low risk for developing malignancy.

b. Risk for progression to carcinoma has generally been correlated with atypical hyperplasia (approximately 25%). For simple and adenomatous hyperplasias, the risk for progression is low (2% or less).

f. Malignant Tumors

1. Cervical Carcinoma (invasive)

a. Gross

1. Exophytic (fungating)

776

Legend A large exophytic tumor (squamous cell carcinoma) is protruding from the cervix.

777 777¥26321

Legend A section through an exophytic squamous cell carcinoma demonstrates the bulging mass (red arrow) in relation to the deeper normal cervical tissue (green arrow).

2. Ulcerating

3320 3320¥26312

Legend The lesion is an ulcerating squamous cell carcinoma that is replacing most of the exocervix. The arrow indicates the endocervical os. The smooth pink mucosal tissue surrounding the tumor is vaginal cuff.

3321 3321¥26313

Legend A small ulcerating lesion is present rather high in the endocervix. Although unusually high in the cervix, this was histologically an early invasive squamous cell carcinoma.

3. Infiltrative

b. Microscopic

1. Large cell nonkeratinizing. Most common and has best prognosis.

3318

Legend Irregular, jagged nests of plump, polygonal cells invade the cervical stroma. Lymphocytes are also present in the stroma.

3319 3319¥26311

Legend The irregular nests and strands of nonkeratinizing squamous cells are seen infiltrating the stroma around an unremarkable endocervical gland.

3368 3369 3390

2. Large cell keratinizing

3. Small cell undifferentiated: Least common with worst prognosis.

4. Adenocarcinoma: Tends to be asssociated with a more aggressive course than squamous lesions. HPV 18 DNA more frquently found in adenocarcinomas.

c. Clinical Course

1. Classical presenting sign is abnormal bleeding, usually postcoital bleeding. Usually found in the 40-60 year age group.

2. Microinvasive carcinoma The earliest invasive lesion, termed microinvasive carcinoma, is defined as less than 3mm of invasion below the basement membrane. Risk of lymph node metastasis is very low so that prognosis is excellent with conservative therapy.

3. Local Extension The tumor grows in an expansile fashion, infiltrating normal tissues. An advanced tumor may directly involve the vagina, pelvic side wall, bladder, and rectum. Compression of the ureters due to advanced local disease is the most common cause of death due to cervical carcinoma. This compression causes ureteral obstruction with resulting hydronephosis and, ultimately, renal failure.

1440 1440¥26303

Legend This image illustrates the extension of squamous cell carcinoma into adjacent tissues. The tumor (encircled in red) involves the vagina , endometrial cavity and urinary bladder and rectum. Surgery to remove the affected tissue en bloc was performed after recurrence following radiation therapy.

4. Vascular Invasion

a) Regional Lymph node metastasis (pelvic and para-aortic) occur commonly.

778 778¥26322

Legend The presence of tumor cells within the lumen of a capillary-like space (arrow) is evidence for aggressive growth potential in squamous carcinoma of the cervix and has been correlated with increased risk for regional lymph node metastasis.

b) Invasion of veins occasionally occurs and is a particularly poor prognostic sign, correlating with distant, blood orne metastasis.

5. Distant Metastases Occur late in the disease, usually involving lungs, liver and other structures.

d. Prognosis

Correlates with stage of disease. Five year survival range from 80-90% for Stage I to10-15% for Stage IV.

2. Endometrial Carcinoma

Now the most common invasive cancer of the female genital tract. Unfortunately Papanicolaou smears are not effective as a screening tool for endometrial carcinoma. Usually found after menopause in the 55-65 year old age group.

a. Pathogenesis

1. Many endometrial carcinomas appear to arise in a background of abnormal estrogen metabolism.

2. Constitutional complex of symptoms, frequently associated with women who have endometrial carcinoma.

a. Obesity

b. Low Parity

c. Hypertension

d. Diabetes mellitis

e. Late menopause

3. The above complex of constitutional characteristics suggest the possibility of an underlying hormonal abnormality. Evidence suggests hyperestrinism. This includes:

a. Chronic anovulation, resulting in unopposed estrogen stimulation of the endometrium.

b. Association of endometrial carcinoma with estrogen secreting ovarian tumors, i.e. theca-granulosa cell tumors.

c. Evidence that weak androgen precursors from the adrenals and ovarian stroma are aromatized to estrone, a weak estrogen, in body fat. This contributes to the overall estrogen levels in the body.

d. The association of endometrial carcinoma in young women with high dose-estrogen-containing sequential oral contraceptives. (These are no longer available for use.)

b. Pathologic Features

1. Gross Appearance

a. Polypoid tumor

b. Diffuse involvement of endometrium

3332 3306 3307

2. Microscopic Appearance

a. Adenocarcinoma (85%)

3330

Legend The tall columnar epithelium and well-defined gland formation illustrate a well-differentiated adenocarcinoma. Note the sparsity of stroma in between the glands.

b. Adenocarcinoma with squamous differentiation (10-15%)

1. Adenoacanthoma: squamous component is histologically bland resembling squamous metaplasia.

2. Adenosquamous carcinoma: squamous component is overtly malignant and comprises 10% or more of the tumor.

c. Rare cell types

1. Papillary serous carcinoma: resembles ovarian serous carcinoma; particularly aggressive form of endometrial carcinoma.

3371

2. Clear cell carcinoma

3. Secretory carcinoma

4. Mucinous adenocarcinoma

c. Clinical Course

1. Presenting complaint: Abnormal vaginal bleeding (usually post menopausal)

2. Mechanisms of progression

a. Myometrial invasion

3270 3270¥26306

Legend Well differentiated adenocarcinoma has invaded through the muscle bundles of the myometrium (green arrow). The adenocarcinoma is indicated by the red arrows.

b. Ovarian metastasis

3429 3429¥26315

Legend Metastases to the ovary are usually bilateral as in this instance.

c. Regional lymph nodes

d. Distant metastases: Late occurrence with grave implications

d. Prognostic Factors

1. Tumor Grade: Relative percentage of glandular and solid areas; A solid growth pattern is less differentiated than a glandular pattern and is therefore, less favorable.

2. Depth of myometrial invasion

3. Surgical-Pathologic stage

4. New technologies are under investigation including

a. Estrogen/Progesterone receptors

b. DNA ploidy

e. Outcome:

Favorable; most (80%) patients present with stage 1 disease and favorable histologic grade. Five-year survival for such patients is nearly 90%.

3. Uterine Sarcomas

Leiomyosarcoma Malignant smooth muscle tumors that originate from myometrium. Peak incidence 40-60 years of age.

1. Gross Appearance

Bulky, fleshy tumors with a gray-tan fish flesh appearance. Focal necrosis and hemorrhage are common.

a. May be a bulky tumor invading into the myometrium. b. or polypoid lesion projecting into the endometrial cavity.

2. Microscopic Appearance

Variable. Elongated spindle cells that variably grow in a fascicular pattern, mimicking a benign leiomyoma. However, the nuclei are generally pleomorphic with increased mitotic activity (greater than 10 mitoses/10 high power fields).

3327

Legend This illustrates the extreme pleomorphism that can occur in high grade leiomyosarcoma.

3372

3. Clinical Course

Variable with strong tendency to recur and metastasize; blood borne metastases to lungs are common, although direct extension into the peritoneal cavity also occurs.

3328

Legend Multiple small nodules are scattered throughout the lung. These are nodules of metastatic leiomyosarcoma (same patient as Slide 3327).

PELVIC MASS
Non-neoplastic Ovarian Cysts
Major importance of these lesions rests in the clinical problems in distinguishing these benign causes of ovarian enlargement from carcinomas.

1. Follicular cysts*

Derived from the ovarian follicles

a. Solitary follicular cyst: Very common; usually regress spontaneously or with hormonal treatment. Lined by granulosa cells.

b. Corpus luteum cyst: Ovulation is accompanied by a variable amount of bleeding into the center of the follicle. This may be sufficient to cause clinical enlargement of the ovary.

349

Legend Ovulation causes a rupture of the ovarian capsule at the point of ovulation. This is associated with bleeding into the lumen of the follicle. This photograph depicts an involuting cystic corpus luteum that contains an organizing blood clot, giving the gross appearance of a hemorrhagic cyst. Occasionally, a hemorrhagic corpus luteum may be large enough to be palpable as an enlarged ovary on pelvic examination.

c. Theca-lutein cyst

3288

Legend The superficial cell layers in this ovarian cyst represent normal granulosa cells. However, beneath these cells are several layers of luteinized (eosinophilic) theca cells. In a normal corpus luteum, the granulosa cell layer is also luteinized. The pattern is usually associated with over stimulation by gonadotrophins as may happen in twin gestations or gestational trophoblastic disease.

3303

Legend The ovaries show multiple, enlarged cysts which cytologically were demonstrated to be theca lutein cysts. This patient had choriocarcinoma which resulted in over stimulation of the ovaries by human chorionic gonadotrophin. The tumor can be seen to be emerging through the serosal surface of the wall of the uterus on the left.

2. Endometriosis (endometriosis external)

Endometriosis is defined as the presence of functional endometrial glands or stroma in an abnormal location (outside the uterus).

Gross Appearance

A spectrum of changes can be seen. Usually, the affected tissues contain cysts (less than 1 mm. to greater than 10 cm.) that are filled with blood or its breakdown products. The cyst contents vary from a blue-black tarry color to light chocolate brown. Fibrous adhesions may extend from the effected areas.

Microscopic Description

The cyst walls are lined by endometrial glands and stroma. The stroma typically contains hemosiderin laden histiocytes. In some areas, the endometrial tissue is associated with fibrous connective tissue adhesions.

The most frequent locations include (in decreasing order of frequency):

a. Ovaries - Endometriosis in the ovary frequently presents as cystic enlargement, opening the cyst reveals old blood, frequently with a "chocolate" appearance)

794

Legend Endometriosis, left ovary.

b. Uterine ligaments

c. Rectovaginal septum

d. Pelvic peritoneum

e. Appendix, intestine, laparatomy scars, umbilicus

1775 1776

f. Extremely rarely, lungs, pleura, lymph nodes.

Clinical Aspects

a. Endometriosis is a major cause of infertility, pelvic pain, dysmenorrhea and other problems.

b. It is found in women in their active reproductive years, typically the third and fourth decades.

c. Symptoms are related to the response of the ectopic endometrium to the ovarian hormones which includes bleeding.

d. Infertility is related to:

1. Serosal scarring of the fallopian tubes.

2. Anovulation of unknown etiology.

Ovarian Tumors
Tumors of surface (coelomic) epithelium
Common tumors thought to derive from the invagination and metaplasia of the germinal epithelium covering the ovary . Small germinal inclusion cysts are commonly found in the ovarian cortex of many ovaries. These may represent the non-neoplastic analog of epithelial tumorigenesis in the ovary.

3279

Legend The small cyst in the ovarian cortex is lined by a flattened simple epithelium. This is termed a germinal inclusion cyst and forms as an invagination of the germinal epithelium. The lining epithelium may undergo metaplasia to mullerian derivatives in a manner analogous to the development of epithelial tumors of the ovary.

a. Biologic Spectrum

1. Benign

a. Cystadenoma* - Benign cystic epithelial tumor, commonly multicystic.

348

Legend This ovary shows a multiloculated cystic appearance. The fact that the cyst walls are very thin and delicate, without papillary excrescences suggest a benign process. Histologically, this was a serous cystadenoma. The cysts were lined by a single layer of ciliated columnar epithelium.

346

3274 3274¥26308

Legend In this serous cystadenoma, papillary excrescences (green arrows) are noted in addition to the thin walled cysts (red arrows). Microscopically, the papillary areas show fibrous connective tissue with the overlying simple epithelium.

3245

Legend A multiloculated, cyst-within-cyst pattern is frequently seen in the mucinous cystadenomas. Mucous-like material is secreted by the cells and is present within the cyst. (See 3248)

3248

Legend The cyst walls are lined by mucous containing tall columnar epithelial cells. Frequently these mucin secreting cells have characteristics of intestinal type differentiation. However, endocervical type differentiation can also be seen.

b. Solid: A stromal component is prominent in addition to the epithelial one.

3243

Legend This image shows a mixed pattern consisting of a dense collagenized stroma that is associated with epithelial lined cysts. This pattern is typical for an adenofibroma. The epithelium may be serous, mucinous, or endometriod. In addition, some tumors have a predominantly cystic gross appearance and qualify for the term cystadenofibroma. The relative proportion of these components is variable.

3246

Legend This gross appearance is typical for a cystadenofibroma in which the predominant pattern is solid with a few cystic spaces also present.

3361

Legend This image demonstrates a surface papilloma of the ovary. It is recognizable by the presence of multiple tiny surface excresences. Histologically, these are small papillary structures composed of fibrous connective tissue covered by columnar epithelium. This histologic pattern is demonstrated on the next Image 3363.

3363

2. Borderline (Low malignant potential*) These tumors have features intermediate between benign and malignant. While these tumor usually have an excellent prognosis, some patients will die of their disease.

803

Legend Papillary serous tumor of low malignant potential (borderline) have histologic features intermediate between papillary adenofibroma and true adenocarcinoma. Excrescences show a connective tissue core covered by piled up, hyperplastic epithelium.

3283

Legend This papillary structure would appear as a mulberry-like excrescence within a cystic space. In the absence of stromal invasion elsewhere in the tumor, this pattern suggests papillary tumor of low malignant potential.

308

Legend Mucinous tumors of low malignant potential can seed the peritoneal cavity with mucin secreting epithelium. The mucous material can massively accumulate in the peritoneal cavity giving rise to pseudomyxoma peritonei*.

3. Carcinoma

Epithelial tumors are the most common malignant tumors of the ovary accounting for approximately 90% of primary ovarian malignancies.

37

Legend The two structures represent cut surfaces of both ovaries in this patient with papillary serous cystadenocarcinoma. While most cases show a mixture of cystic and solid elements, this case shows a solid pattern totally replacing the ovaries and involving the surfaces of the ovaries. This patient had extensive peritoneal seeding at the time of diagnosis.

3286

Legend This image represents a low power view of a well differentiated papillary serous cystadenocarcinoma. On the right-hand side of the image is a large cyst-like space that is filled with papillary projections. The fibrous connective tissue cores are covered by piled up epithelial cells. At high power, these represent malignant cells. On the left-hand edge of this large cystic space, fragments of psammoma bodies can be seen.

854

Legend This large ovarian tumor has a smooth exterior surface. The interior surface contains multiple papillary nodules that are suspicious for a neoplastic process. Histologically, this was demonstrated to be a papillary serous cystadenocarcinoma. Note the coarse, solid nodules are different from the thin walled cysts of benign lesions.

857

Legend This represents a close-up view of the gross papillary nodules of the cystic papillary serous carcinoma noted above.

855

Legend This pattern represents the papillary excresences that may be seen on the external surface of a papillary serous cystadenocarcinoma of the ovary. This is seen in the enlarged ovary on the right side of the image. The malignant nature of these excresences can be determined only by microscopic examination.

3242

Legend This papillary serous carcinoma displayed a variant pattern in which the lesion is present on the external surface of the ovary. A cystic component is lacking in this lesion. It has a similar biological potential to a cystic lesion in which the malignant cells have penetrated to the external or peritoneal surface.

3247

Legend This represents the cut surface of a predominantly solid mucinous cystadenocarcinoma. The surface has a glistening mucoid appearance. Frequently there is a mixture of cystic and solid areas. The solid areas show these dimensional masses of tumor cells. Areas of necrosis are soft and frequently hemorrhagic.

330

Legend Although the hemorrhagic cyst suggests endometriosis grossly, the presence of solid, focally necrotic tissue nodules within the cyst is evidence that this represents a carcinoma. Histologically, this lesion was endometrioid adenocarcinoma.

b. Histologic Subtypes

1. Serous*Tumors

Fallopian tube differentiation. Serous tumors are the most common of the epithelial tumors. They show cystic, papillary or solid patterns. Small laminated calcified structures, psammoma bodies, are frequently seen.

3359

Legend This histologic picture represents a papillary serous cystadenocarcinoma. The fibrous connective tissue cores are covered by malignant cells. This demonstrates the papillary nature of the lesion. In addition, the epithelium (which is seen as the blue areas) are piled up in multi-dimensional layers. This distinguishes the malignant tumor from the benign lesions in which the papillae or cysts are lined by a single epithelial layer.

2. Mucinous*Tumors

Endocervical or gastrointestinal differentiation

3. Endometrioid*

Endometrial differentiation; commonly arise in the background of endometriosis. (However, endometriosis is not considered to be premalignant.)

338

Legend Unlike the typical serous carcinoma, this well differentiated endometrioid carcinoma has a glandular rather papillary configuration. Tall columnar epithelium typical of carcinoma of the endometrium is also seen in the primary ovarian carcinoma.

4. Clear Cell Carcinoma

Benign counterpart is unclear; It may be an endometrial derivative.

3263

5. Brenner Tumor*

Urothelial differentiation.

3365

Legend Epithelial islands are present surrounded by a fibrotic stroma.

3366

3367

Legend The epithelial cells mimic urothelial differention.

c. Pathogenesis

Poorly understood. Risk factors include nulliparity and family history. Some authors have noted that the peritoneal cavity (and the surface of the ovaries) is open to the external environment through the vagina, uterus and fallopian tube. This could indicate a route for exposure to carcinogens. This has not however been substantiated.

d. Clinical Course

1. Presenting complaint. Lower abdominal pain or abdominal enlargement. These tumors are commonly metastatic at the time of diagnosis.

2. Direct penetration of the tumor through the ovarian capsule is typical with implantation of tumor onto the peritoneal surfaces.

855

Legend The ovarian tumor is predominately cystic but the granular excresences on the lower half of the mass indicate peritoneal extension.

664

Legend The structure is the tumor studded, fibrotic omentum from a patient with massive intraperitoneal metastases from ovarian carcinoma. Because of the relatively thin ovarian capsule, intraperitoneal extension is common.

3. Ascites*: The accumulation of excess peritoneal fluid. In ovarian carcinoma, tumor cells penetrate into the peritoneal cavity and grow in the accumulated fluid as in a cell culture medium. The fluid accumulation is due to blockage of lymphatics, elaboration of protein and fluid by the tumor and irritation of peritoneal surfaces. Tumor implants settle out and attach to peritoneal surface throughout the peritoneal cavity.

3808

Legend Groups of adenocarcinoma cells are present with psammoma bodies.

3810

Legend Groups of adenocarcinoma cells are present with psammoma bodies.

4. Lymph node metastases: Frequently occurs as part of disseminated carcinomatosis.

5. Blood borne metastasis: Late manifestations, involving the liver, lungs, bone marrow.

e. Prognosis

1. Stage: Survival related to stage. Unfortunately, most patients present at an advanced stage accounting for the relatively poor survival rates.

2. Tumor markers:

CA125*: High molecular weight glycoprotein present in over 80% of serous and endometrioid carcinomas. Rising serum levels can be used to monitor recurrence.

CEA: Carcinoembryonic antigen: Originally described in colon carcinomas, the antigen is present on a wide variety of carcinomas, including ovarian. Rising serum levels can be used to monitor recurrence.

3. Ploidy and cell cycle kinetics

4. Hormone receptors: Estrogen and progesterone receptors

Germ Cell Tumors
9268 Robbins Figure 24-50

a. Histologic Subtypes

1. Teratoma*: The most common germ cell tumor

a. Benign cystic teratoma (Dermoid cyst)

3252

1. Gross: Usually a simple cyst containing hair admixed with greasy yellow-white, sebaceous material. Frequently, a single nodule is present in the wall which contains hair shafts, teeth or other tissues.

797 797¥26325

Legend This x-ray of a benign cystic teratoma shows a definite malformed tooth, a relatively common finding.

798

Legend This ovary mass, when opened, revealed greasy, sebaceous material and hair. This appearance is typical of benign cystic teratoma.

2. Microscopic: Usually a combination of multiple mature tissues is present including epidermis with adnexal structures, neural tissue, respiratory epithelium, bone, etc. Lesions that contain thyroid tissue are termed struma ovarii.

3250

3252

Legend Ciliated respiratory epithelium is present at the surface. At the lower half of the image, thyroid follicles can be seen.

b. Immature teratoma: Rare tumor with immature cell types including primitive neuroectoderm. Aggressive tumor in contract to the benign cystic teratoma.

c. Malignant transformation in a benign cystic teratoma: Rare; occurs in post menopausal women. Squamous cell carcinoma is the most common histologic tumor to evolve.

2. Dysgerminoma*: analogous to testicular seminoma; resembles primitive germ cells. Malignant tumor but responds to radiation therapy.

3. Endodermal sinus tumor (yolk sac tumor): mimics differentiation of extraembryonic membranes; Frequently secretes alpha fetoprotein*, which can be used to monitor recurrence.

4. Choriocarcinoma: rare; usually occurs as part of a mixed germ cell tumor; produces human chorionic gonadotropin (HCG).

5. Other germ cell tumors

Sex Cord - Stromal Tumors:
Derived from the ovarian stroma and follicular lining cells which originate embryologically from sex cords*. Frequently secrete hormones; tend to occur in premenopausal women.

Histologic Subtypes

Granulosa-Theca cell tumors*:

Estrogen secreting: Most frequent of this group. Associate with long-term survival but late occurrence common; considered a low grade malignancy.

851 851¥26326

Legend Granulosa cell tumors frequently show microcystic areas called Call-Exner bodies. Call-Exner bodies (arrow) can sometimes be recognized in the normal granulosa layers of normal follicles.

3275

Legend Normal developing follicle in a premenopausal woman with a Call-Exner body in the granulosa cell layer.

Fibroma*: (Fibrothecoma):

A benign stromal tumor that is occasionally associated with Meigs' Syndrome, which is defined as combination of ovarian tumor, hydrothorax and ascites. The cause is unclear; however, when the bulky ovarian tumor is removed, the effusions disappear.

3265

Sertoli-Leydig cell tumors (Arrhenoblastoma):

Sex cords of the embryonic gonad develop into the granulosa-theca cells of the ovary and the Sertoli-Leydig cells of the testes. Rarely, an ovarian tumor shows Sertoli-Leydig differentiation. May be androgen secreting.

852

Uterine Enlargement
Adenomyosis* (Endometriosis interna)

1. Adenomyosis is defined as the presence of endometrial glands and stroma deep within the uterine myometrium (1 low power microscopic field or 2-3 mm. below endometrial-myometrial junction).

405 405¥26317

Legend Endometrial glands and stroma extend through the myometrial muscle fibers well below the endometrial-myometrial junction.

2. It is thought to represent down growth of the basalar endometrium between the smooth muscle bundles of the myometrium.

3. It has been associated with an enlarged, globular uterus with hypertrophied uterine walls, although the uterus may be grossly normal in some cases. Occasionally, 2 - 5 mm cysts containing red-brown material can be seen grossly in the myometrium. This reflects the cyclic bleeding of the entrapped endometrium in response to ovarian hormone levels during the menstrual cycle.

1764 1765

Leiomyomas: refer to Leimyomas under "Abnormal Uterine Bleeding".

Malignant tumors of the Endometrium and Myometrium: refer to "Endometrial Carcinoma" under "Bleeding Secondary to Organic Disorders".


Differential Diagnosis of Pelvic Pain
Pamela Talley, M.D.
Peer Review Status: Externally Reviewed by Mosby


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GI
 GU
 GYN
Appendicitis
Diverticulitis
Inflammatory bowel
Irritable bowel
Bowel obstruction
Inguinal hernia
 Pyelonephritis
Ureteral stone
Cystitis
 Ectopic pregnancy
Spontaneous abortion
Pelvic inflammatory disease
Bleeding corpus luteum cyst
Adnexal torsion
Mittelschmerz
Endometriosis



Cytopathology Reporting Systems for Papanicolaou Smears
Pamela Talley, M.D.
Peer Review Status: Externally Reviewed by Mosby


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Class System
 World Health Organization System
 Cervical Intraepithelial Neoplasia System
 Bethesda System
I
 Normal
 Normal
 Within normal limits
II
 Inflammation
 Infection, reactive, reparative
III
 Dysplasia
Mild
Moderate
Severe
 CIN-1
CIN-2
 Squamous intraepithelial lesions
Low grade
High grade
IV
 Carcinoma in situ
 CIN-3
V
 Invasive squamous cell carcinoma
Adenocarcinoma
 CIN-3
Invasive squamous cell carcinoma
Adenocarcinoma
 Squamous cell carcinoma
Adenocarcinoma



Table 8-1: Hepatitis B Vaccination Schedule for Infants
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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Hepatitis B Vaccine
 Infant Age
 Other Infants/Children
Dose 1
 2 wk, 1 or 2 mo
 Time 0
Dose 2
 2 or 4 mo
 1 mo after dose 1
Dose 3
 9 mo
 6 mo after dose 1



Table 8-2: Management Protocol Based on Biophysical Profile
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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Score
 Interpretation
 Recommended Mangement
10
 Normal infant; low risk of chronic asphyxia
 Repeat BPP at weekly intervals; repeat twice weekly in diabetic patients and patients 42 or more wk gestation
8
 Normal infant; low risk of chronic asphyxia
 Repeat BPP at weekly intervals; repeat twice weekly in diabetic patients and in patients 42 wk or more gestation; oligohydraminos is an indication for delivery
6
 Suspect chronic asphyxia
 If 36 or more week gestation and conditions are favorable, deliver; if less than 36 wk and L/S less than 2.0, repeat test in 4-6 hr; deliver if oligohydraminios is present
4
 Suspect chronic asphyxia
 Deliver if 32 or more wk gestation; if less than 32 wk, repeat BPP
0-2
 Strongly suspect chronic asphyxia
 Extend testing time to 120 min; indication for delivery: persistent score 4 or less, regardless of gestational age

*Adapted from Gabbe SG (ed): Obstetrics: Normal and Problem Pregnancies, ed 2. New York, Churchill Livingstone, 1991. Used by permission.



Table 8-3: Upper Limits of Normal Serum Glucose Levels (mg/dl) on 3-hour Glucose Tolerance Tests
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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Fasting
 1 hr
 2 hr
 3 hr
105
 190
 165
 145



Table 8-4: Interpretation of Fetal Scalp Scalp pH
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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Fetal Scalp Blood pH
 Interpretation
 Management
7.25 or more
 Normal
 Continue FHR monitoring and resample if appropriate
7.20-7.24
 Preacidotic
 Consider resampling and continue FHR monitoring
7.19 or less
 Fetal acidosis
 Resample in 5-10 min and prepare for immediate delivery if low scalp pH confirmed



Table 8-5: Bishop Scoring System
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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 Score[1]
Cervix
 0
 1
 2
 3
Position
 Posterior
 Midposition
 Anterior
 ---
Consisttency
 Firm
 Medium
 Soft
 ---
Effacement (%)
 0-30
 40-50
 60-70
 80 or more
Dilatation (cm)
 Closed
 1-2
 3-4
 5 or more
Station
 -3
 -2
 -1
 +1, +2

*Adapted from Driscoll CE, et al: Handbook of Family Practice. St Louis, Mosby-Year Book, 1986. Used by permission.

[1]A Bishop score of 9 or greater indicates that induction should be successful.



Table 8-6: Differential Diagnosis of Puerperal Fever
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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Diagnosis
 Risk Factors
 Clinical Features
Endomyometritis
 Chorioamnionitis, prolonged rupture of membranes and labor, multiple vaginal examinations, cesarean section, retained products, contact with group A streptococci carrier, carriage of group B streptococci, indigent patient, internal monitoring (?), manual placental removal (?)
 Fever, malaise, abdominal pain, uterine tenderness, purulent lochia, leukocytosis; usually within 48 hours of delivery
Pelvic abcess
 Pelvic infection with delayed anaerobic therapy
 Continued fever, pain, ileus; pelvic mass; usually after day 5
Septic pelvic thrombophlebitis
 Pelvic cellulitis
 Continued spiking fever, with or without pain, unresponsive to antibiotics; possible tender mass; diagnostic response to intravenous heparin
Wound infection
 Cesarean section in labor, emergency surgery, electrocautery, open drains, obesity, diabetes
 Fever; tender, erythematous, or fluctuant incision; drainage of blood or pus; usually after day 5
Pulmonary atelectasis
 Recent general anesthesia, abdominal incision, narcotic analgesics
 Fever usually within 48 hours; poor inspiratory effort; dullness, decreased breath sounds, or rales
Pyelonephritis
 Unrecognized bacteriuria, bladder trauma, catheterization
 Fever, malaise, costovertebral angle tenderness, pyuria
Deep vein thrombosis
 Traumatic delivery, cesarean section, delayed ambulation, varicose veins
 Fever; lower-extremity pain, swelling, and pallor
Mastitis
 Usually breast-feeding, contact with Staphylococcus aureus carrier
 Usually 3-4 wks postpartum; fever, malaise; swollen, tender, indurated breast

*Adapted from Niswander KR )ed): Manual of Obstetrics: Diagnosis & Therapy, ed 3. Boston, Little, Brown, 1987. Used by permission.



Shoulder Dystocia
Barcey T. Levy, M.D. and Pamela L. Brown, M.D.
Peer Review Status: Externally Reviewed by Mosby


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I. INCIDENCE

Directly related to fetal size: greater than2500 g, 0.15%; greater than4000 g, 1.7%; greater than4500 g, 10.0%

II. DIAGNOSIS

Suspect shoulder dystocia if there is reason to suspect macrosomia (gestational diabetes, history of large infants, large maternal size, prolonged gestation) or if the second stage is prolonged. Consider cesarean section. In vaginal deliveries, suspect dystocia if the head pulls back against the perineum after delivery and external rotation is difficult

III. MANAGEMENT

A. Ensure adequate maternal anesthesia and cut a very generous episiotomy

B. Attempt McRobert's maneuver. The mother's thighs are hyperflexed, bringing her feet "to her ears.'' Have an assistant apply suprapubic pressure. This causes the shoulder to move under the symphysis pubis. Attempt delivery with gentle downward traction

C. Attempt the Wood's screw maneuver. Gently rotate the posterior shoulder by pushing on the posterior aspect of the scapula until the shoulder passes under the symphysis and can be delivered as the anterior shoulder

D. If this is unsuccessful, try delivering the posterior arm first, then rotating the anterior shoulder into the oblique position for delivery

E. If all else fails, one may attempt deliberate fracture of the clavicle of the impacted shoulder. The thumb and forefinger are used to push the clavicle outward to avoid a pneumothorax. Although the fracture will heal, damage to cervical nerve roots may occur and cause permanent sequelae


 What's Your Diagnosis?


A 22 y/o primigravid presents with a fetus in transverse lie at 35 weeks. A sonogram performed at that moment confirmed the presence of malpresentation. The following longitudinal view of the lower uterine segment shows the cervix (Cx) and maternal bladder (Bl). The cause of the malpresentation in this case would be?






Answer:

Vasa Previa is an uncommon finding with an occurrence of 1/3000 deliveries. It is defined as a velamentous insertion of the cord in the lower uterine segment. It is considered one of the most potentially lethal fetal condition due to the risk of exanguination which can occur in up to 75% of cases.


A 20 y/o primigravid is referred due to an abnormally elevated maternal serum alpha feto protein. The sonographic image of the fetal head is a classic finding.

1 What is this finding called?

2 What anomaly would you expect to find?





Answers:

1 - A lemon sign.

2 - Myelomeningocele

The lemon sign is present in over 95% of cases of myelomeningoceles. It is caused by indentation of the frontal bones due to a decrease in intracranial pressure brought about by displacement of the brain through the foramen magnum as occurs in cases of open neural tube defects. Although it may be a transitory finding in a small percentage of the normal population, its identification should prompt a careful surge for spinal defects.

The following sonogram was an incidental finding during a sonogram performed at 20 weeks

1 - What is this finding?

2 - To which condition is it associated?

3 - What procedure should be offered?

4 - If the Maternal serum alpha feto protein is normal, can we exclude the risk of this anomaly?




Answers:

1- Abnormal nuchal fold, defined as a thickness of over 5 mm measured from the external bone margin to the external skin surface at the level of the posterior fossa in a transverse view of the fetal head.

2- There is a higher risk of chromosomal abnormalities such as trisomy 21 and monosomy XO

3- A genetic amniocentesis is indicated

4- No, an abnormal alpha feto protein level is only present in 23% of fetuses with trisomy 21 and even using triple markers (Estriol, HCG and MSAFP) the sensitivity is only 65%, therefore if a finding such as this one is present, the risk of a chromosomal abnormality can not be excluded by any other finding other than a normal karyotype.


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"At Risk" Pregnancies

While obstetric complications may occur in any pregnancy at any time, it is recognized that certain categories of patient are particularly 'at risk'. In these categories, both maternal and perinatal mortality are substantially increased. The accompanying list is presented to remind all those practising obstetrics of these dangers. It is recommended that patients falling into these groups should be assessed carefully and that if more than minor complications exist, consideration should be given to referral of the case to an obstetrician with special experience.

1. General Factors

age (early teenage, later reproductive years);
social class (underprivileged);
aboriginality;
parity (primigravida and gravida 4+);
height (short stature);
weight (overweight and underweight);
dietary aberrations;
drug addiction and abuse of alcohol or tobacco;
mental disturbance.
2. Maternal Diseases

cardiovascular disease including hypertension;
diabetes mellitus;
anaemias (all types);
chronic renal disease including recurrent urinary infection;
past history of venous thrombosis and/or pulmonary embolism.
3. Family History of a Genetic Disorder

4. Bad Obstetric History

previous Caesarean section;
previous abortion, including habitual abortion;
previous perinatal mortality;
previous premature labour or placental insufficiency.
5. Diseases Peculiar to Pregnancy

preeclampsia;
rhesus and other blood group incompatibility.
6. Bleeding in Pregnancy

threatened abortion;
abruptio placentae;
placenta praevia.
7. Obstetric Difculties Discovered Antenatally

malpresentationespecially breech presentation and transverse lie;
disproportion.
Multiple Pregnancy
placental insufciency and retarded intrauterine growth;
prolonged pregnancy (past 42 weeks);
premature rupture of the membranes.
8. Patients Having Inadequate Antenatal Care

failure to attend for regular antenatal checks;
nonbooked cases;
late booked cases.
9. Difficulties Discovered During Labour

failure to progress satisfactorily, including prolonged labour;
fetal distress;
malpresentation.

Pregnancy I
I. Overview
A. Over 6 x 106 begun in U.S. each year, more than 1/2 are unplanned, results in about 3.6 x 106 births/year.
B. Length: 38 weeks post-conception or 40 weeks from LMP. Range is 37 - 42 weeks.

1. about 5% of women deliver on their due date.

2. 50% of women deliver within 10 days of due date.

C. Terms

1. zygote- fertilized egg, single cell.

2. embryo- up to 8 weeks.

3. fetus- 9 weeks on.

II. PRE-PREGNANCY COUNSELING
(before a planned pg or very early in an unplanned pg)

A. Stop all drugs, alcohol, cigarettes (or at minimum cut back to less than 1/2 pack/day).

B. If you know you have a health problem (HTN, diabetes, seizure sidorder, migraine headaches) get a medical check-up before you get pregnant. These problems, or the medication for them can put you and/or your baby at risk.

C. Survey your environment (workplace, home, refrigerator, etc) for unhealthy exposures.

1. Workplace: what's safe and what's not safe?


Only 4 out of 60,000 chemicals regulated by the FDA are regulated because of their reproductive effects. We don't know the reproductive effects of most chemicals. FDA has required testing on women only since early 1990s. 2. Dose: Higher doses are more likely to cause any kind of health effects. Most reproductive toxins are found in the workplace (present in high doses), some are found in the environment (chronic exposure). a. Evaluate exposure based on:

dose- how much?
route of exposure: breathing, eating, skin contact.
duration of exposure (1 day, chronic).
toxicity of chemical (depends on sensitivity of patient).
individual response of patient (body size, smoker/non- smoker, etc).

3. How do we know about reproductive toxins?

a. in vitro test (Ames test)- uses bacteria or cells to look for adverse affects of a compound.

b. animal tests- need to use different animals for tests since the effect of a compound on a rabbit may be very different than on a mouse. Humans should be considered at least as sensitive as the most sensitive animal. Spontaneous abortion might be the most sensitive measure of a chemical's toxicity.

c. epidemiological studies- study the pattern of health effects in different populations.

4. Timing of development a. Gametes (reproductive cells or eggs and sperm) of women and men. Women are born with all the eggs they will ever produce already in the ovaries. Men produce sperm continuously (after puberty), make millions/day. Means that damage to reproductive cells can be passed to future generations more easily if it occurs in women than if it occurs in men.

b. After fertilization

i. It takes about 5 days for the embryo to travel down the fallopian tube to the uterus. Once in the uterus, the embryo implants. The placenta not formed until about the 17th day after fertilization. Before the placenta is formed, it is difficult for chemicals to reach the embryo. Once placenta formed, then the transport mechanism used to move nutrients from mother to embryo can also move hazardous chemicals.

c. ALL OR NOTHING PERIOD- about the first 2 weeks of development, during this time an exposure to a hazardous substance will either cause the miscarriage of the embryo (may look like a slightly heavier than normal period, woman may not even know she is pregnant) or cause no damage at all.

d. Organs, systems, and limbs of embryo form at different times. Exposure to a reproductive toxin may cause different effects depending on when the exposure occurred (relative to how developed the embryo was).Habits-

5. Alcohol- don't know what is "safe" amount, recommend 0, an occassional glass is prob. ok.

a. Fetal Alcohol Syndrome (FAS)- facial features, retardation due to regular drinking or heavy binge drinking. Lower levels of alcohol intake can lead to Fetal Alcohol Effect (FAE). Preventable.

6. Smoking- assoc c/ low birth weight babies, preterm labor, placental abruption, miscarriage, and increased risk of neonatal death. Nicotine in circulation constricts blood supply to baby.

7. Other legal drugs-

a. caffeine- 1 - 2 cups/day probably ok, beware decaf processing.

b. artificial sweeteners (Saccharin/Nutrasweet)- don 't know what's safe.

c. OTC medications- check with your practitioner about each one.

Example: Tylenol is ok, aspirin is not (it tends to prolong bleeding). Worrisome to note that most women take 4 OTC preparations in the 1st trimester.

d. Prescription drugs need medical consult.

8. Illegal drugs-

a. Marijuana- no congenital defects seen, but concerns about smoke inhalation and decreased blood flow to placenta (like nicotine).

b. Cocaine/crack- maternal high blood pressure, seizures, placental abruption (cause lack of O2 to fetus), see neurological changes in resulting babies. These children may be the fastest growing and the largest new group of learning disabilities.

c. Amphetamines/speed- similar to cocaine.

d. Heroin- preterm labor, low birth weight babies, neonatal withdrawal takes 3 - 5 days.

9. X-rays- a problem in large doses, avoid if possible, but ok c/ small doses and adequate shielding.

10. Toxins in workplace- solvents, pesticides, styrene are a problem. 1x exposure is probably ok, but large or continuous exposures are bad.

11. Radiofrequency/Microwaves- RF can correlate c/ increased body temp of few degrees. Microwaves safe if meeting current regs.

12. TV/VDTs- negligible emissions. Shielding is available.

13. Hot tubs/saunas- if mom's body temp is above 100oF, can cause birth defects, either turn down or avoid.

14. Laws-

a. Occupational Safety and Health Act.

b. Right to Know legislation. Legally, in CA, your employer must inform you if you work with hazardous materials.

c. Title VII of the Civil Rights Act (Pregnancy Discrimination Act)

d. Fetal Protection Policies
UAW vs Johnson Controls

e. FDA regulations on drug testing, pesticide testing.


Protecting against other toxic effects of a substance also protects against reproductive toxic effects.
Exposures need to be studied on a case by case basis.

D. Start prenatal nutrition/vitamin regime (make sure contains at least 1 mg/day folate or folic acid). This can help reduce the risk that your baby will be born with a serious birth defect known as spina bifida. Spina bifida (or open spine) occurs when the backbone that protects the spinal cord fails to close completely. The unprotected part can be so small that it causes no noticable problems, or so large that it can cause paralysis of the legs ,and bladder and bowel control problems, and hydrocephaly (water on the brain, which has other assoc. problems). Good sources of folate include: citrus fruits and juices, dark green leafy vegies, beans, breads and cereals made with folate-fortified flour, and supplements (pills).

III. CONCEPTION
A. After ovulation, egg travels down fallopian tube. Usually the sperm encounter the egg somewhere in the tube. Egg is fertilized by only 1 sperm, but it may take millions of sperm to overcome the egg's "resistence" to fertilization.

1. Sex of child determined by sperm, which can carry either an X chromosome or a Y chromosome. All eggs carry only an X chromosome. It is the father's contribution that determines sex of child. 2. Identical twins (1 fertilized egg that splits into two viable embryoes, producing two genetically identical individuals) vs fraternal twins (2 eggs each fertilized by a different sperm, no more similar genetically than normal siblings). 3. After fertilization cleavage begins, dividing the single-celled fertilized egg into what will eventually be an individual with billions of cells. All this time the embryo is moving down the fallopian tube towards the uterus (takes about 5 days). Embryo implants in uterus somewhere around day 7 (post-conception, = day 21 since LMP). Implantation bleeding (looks like spotting) may occur at about the time the period would normally be expected, can cause confusion in determining date of LMP.

B. Hormones: embryo produces HCG which sustains corpus luteum to continue to produce progesterone to sustain endometrium until the placenta (part of the fetus) can take over progesterone production at about week 12.

1. Basis for pregnancy test is HCG in urine or blood. The earliest you could see a + pregnancy test is 21 days from LMP. 2. Most home tests reasonably accurate by 1st day menstrual period is late.

3. HCG levels continue to rise, doubling every other day until about day 60, then declines.

IV. FIRST TRIMESTER
- first 1/3 of pregnancy (first 13 weeks).

A. All or none period- the first two weeks post-conception (before missed period). An exposure to a hazardous substance will either kill the embryo, or cause it no harm.

B. Organogenesis- when all major organs, systems, limbs, etc. of embryo are beginning to develop. This is the 1o task during this trimester. It is during this time that the embryo is extremely sensitive to toxic substances.

C. Establishment of placenta on uterine wall. The placenta is a disposable separate organ that is designed to furnish the fetus with O2 and nutrients and dispose of the fetus' wastes. The blood of the fetus and the mother do not come into contact, rather transfer of materials across the placenta occurs.

D. Special 1st trimester problems

1. Ectopic pregnancy- we've discussed this before (infertility lecture). It is a pregnancy that occurs anywhere outside the uterus, most commonly in the fallopian tube, where the developing embryo can cause the tube to rupture which puts the mother' life in danger.

a. rate = 1%

b. predisposing factors- PID, IUD, minipill, previous tubal surgery.

c. sx- late period, signs of pg, +/_ spotting, pelvic pain c/ unusual dizziness.

d. dx- HCG levels, uterus too small for dates, tube enlarged and/or tender, ultrasound (US).

e. tx- methotrexate or surgery to remove pg. Risk of subsequent ectopic increased by the surgery. 2. Spontaneous abortion (or miscarriage) (see infertility lecture)-

a. it is fetal loss at less than 20 weeks.

b. occurs in more than 30% of all pregnancies, may occur so early that woman may not even know she was pregnant, therefore doesn't recognize it as a miscarriage.

c. most miscarriages occur before about 12 weeks. A miscarriage is less likely if fetal heart tones (FHT) heard or heart is seen on US.

d. 50 - 60% may be due to chromosomal damage so severe that the fetus would not have completed development anyway. ("Nature's protection")

e. if a woman has suffered more than 2 miscarriages, there may be an immunologic basis to the cause (mother cannot protect the 1/2 of the fetus that is "foreign" from her own immune system).

f. sx- vaginal bleeding usually accompanied by cramps.

g. may be threatened, inevitable (cervix opened), incomplete (some but not all of fetus or placenta expelled), or complete. May need medical intervention if cramps or bleeding is severe. Otherwise, advise bedrest.

h. tx- nothing except awareness of a grieving period (some families have formal ceremony, etc). Evaluation recommended if a woman has had 3 or more SAB, but even then there is a 75 - 80% chance that the next pg will be normal.

3. Molar pregnancy- a rare condition (1 in 1500 pregnancies) where the placental tissue itself becomes choriocarcinomaa, an aggressive and invasive form of cancer. The fetus, if even present, is non-viable. HCG levels are very high. Need for follow-up is critical. If a woman has already had a molar pregnancy, there is a slightly higher risk (~2%) of another molar pregnancy. The overall risk of having a molar pregnancy is extremely low in young women, but the risk increases with age. In women over 45 the risk of a molar pregnancy is 2-4%. A molar pregnancy does not increase the risk for endometrial cancer later.

E. Maternal physiological changes-

1. Uterus- grows to contain more than 5 liters, enlarges 500 - 1,000x, then returns to its normal size after birth. It is above the pelvic bone by 12th week. Braxton-Hicks contractions (warm ups for labor, woman may not feel during her first preg) occur from end of 1st trimester on.

2. Cervix- softens, becomes swollen and bluish colored.

3. Ovaries- less active, secrete relaxin- a hormone that relaxes ligaments.

4. Vagina- increased vascularity, more secretions, more acidic.

5. Skin- changes in pigment include chloasma (the mask of pregnancy), linea nigra (dark line on abdomen). Face has increased oil production (glow of pg). Vascular spiders, palmer redness.

6. Breasts- enlarge, more tender, areola darkens. Glands begin to produce colostrum last few months of pg.

7. Blood- volume increases by more than 50%. Anemia usually develops as iron stores are depleted.

8. Heart rate- increases 10 - 15 beats/min. Is pushed upward by expanding abdomen. BP usually drops as peripheral resistance (tension in the blood vessels) drops.

9. Respiration- rate is unchanged, but each breath moves more air and O2 extraction becomes more efficient.

10. Urinary system- kidneys filter 50 - 60% more urine, more spilling of protein and glucose into urine. Bladders and ureters compressed by expanding abdomen.

11. Intestinal tract- tone and mobility declines, takes longer for stomach to empty and to move through intestines-->heartburn, bloating, constipation (esp later in pg). Gums enlarge, may bleed. Hemorrhoids (varicose veins of rectum) may bleed.

12. Musculoskeletal- progressive swayback, mobility of pelvic joints.

13. Metabolism-

a. water- retention, exp towards term, increased thirst as blood volume builds.

b. protein metabolism increases to add protein to uterus, breast glands, & fetus.

c. carbohydrates and fats used differently

d. weight gain- "IDEAL" IS 25 - 30 lbs.
fetus (7.5) placenta (1.5) amniotic fluid (2) uterus (2.5)
breasts (1-1.5) blood (3.5) fat (4) water retention (4)
TOTAL = 26 LBS. IMPORTANT NOT TO LOSE WEIGHT IN PG.

F. Usual complaints of early pg- can be understood in terms of above changes.

Breast tenderness, fatigue, bloating, nausea (in 50% of women, may be a reaction to all the HCG being produced or to the 1/2 "foreign" protein of the fetus), food cravings (pica), food aversions, hemorrhoids, headache (sinus congestion), skin changes, hair changes, etc.

G. Emotional changes- vary markedly between women- elation, depression, change in libido (either up or down), ambivalence toward the pg, some introversion (looking inward), some body image problems. A "labile" emotional component.

V. NUTRITION IN PG
A. Four basic food groups (servings/day)

1. Protein (meat, chicken, fish, eggs, tofu, beans, peanut butter, etc)- 3-4.

2. Vegetables and fruits- 5-7.

3. Grains- 6-11.

4. Dairy- 3-4.

B. Specific increases

1. Total calories increase by 25% (300-500 calories/day).

2. Protein requirements increase by nearly 60% (from 44-->74 g/day).

3. Folate (or folic acid) requirements double.

4. Calcium increases by 50% to 1500mg.

5. Iron needs increase 2-4x.

6. Magnesium up by 50%.

7. Vitamin C up 30%.

8. Vitamin E up 25%.

9. All of these needs can be supplied by most prenatal vitamins except for calcium (assumes that women will take in 3-4 dairy servings/day because the calcium is assimilated much better from dairy products than it is from a supplemental pill).

C. Think of it as a positive calorie balance, which provides enough calories for you and for the fetus. This is not a time to diet!

D. Focus on eating nutrient-dense foods instead of junk food or desserts which can offer you only empty calories (but you can spoil yourself occassionally).

VI. SECOND TRIMESTER
(weeks 14 - 26 or so)- characterized by an overall improvement in the way you feel. Nausea resolves, energy increases, abdomen swells and you start to "show", settle in for the pregnancy.

A. Chances of miscarriage markedly decrease. It is at this time that most people tell folks they are pregnant.

B. Quickening- recognize that some of the sensations you are feeling are due to the fetus moving. Firsttime moms at about 20 weeks, other "experienced" moms at 15-18 weeks.

VII. MATERNAL RISK FACTORS/BEHAVIORS
A. Exercise- continue previous activities but don't start new vigorous ones. (Probably by end of pg will be cutting back maybe 20%) Avoid activities that require excellent balance, avoid SCUBA. Keep in mind that you could compromise blood flow to the fetus if too much blood is diverted to the skeletal muscles. A benefit is an improved perception of labor's difficulty. Kegel exercises- contract and relax muscles quickly for 10 seconds, rest 10 seconds, then contract and hold for 10 seconds (or as long as possible). Repeat as long as possible, up to 150/day.

B. Sex

1. safe through pg, until cervix starts to dilate. 2. often recommended last 2-3 wks of pg to help /c cervical ripening, semen contains prostaglandins that help this process along.

C. Advanced maternal age- 35 or older at time of birth

1. Imp. c/ increased # of women delaying childbearing.

2. concerns are increased risk of chromosomal abnormalities, pre-existing health conditions, & special conditions such as pre-eclampsia. Pre-existing health conditions include: HTN, diabetes, kidney disease, heart problems. Most older moms do extremely well.

3. Monitor with prenatal diagnosis.

D. Teenage moms- increased risks often assoc c/ specific behaviors (e.g. unawareness of affects of drugs, alcohol, poor nutrition on fetus, warning signs, later entry into prenatal care).

VIII. PRENATAL MONITORING
A. Regular visits c/ a health care provider are imp. (ob/gyn, fp, cnm).

1. Initial complete exam, then visits once a month until 7th month, then 2x a month until 9th month, then once a week until birth.

2. Check weight gain/loss, BP, fetal growth, position of fetus, urine (for signs of protein, glucose, infection).

3. Listen for FHT every visit c/ Doppler (audio-ultrasound), first heard ~10 - 12 weeks from LMP.

B. Routine tests (done on most women)

1. CBC, syphyllis, hepatitis, rubella, blood type, Rh. Now usually include HIV, other STD screens, toxoplasmosis, Varicella (chickenpox).

a. Toxoplasmosis (protozoan)- causes mild flu-like sx in adults, 50% exposed before age 50. Causes blindness, mental retardation, other birth defects to fetus if mom exposed during pregnancy. Found in raw or undercooked meat and in cat feces (pg women should not handle raw meat or touch cat litter box, should wear gloves when gardening to prevent accidental exposure).

b. Rubella (German measles)- a virus that causes mild flu-like sx and a rash in adults and children. Some women were never exposed or immuniztions didn't "take" and contract it in pg. Causes congenital deafness, heart problems and mental retardation to fetus.

C. Other tests offered.

1. AFP (Alphafetoprotein)- mandated by CA to be offered between weeks 14-20. In widespread use where US not available. Used to detect congenital spina bifida, anencephaly (all or most of brain is missing), microencephaly (a large part of brain is missing), abdominal wall problems, and may also pick up Down's syndrome. Lots of false + but almost never a false -. Follow up US is done to rule out false +.

2. Glucose screening- offered at ~28 weeks to rule out gestational diabetes, routine use being called into question.

3. Group B Strep- a bacterium that occurs in the vagina of women, can cause serious infection in neonates, screening and monitoring is controversial.

4. Ultrasound (US)- used by many practitioners to confirm dates and scan for fetal anatomy surveillance (esp. the location of the placenta). There is no evidence to show any long-term ill effects and we are into the 2nd generation of women receiving it. New data indicates that there is no indication for routine use (no benefit medically in many cases).

D. Special tests for chromosomal analysis in women over 35:

1. Amniocentesis- done at 14-16 weeks. A needle is passed through the abdomen into the amniotic sac and a bit of the amniotic fluid is removed, along with some of the shed cells from the fetus. Cells are grown up in a lab, and chromosomes are examined.

a. benefits: detects chromosomal abnormalities.

b. risks: SAB, infection leading to fetal loss in 0.5% to 1% of cases.

c. done at 14-16 weeks and takes 10-14 days to grow cells-->some women feel fetal movement by then, harder to terminate.

2. Chorionic Villous Sampling (CVS)- newer technique, done at 9-11 weeks. Needle is passed via a catheter through the cervix or through the back wall of the vagina or through the mother's abdomen to retrieve a small piece of tissue from the placenta. This technique allows retrieval of more cells than with amniocentesis so it doesn't take as long to grow enough cells in the lab.

a. preferred technique for early dx since it's done earlier and takes less time.

b. risk is 1% to 1.5% of fetal loss by disrupting the pg. One study reports a group of congenital malformations in CVS babies, maybe due to hypoxia.

E. need for prenatal classes that include birth and parenting preparation.


Pregnancy II
I. ANEMIA
- probably the most common problem in pg. A deficiency of iron caused by the expansion of total blood volume without an associated increase (or availability) of iron.

A. Measured by hemoglobin (Hb) levels.

1. Hb is the molecule in the blood responsible for O2 transport. Decreased Hb levels are assoc. c/ decreased ability of body to do "work".

a. Pg women with Hb level of 11 g/dl or less are often considered anemic.

2. Concern is for the normal or greater blood loss that will occur with birth. In the presence of severe anemia a woman may require blood transfusion(s) which could obviously be avoided if Hg levels sufficiently high to allow for some blood loss.

B. Treatment is to increase amount of iron in diet.

1. Foods rich in iron: red meat, iron-fortified cereals, dried apricots, (raisins and prunes to a lesser extent), spinach, lima beans, soy beans, clams*, oysters*.

2. Iron supplement- ferrous sulfate (cheap). Side effects are constipation (so prunes may be a good choice again), stomach upset, dark stools.

3. Iron absorption is increased when iron supplements or iron-rich foods are accompanied by vitamin C (ascorbic acid)-rich foods or supplements.

II. PRETERM LABOR
- labor starting before 37 weeks. ~10% of pg end in preterm delivery, which accounts for 75% of all perinatal mortality (death of fetus/baby at or about the time of birth).

A. Causes are not usually known, although may be triggered or assoc with urinary tract infections, bacterial vaginosis, infection of the uterus (amnionitis) or distension of the uterus (due to multiple fetuses or too much amniotic fluid).

B. Premature birth is assoc with many problems for newborns (immature lungs, immature nervous system, immature digestive systems that isn't ready for oral nutrition yet, eye damage from oxygen therapy, vitamin deficiencies, etc. General prognosis for preterm babies- (the further along they are the better their chances are):

1. less than 28 weeks- 20% chance of survival. Need to be in a Neonatal Intensive Care Unit (NICU) for prolonged (and expensive) stay.

2. 28-32 weeks- babies may be in NICU and may have many complications, but each week further along the pregnancy continues adds about 10% to their chances of survival.

3. 32-34 weeks- need NICU, but most babies survive.

4. 34-37 weeks- need NICU initially, but most babies do well.

C. Respiratory immaturity- The lungs are one of the last organs to mature in a fetus. If the lungs can't pass O2 to the blood the baby will have severe brain and organ damage or may die. Most of the advances in treating preterm infants depend on the ability to help the lungs mature. One advance is the use of a surfactant, which is sprayed directly into the lungs at birth and helps overcome respiratory immaturity.

D. Tx- includes bedrest (to keep fetal pressure off the cervix and decrease uterine irritability) and tocolytic therapy (drugs), all aimed at stopping labor and giving fetus more time in the uterus to continue to develop, so that the baby is as mature as possible when it is born. Sometimes the drugs and bedrest work only for the short term, but this can give healthcare providers enough time to administer cortiocsteroids to the mother which actually help the fetus' lungs mature faster.

E. Who is at risk for preterm labor?

1. Women with any of the conditions mentioned under "A. Causes"

2. a prior preterm delivery increases a woman's risk from 7% to 15%.

3. teenagers.

4. women who have had inadequate nutrition or inadequate or delayed access to prenatal care.

5. smokers.

6. women with chronic high blood pressure (HTN).

III. PRE-ECLAMPSIA & ECLAMPSIA
(old name is "toxemia of pregnancy")-
A. Occurs in ~10% of pgs, usually occurs after 20 weeks.

1. sx- a set of 3.

a. hypertension (HTN, high blood pressure)- BP 140/90.

b. weight gain (>2 lb/ week), water retention and swelling (edema, "dentable" feet, ankles, legs, face, hands, etc).

c. protein in the urine (proteinuria)- a sign that the kidneys are not functioning properly.

2. Results in spasm of woman's blood vessels. Many organs of woman can be affected (brain and central nervous system [CNS], liver, kidneys, heart, blood's clotting ability).

3. Effect on fetus- loss of circulation to the fetus, detachment of placenta from uterine wall (placental abruption), both of which reduce the amount of O2 the fetus receives.

B. Cause is unknown, although there seems to be some male factor affecting risk: women are more at risk during first pregnancy, and again if a subsequent pregnancy is with a different partner.

C. Treatment of mild to moderate pre-eclampsia

1. increased surveillance of woman (fetal heart rate {non-stress test], US to check fetal growth and amniotic fluid volume, blood tests to evaluate the mother's liver, kidney and clotting factors).

2. bedrest.

3. Often this is enough to reduce blood pressure, proteinuria, and water retention enough to allow normal development of fetus, cervical ripening and vaginal delivery. If patient is not responding to bedrest, hospitalization and expeditious delivery of the baby (via induction of labor or cesarian section) may be necessary.

D. If pre-eclampsia is left untreated it can progress to eclampsia.

1. sx- all of the sx for pre-eclampsia + seizures.

E. Treatment of severe pre-eclampsia or eclampsia

1. delivery of baby as soon as possible. If fetus is still very immature, mother will be hopitalized for intense surveillance, bedrest, and will be given magnesium sulfate to prevent seizures until fetus is mature enough to survive outside the uterus. Continuous evaluation of the risks and benefits of non-intervention vs premature delivery is needed.

IV. DIABETES
- occurs in up to 6% of pg. Woman's blood sugar (glucose) level is higher than normal. Sugar (glucose) is spilled into the urine.

A. Types:

1. Pre-existing diabetes- woman knows before she gets pregnant that she is a diabetic.

2. Gestational diabetes- the condition develops during pg, as a result of interaction of two hormones (insulin and human placental lactogen). Usually develops late in 2nd trimester or early in 3rd trimester. Gestational diabetes disappears after delivery.

B. effect on fetus-

1. macrosomia (large babies)- increased risk of shoulder dystocia (head comes out but shoulders get stuck, can result in nerve injury to arms ranging in severity from impairment to total loss of use) if delivered vaginally. Cesarian section may be recommended.

2. delayed fetal lung maturity.

3. higher risk for birth defects if woman's blood sugar levels are not well-controlled during first 8 weeks of pg.

4. stillbirth.

C. Tx-

1. by diet alone, to regulate the amount of sugar the mom takes in. This helps many women.

2. take insulin. None of the oral therapies for diabetes are safe during pg, so insulin must be administered by injection. Woman must do frequent (3-4x/day) fingerstick blood sugar testing to make sure insulin levels stay in the normal range. Frequent adjustments in the dose of insulin may be necessary throughout the course of the pg.

D. Tests- screening test usually done ~28 wks for women with risk factors (family history of diabetes, previous large baby, previous stillbirth, excessive weight gain in pregnancy)

1. Glucose challenge test: Woman drinks a drink which contains 50 g of glucose. 1 hr later her blood is tested. By that time, normally her blood sugar levels should have gone up, stimulating the production of her own insulin, which moves the glucose out of the blood and stores it for future use. This causes blood sugar levels to decline. If blood sugar levels are still high after 1 hr, further testing will be done, and her diet may be altered. If diet alone is not enough to regulate blood sugar levels, she will probably have to take insulin.

2. Hemoglobin A1C test: This is a blood test that can determine if a woman's blood sugar levels have been stable for the previous 3-4 mos.

E. Surveillance of fetus as pregnancy approaches term to assess size of the fetus.

V. THIRD TRIMESTER BLEEDING
A. Placental abruption- sx is bleeding with cramps or severe pain. This condition is caused by the placenta detaching from the uterus too early, threatening the nutrient and O2 supply to the fetus. Mild abruption occurs occasionally, where most of the placenta stays in contact with the uterus and the fetus survives, but abruption is often extensive enough that the fetus' life is at risk. Tx is fast delivery of the baby (with cesarian section) to save the baby's life and minimize the amount of brain damage that may occur. Cocaine, chronic HTN, and pre-eclampsia all increase the risk of abruption.

B. Placenta previa- sx is painless bleeding. In this condition, the placenta is located on top if the cervix, so as soon as cervix begins to dilate (before or during early labor) the placenta starts to separate from the uterine wall, causing bleeding and reduction of O2 supply to the fetus. Dx is by US to determine the location of the placenta during the pg. Tx is to deliver the baby before the placenta, do this with a cesarean section.

VI. BREECH PRESENTATION
- the position of the baby in the uterus at the time of delivery is such that the head will come out LAST instead of first.

A. Types of breech

1. Frank breech- baby enters birth canal buttocks first (folded at hips, legs and head come out last). Least dangerous of all breech positions, buttocks can dilate cervix totally and stretch the vagina. Problem: head does not have enough time to mold, elongate to fit thru pelvis, may still be risk of head getting stuck (fetal head entrapment). Umbilical cord may cease to function before head delivered and baby can suffer from lack of O2.

2. Non-frank breech-

a. Buddha position (complete breech- sitting cross-legged)

b. 1 leg down, 1 leg up (footling breech).

c. Both legs down (double footling breech).

d. all of these positions dangerous since umbilical cord can be between baby's legs and circulation cut off.

e. Usually require immediate c-section.

B. Breech with twins: if 1st twin out was head first (vertex), then if 2nd twin is breech but not larger than 1st, twin #2 can be delivered breech. (Twin #1 has already done all the work of dilating cervix.)

C. Use semi-upside down position to encourage fetus to turn.

D. External version- at 36 - 37 wks, clinician puts hands on woman's belly and puts pressure on baby in the uterus, trying to turn the baby so the head is down. Done while monitoring the baby's heart rate to watch for cord problems. If a complication, baby is mature enough to deliver immediately /c c-section.

VII. TWINS (AND OTHER MULTIPLE GESTATIONS)
A. Higher risk than singleton pg, must nourish 2 babies (or more), is more metabolic work for the woman, there is higher weight gain.

1. High risk of preterm labor and premature delivery.

2. Recommend "couch potato" activity and freq. visits to clinician from 6th month on.

3. If there is only 1 placenta for all the babies (in case of identicals), there is:

a. Higher risk of miscarriage as 1 twin may get more blood flow than the other. Will do US to make sure twins are about equal in size and growth.

b. cord accidents occur more freq.
Twins /c separate sacs and placentas are at less risk.

4. Higher risk of IntraUterine Growth Retardation (IUGR)- not showing adequate growth, or growing asymmetrically (less abdominal growth than head or leg growth).

5. Higher freq of pre-eclampsia and gestational diabetes.

6. More risk of heavy blood loss and anemia in woman due to extreme distention of uterus at full-term. May need agressive use of medications to contract uterus after delivery (as uterus contracts, it causes a reduction in blood loss).

7. If twins not "lined up" correctly for delivery, may need cesarean section. Triplets and higher multiples are almost always delivered by cesarean section.

VIII. POSTDATES OR POST-TERM- 41 - 42 wks.
A. few clinicians willing to let pg go more than 2 wks overdue, due to increased risk of stillbirth, fetal distress (fetal bowel movement or meconium, baby can inhale meconium--> need respiratory therapy).

B. Interventions:

1. "Stripping" the fetal membranes: when done weekly starting at about 38 weeks, reduces the number of days to labor onset (from more than 12 down to 8).

2. Induction

a. prostaglandin gel (Prostin) placed into cervix 3X throughout the course of a day (relatively gentle).

b. pitocin via IV (synthetic oxytocin, sometimes less gentle).

CCASH - Division of Obstetrics

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http://www.clininfo.health.nsw.gov.au/hospolic/infoccah/032dmm18.htm - E9E1916. The use of Diagnostic Ultrasound in Obstetric Practice
First Trimester
Threatened Abortion
Recurrent Abortion
Clinical Suspicion of Ectopic Pregnancy
Pregnancy Following Ovarian Stimulation
Prior to Cervical Suture
Uterus Not Equal to Dates
Hyperemesis Gravidarium
Prior to Booking CVS or Amniocentesis
Very High Risk Pregnancy
Previous Fetal Abnormality
Second Trimester
Second Trimester Assessment
Previous Fetal Abnormality or High Risk of Fetal Abnormality
Antepartum Haemorrhage
Threatened Premature Labour
Suspected Premature Rupture of Membranes
Slow Growth of Uterus
Suspected Polyhydramnios
Third Trimester
Suspected Intrauterine Growth Retardation
Clinical Polyhydramnios
Previous IUGR or Stillbirth
Moderate/Severe Hypertension (Mean Diastolic Blood Pressure >100)
Diabetes and Renal Disease
Low-Lying Placenta on 18 week scan
Antepartum Haemorrhage
Malpresentation
Multiple Pregnancy

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16. The use of Diagnostic Ultrasound in Obstetric Practice
First Trimester
An ultrasound examination should not be used as a substitute pregnancy test.

Threatened Abortion
Scan at time of bleeding. If further bleeding thereafter, a repeat scan only if continuos wave Doppler examination (Sonicaid) does not detect fetal heart tones.

Recurrent Abortion
• (>2 previous spontaneous abortions)

• Scan at six (6) to ten (10) weeks.

• No repeat in the first trimester unless fetal heart tones not heard on Doppler examination.

Clinical Suspicion of Ectopic Pregnancy
• Including previous tubal surgery.

• PID or previous ectopic and pregnancy in association with an IUCD.

Pregnancy Following Ovarian Stimulation
• Pelvis mass (>3-4cm) in association with pregnancy.

Prior to Cervical Suture
• If not previously performed earlier in the pregnancy.

Uterus Not Equal to Dates
• Scan if discrepancy of four (4) weeks or more.

Hyperemesis Gravidarium
• Patients who require admission should have a scan performed (to exclude hydatidiform mole).

Prior to Booking CVS or Amniocentesis
Only if real doubt about gestational age or if there are geographical considerations.

Very High Risk Pregnancy
• Severe RH

• Diabetes

• previous IUGR

• Previous premature labour

• Scan if any doubt about gestational age.

Previous Fetal Abnormality
• Patients where accurate knowledge of gestational age is critical eg. Previous microcephaly or short limb dwarfism.

Second Trimester
Second Trimester Assessment
• While a policy of all patients having an ultrasound examination at 18 - 20 weeks is recognised for its clinical value undertaken by competent personnel, it is not considered mandatory and should be left to the discretion of the doctor after discussion with the patient.

• Elective examinations (eg. for confirmation of dates and exclusion of multiple pregnancy) are best performed at this stage.

• There should be an expectation that no more than 5% of patients will have a report of a low-lying placenta.

Previous Fetal Abnormality or High Risk of Fetal Abnormality
• Additional scan may be indicated depending on the specific anomaly to be excluded eg. hydrocephaly, congenital heart disease.

Antepartum Haemorrhage
• Scan if no previous second trimester examination or if more than four (4) weeks since "second trimester assessment".

Threatened Premature Labour
• Only if no previous "second trimester assessment" or if reasonable prospect of survival.

Suspected Premature Rupture of Membranes
• If clear evidence of PROM and if a normal fetus seen on a recent scan, a repeat ultrasound examination should be deferred until there is a reasonable prospect of survival.

Slow Growth of Uterus
Suspected Polyhydramnios
• Fundal height > 4cm above the mean for dates would be one criterion. (NB Lack of growth cannot be detected less than ten (10) days between ultrasound examinations).

Third Trimester
Suspected Intrauterine Growth Retardation
• eg. greater than 2cm below the mean for dates or no growth over two successive visits. (NB: Lack of growth cannot be detected unless less than ten (10) days between ultrasound examinations).

Clinical Polyhydramnios
• Fundal height > 4cm above the mean for dates.

Previous IUGR or Stillbirth
• Scan before time of previous problem or at six (6) weekly intervals.

Moderate/Severe Hypertension (Mean Diastolic Blood Pressure >100)
• Scan not indicated if hypertension/PET only mild.

Diabetes and Renal Disease
• Scan at six (6) weekly intervals.

Low-Lying Placenta on 18 week scan
• Repeat scan 32-34 weeks. This should be required in no more than one (1) in twenty (20) patients.

Antepartum Haemorrhage
• A repeat scan is indicated. If scan normal, there is little value in further ultrasound examination in the event of further bleeds.

Malpresentation
• After 36 weeks and only if vaginal delivery is planned.

Multiple Pregnancy
• Repeat scans at 25, 30 and 35 weeks.


CCASH - Division of Obstetrics

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http://www.clininfo.health.nsw.gov.au/hospolic/infoccah/032dmm24.htm - E9E2522. Management of Primary Post Partum Haemorrhage (PPH)
Management Outcome
Definition
Aetiology
Policy Statements
General Management of Primary PPH
Most Common Causes of Primary PPH
Management of Haemorrhage from the Placental Site
Prior to the delivery of the placenta - atonic uterus
Treat hypovolaemia (Haemacell/SPPS)
Primary Postpartum Haemorrhage - Traumatic
Aetiology
Signs and Symptoms
Management
Requirements
Bleeding Disorders

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22. Management of Primary Post Partum Haemorrhage (PPH)
Management Outcome
Blood loss has been minimised, shock treated and intravascular volume replacement initiated.

Definition
Bleeding in excess of six hundred (600) mls from the genital tract during and after the third stage of labour up until twenty four hours post partum.

Aetiology
1. Uterine atony

2. Trauma to the uterus, cervix and/or genital tract.

3. Coagulation disorders.

4. Uterine inversion.

Policy Statements
1. Patients predisposed to PPH and/or predisposed to adverse outcome(s) from blood loss of less than 600mls (eg. anaemia) must have intravenous fluids in progess (or venous access available) intrapartum.

2. A patient experiencing PPH must never be left unattended.

3. Visiting Medical Officer or Registrar Medical assistance must be sought immediately PPH is diagnosed.

4. While awaiting such assistance, the following procedures should be initiated.

(a) Venepuncture - collection of blood for Crossmatch.

(b) Cannulation - two appropriate sized wide bore cannulas should be inserted.

(c) Syntocinon Forty International Units (40IU) in one litre of Hartmann’s Solution commenced.

(d) Administration of a bolus dose of Intravenous Syntocinon Ten International Units (10 IU).

(e) Commencement of volume expanders (Haemacell/SPPS).

(f) Consider IM Syntometrine or Ergometrine if not contraindicated.

(g) Catheterise if indicated.

General Management of Primary PPH
1. Determine the cause (atonic, traumatic, coagulation disorder)

2. Manage the cause.

3. Monitor for shock - vital signs, colour, dyspnoea.

4. Treat shock:

(a) elevate the legs. Do not elevate the foot of the bed.

(b) Administer facial oxygen 8L per minute.

(c) Maintain warmth. Do not overheat.

(d) Reassure patient and support person(s).

ALERT

ESTIMATION OF BLOOD LOSS SHOULD BE CONTINUOUS AND PROGRESSIVE. WHERE POSSIBLE BLOOD AND BLOOD CLOTS SHOULD BE MEASURED. LOSS ONTO PADS AND BEDCLOTHES SHOULD BE ESTIMATED AND INCLUDED IN THE TOTAL BLOOD LOSS ESTIMATION.

Most Common Causes of Primary PPH
1. Atony of uterine muscle - eg.

(a) Prolonged labour

(b) Overdistended uterus

(c) Grande Multiparity

(d) Precipitate labour

(e) Maternal exhaustion

(f) Abnormalities of the uterus

(g) Analgesia (general or epidural anaesthetic)

(h) Full bladder

(i) Mismanagement of the third stage ie. "fiddling with the fundus"

(j) Pre-eclampsia

(k) Antepartum Haemorrhage

2. Partial separation of the placenta.

3. Retained placenta.

4. Retained placental fragments

5. Lacerated vessel(s).

6. Clotting defects.

Management of Haemorrhage from the Placental Site
Prior to the delivery of the placenta - atonic uterus
1. With the flat of the hand, massage the uterus to promote a contraction.

2. Administer appropriate Oxytocic.

(a) Intravenous Syntocinon 10 IU Bolus if venous access is either available or can be quickly provided.

AND/OR

(b) Intramuscular Syntometrine 5 Units or Ergometrine if venous access is not readily available and Ergot preparations are not contraindicated by maternal hypertension.

OR

(c) 10 IU Syntocinon IMI if venous access is not available and Syntometrine is contraindicated.

3. The bladder should be catheterised if indicated.

4. Provided the uterus is contracted, deliver the placenta by combined cord traction and support of the body of the uterus (ie. supra-pubic counter traction).

ALERT

THE UTERUS MUST BE WELL CONTRACTED THROUGHOUT THE PROCEDURE FOR POINT 4. TO AVOID INVERSION OF THE UTERUS.

5. If the uterus is contracted and Point 4 is unsuccessful (ie. the Placenta is retained) and heavy bleeding continues, prepare for immediate manual removal of placenta. This procedure may be carried out in Delivery Suite if the patient has an effective epidural or in Operating Theatres under general anaesthetic.

6. If Point 4 is successful (ie. the placenta is delivered)

(a) Maintain vigilant observation of blood loss, vital signs and uterine contraction.

(b) It may be necessary to "rub up" a contraction and express clots from the uterus.

(c) It may be necessary to repeat administration off appropriate oxytocic.

(d) It may be necessary to apply continuous fundal massage in order to maintain a contraction and stem the blood flow.

(e) Examine placenta and membranes for "completeness". If "incomplete", and bleeding is continuing, prepare for dilatation and curettage in operating theatres.

(f) If placenta and membranes are complete and bleeding is continuing Bi-manual compression may be required.

Commence Intravenous Syntocinon 40IU in a litre of Hartmann’s titrated to control bleeding.

Treat hypovolaemia (Haemacell/SPPS)
If bleeding continues despite the above procedures, prepare for:

1. Administration of Prostaglandin directly into the uterine muscle by the Medical Officer.

2. Transfer to Theatre for investigation under anaesthetic (and possible hysterectomy).

Primary Postpartum Haemorrhage - Traumatic
Aetiology
1. Trauma to the upper or lower uterine segment (ruptured uterus).

2. Trauma to the cervix, vaginal wall, the area surrounding the urethra or trauma to the perineal tissues.

Signs and Symptoms
1. A steady trickle or flow of bright blood rather than intermittent.

2. Unless the trauma involves extensive lower segment damage or upper segment rupture, the uterus is likely to be well contacted.

Management
1. Determine the location

(a) thorough examination of all visible trauma in a good light.

(b) Examination of cervix an vaginal walls and uterus.

Requirements
1. Adequate lighting

2. Stirrups

3. Medium and large Graves Speculum

4. Uterine packing gauze

5. Uterine packing forceps

6. Emergency instrument set.

Note If trauma is extensive or involves the uterus, the patient will require to be transferred to theatre for repair.

ALERT

CONTINUOUS LIGHT BLOOD LOSS MAY BE AS FATAL AS TORRENTIAL BLEEDING. CONTINUING BLOOD LOSS WHICH CONSTITUTES GREATER LOSS THAN NORMAL LOCHIAL LOSS MUST BE PROGRESSIVELY ASSESSED AS FOR HEAVY BLEEDING. ITS CAUSE ASCERTAINED AND MANAGED AS FOR HEAVY LOSS.

Bleeding Disorders
1. Administration of packed cells may be indicted if anaemia is present.

2. Observe clotting time of blood. If blood takes longer than six (6) to eight (8) minutes to clot, suspect hypofibrinoginaemia. Intravenous Infusion of fresh whole blood or fresh frozen plasma should be commenced if indicated.

3. Prepare for CVP and/or transfer to critical care.



CCASH - Division of Obstetrics

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http://www.clininfo.health.nsw.gov.au/hospolic/infoccah/032dmm26.htm - E9E2724. Guidelines for the Management of Rhesus Negative Patients
Preamble
Management
Interim Policy
Anti-D Immunoglobin Administration
Outcome
Policy Statements
Patient Information Sheet and Consultant Form
RH (D) Immunoglobulin (ANTI-D)
This Document to be retained with Patient Records

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24. Guidelines for the Management of Rhesus Negative Patients
Preamble
It a patient with a Rhesus negative blood group has a conceptus that is Rh positive, sensitisation of the mother can occur. Rhesus gammaglobulins cross the placenta into the fetal circulation and cause haemolysis of fetal red cells, anaemia and congestive cardiac failure (hydrops fetalis). The most likely time for sensitisation of the mother is during delivery. This will not affect the delivered child, but the antibodies can cause problems in a future pregnancy.

Management
Management of an Rh negative pregnant woman consists of the regular examination of maternal serum for Rh antibodies at booking and at 28-30 and 32-34 weeks gestation. Anti D gammaglobulin should also be administered at times when feto-maternal haemorrhage is likely eg.

• Abortion

• antepartum haemorrhage/threatened miscarriage.

• Amniocentesis.

• External cephalic version.

• Abdominal trauma.

• Within 72 hours of the delivery of an Rh positive child.

Anti D gammaglobulin will remain effective within the maternal circulation for up to six weeks after administration but this will vary with the size of any fetomaternal haemorrhage. The standard dose for Anti D is two (2) ampoules (=1.0 ml) but larger amounts may be necessary if a fetomaternal haemorrhage of > 12 ml has occurred. This can be quantified by a Kleihauer test but a simpler way is to perform a Coombs test for passively acquired Anti D 24-48 hours after its administration. If detectable then this is presumptive evidence of sufficiency to prevent maternal sensitisation.

A Coomb’s test for Anti D gammaglobulin in the maternal circulation is recommended when there may have been a large fetomaternal haemorrhage eg.

• Accidental Antepartum Haemorrhage.

• Delivery by Caesarean section.

• Manual removal of placenta.


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Compiled by Dr J. Palmer, Divisional Medical Manager AND

Anti-D Immunoglobin Administration
In response to a directive from The Royal Australian College of Obstetricians and Gynaecologists received on 23 March 1995, the following Interim Policy is to be adhered to from 23 March 1995.

As an interim measure, the RACOG recommends that the administration of Anti-D Immunoglobulin to Rhesus Negative women be limited to the following circumstances.

1. Use after delivery.

Rh D Negative women who have no Rhesus antibodies if the baby is RH D Postive. Dose requirements should be assessed on the basis of a Kleihauer count.

2. Miscarriage

3. Termination of pregnancy

4. Genetic studies where transplacental access is needed or puncture of fetal blood vessels is performed.

5. Trauma and APH on the basis of Kleihauer count.

It should be noted that the use of Anti-D immunoglobulin is currently used in a number of situations which are now not recommended.

1. External cephalic versions, unless indicated by a Kleihauer count.

2. Ectopic pregnancy.

3. Threatened miscarriage.

4. Prophylactic use of Anti-D during pregnancy.

Outcome
Anti-D will have been administered to pregnant and post partum women within the guidelines of The Royal Australian College of Obstetricians and Gynaecologists.

Policy Statements
1. All Rh negative women who deliver are to have a Kleihauer test one (1) hour after delivery.

2. All Rh negative women who are admitted with an antepartum haemorrhage or abdominal trauma are to have a Kleihauer test on admission.

3. Prior to administration of Anti-D, the Kleihauer result is to be obtained.

4. If Anti-D is required, the patient is to be given a Patient Information Sheet.

5. Prior to administration of Anti-D, a Medical Officer will explain the Patient Information Sheet.

6. If the patient refuses an Anti-D injection, that fact is to be recorded by the Medical Officer in the history and progress notes.

7. Dosage of Anti-D

(a) Antepartum Haemorrhage

or Abdominal Trauma

* Negative Kleihauer

* Positive Kleihauer
 No Anti-D

One (1) Ampoule Anti-D
(b) Post Delivery

* Negative Kleihauer

* Positive Kleihauer
 Positive Baby’s Blood Group

Positive Baby’s Blood Group
 One (1)Ampoule of Anti-D

Two (2) Ampoules of Anti-D

Interim Policy authorised by Dr J. Palmer, Divisional Medical Manager, Division of Obstetrics.

11 April 1995

Patient Information Sheet and Consultant Form
RH (D) Immunoglobulin (ANTI-D)
You have been advised to have an injection of Anti-D Immunoglobulin. Since Anti-D immunoglobulin was made available to Rh (D) Negative post partum women from 1970, there has been a 96% decrease in infant deaths from Rhesus Disease.

Anti-D is recommended to be given when there is a risk of blood group incompatibility causing problems for the baby in the current or future pregnancies.

It is, therefore, an essential preventive treatment for Rh (D) negative women who have had a Rh positive baby.

With all medical products prepared form human blood and plasma there is a possibility of the transmission of infectious diseases. This is controlled as far as possible by strict regulations on who can donate blood and testing of donated blood products. The manufacturing process of this product does not include a specific step to ensure viruses such as HIV, or Hepatitis A, B or C are inactivated, however there have been no recorded cases of transmission OF these diseases from this product and over 10 million doses have been administered overseas since 1968.


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Prelabour rupture of membranes (PROM)
Introduction:
        Types of PROM:
               PROM at term
               or pre-term PROM
Causes:
        Maternal:
               Infections
               Polyhydramnios
               Trauma / coitus
               Cervical incompetence
        Fetal:
               Multiple pregnancy
               Malpresentation
Complications:
        Cord prolapse
        Preterm labour
        Infections
Management:
        Depends on whether PROM at term or preterm
        Balance between maternal risk of infection & prematurity in baby.
        Admit all cases
        Check dates
        Take history
        Physical examination:
               General examination
               Abdominal examination (assess cause)
               Sterile speculum examination (to confirm PROM)
                       Visualise
                       Do high vaginal swab
                       Nitrate amnicator test
        Do FBC (exclude infection)
        Start pad chart
        Start fetal movement chart
        4 hourly parameters for mother
        Start empirical IV antibiotics until HVS culture negative
        AT TERM:
               In addition:
                       Continuous CTG
               Wait 24 hours for spontaneous labour (80%)
               Else, assess cervical score
               if favourable induction of labour done
        PRETERM PROM 34-37 WEEKS:
               No VE
               Monitor mother & fetus
               Wait > 24 hours for spontaneous labour
        PRETERM PROM < 34 WEEKS:
               No VE to be done.
               In the absence of infection,
                       give tocolytic for 48 hours
                       + IM dexamethasone 2 doses 12 hours apart
                       (for lung maturirty, weekly)
               Meanwhile continue to monitor mother & fetus
        AT ANY TIME BEFORE TERM OR 24 HOURS:
               Indications for delivery:
                       Infection
                       Fetal distress
                       Term & greater than 24 hours
               Do stimulation of labour, not IOL


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Special Risk Pregnancies


I. Introduction

Definition

(1) Elderly primiparous: A primipara aged ³ 35 years

(2) Teenage pregnancy: Usually defined as < 16 years old

(3) Grand multipara: ³ 5 viable deliveries

(4) Recent immigrant


II. Elderly Primiparous

A. Antenatal Complication

Maternal

(1) DM

(2) Antepartum haemorrhage

(3) HT in pregnancy

(4) Fibromyoma complicating pregnancy -> Malpresentation, IUGR, PPH

(5) Spontaneous abortion

1, 3 & 4 -> Age dependent
2 -> Placenta praevia, placenta abruption

Fetal

(1) &shy; Perinatal mortality (PNM)

(2) &shy; Chromosomal abnormality

eg. Down’s syndrome Age Risk

35 1 in 360

40 1 in 100

45 1 in 50


B. Intrapartum: Labour & Delivery

(1) Induction rate > 20% (Normally, in general population: 5-15%)

(2) Caesarean section (CS) rate > 40% (In general population: 15%)

Maybe due to &shy; concern

(3) Instrumental delivery rate: Unchanged

(4) NOT at &shy; risk of preterm delivery

(5) Uterine dysfunction

(6) &shy; fetal distress

(7) &shy; puerperal psychosis & difficulty in lactation


III. Teenage Pregnancy

A. Introduction

(1) More in under-developed countries, black > White & &shy; numbers in HK

(2) USA: 1in 5 pregnancies < 18 years old

(3) Most pregnancies are terminated

(4) 43% No contraception: ie. Unplanned

35% Wanted

4% Unwanted

61% Mixed feeling


B. Complication

Medical

(1) Anaemia: Iron or Folate deficiency or Both

(2) Gestational HT

(3) Preterm delivery -> Prematurity (Important cause of PNMR)

(4) Low birth weight: IUGR / Constitutionally small

a. Irregular cycle -> LMP NOT sure -> IUGR or Constitutional small ?

(5) Small bony pelvis: But NO &shy; incidence of cephalopelvic disproportion (CPD) or CS

(6) High perinatal mortality

(7) STD: Syphilis, Gonorrhea, Herpes. Chlamydia, HIV

Therefore, we must screen for STD in all these young girls

(8) Late booking: Main reason for complications

It may be due to

Denial
Irregular cycle -> Not aware of amenorrhoea
Poor sexual knowledge
Doctor unaware
(9) Sudden infant death syndrome

(10) Child abuse


Psycho-social

Usually come from broken family with parents divorced or working whole day
Poor school attendance pr performance
Financially tight
Ambivalent about pregnancy
Rejected by parents
Boyfriends run away
Humiliation from peers / neighbours
Irregular attendance to antenatal visit
Smoking or Alcoholism or even Drug abuse
Long term psychological sequelae especially when baby is given for adoption
Counseling before discharge
Contraception

A group of patient who are socially deprived, diet deficiency
More related to psychosocial problem rather than age itself
3 U
- Unmarried

- Unsupported

- Unemployed


In summary, the complications are related to

1. Their marital status

2. Timing of antenatal status

3. Socioeconomic status

Nutritional state
Smoking
Drinking
Drug abuse

C. Management

(1) Counseling before discharge

a. Work / School

b. Contraception

Say `NO’
Oral contraceptive pills: Compliance?, No protection to STD
IUCD: NOT good because of possible infection
Depo-Provera may have irregular bleeding
Condoms
Rhythm
Coitus interruption: NOT safe
Post-coital contraception

Even the patients have employed hormonal contraceptive methods, use of condoms are also encouraged because of the risk of STD

c. Danger of promiscuity: Cervical cancer, Venereal disease, HIV


IV. Grand Multipara

A. Antepartum Complication

Anaemia: mother without enough time to recover from previous pregnancies, iron or folate or both deficiency
Antepartum haemorrhage
HT: age related
Multiple gestation
Malpresentation: laxity of abdominal, uterus lax, Disorientated uterine axis -> high chance of unstable lie, oblique lie
Macrosomia?:&shy; Number of pregnancy -> &shy; baby size
Physical & mental stress on repeated child bearing
False sense of severity both in the doctors & patients eg. Late attendance & frequently defaulted
Poor socio-economical conditions eg. Poor, Overworked, Malnourished, Anaemia, Poor nutrition after successive pregnancies
&shy; Congenital abnormality: because of &shy; age

B. Intrapartum: Labour & Delivery

(1) Dystocia

It is due to

Repeated damage of uterine muscle -> fibrosis
Fat deposit

(2) Obstructed labour

It is because

Malpresentation
CPD related to &shy; baby size, &shy; lumbar lordosis, &shy; angle of inclination of uterus

(3) Uterine rupture: Even the presenting part NOT descent, Cervix may continue to dilate.

It is because &shy; number of pregnancy, &shy; risk of obstructed labour. Uterus contracts stronger & stronger -> May cause Fetal death or Constrict ring in uterus & Rupture

Rupture is treated by suture or hysterectomy


(4) Cord prolapse: &shy; chance in Malpresentation

(5) Precipitating labour: Trauma to fetus eg. Intra-cranial haemorrhage


(6) Post-partum haemorrhage (PPH)

It is related to

a. Big baby -> Uterus Over-distention + _ Uterine atony

b. Uterine degeneration & fatty change +

c. Placental adhesion

Syntocinon is contra-indicated


(7)&shy; Maternal & Perinatal mortality with &shy; parity

Advise contraception before discharge


V. Recent Immigrants eg. China, Vietnam

There are several points to note

Different disease patterns eg. TB, Worm infestation (In one study, nearly all of those with anemia have infestation), STD
Socioeconomic status: Lack of social support, Language problem, Financial status
Previous uterine surgery eg.
In China, Classical CS
Cornual implantation: for reversal of tubal ligation, may &shy; risk of placental adhesion -> PPH
&shy; TOP -> &shy; chance of placental adhesion


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GYNECOLOGIC PATHOLOGY- OVARY

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I. OVARY: HISTOLOGY
II. OVARY: NON-NEOPLASTIC AND FUNCTIONAL CYSTS
III. OVARY: POLYCYSTIC OVARIAN DISEASE (PCOD)
IV. OVARY: STEIN-LEVENTHAL SYNDROME
V. OVARY: STROMAL HYPERTHECOSIS
VI. OVARY: NEOPLASMS
VII. OVARY: CANCER
VIII. OVARY: TUMORS
IX. OVARY: MATURE CYSTIC TERATOMA
X. OVARY: IMMATURE MALIGNANT TERATOMA
XI. OVARY: MONODERMAL TERATOMA
XII. OVARY: DYSGERMINOMA
XIII. OVARY: ENDODERMAL SINUS TUMOR (YOLK SAC TUMOR)
XIV. OVARY: CHORIOCARCINOMA
XV. OVARY: EMBRYONAL CARCINOMA
XVI. OVARY: POLYEMBRYOMA
XVII. OVARY: SEX CORD- STROMAL TUMORS
XVIII. OVARY: GRANULOSA-THECA CELL TUMORS
XIX. OVARY: THECA-FIBROMAS
XX. OVARY: SERTOLI-LEYDIG CELL TUMORS
XXI. OVARY: HILUS CELL TUMOR
XXII. OVARY: PREGNANCY LUTEOMA
XXIII. OVARY: GONADOBLASTOMA
XXIV. OVARY: METASTASIS



I. OVARY: HISTOLOGY
Average 4 cm during reproductive life
Cortex- spindled stroma which contains follicles at different stages of maturation
Medulla--loose stroma with hilus cells-steroid producing
Follicle
Theca and granulosa cells
Graafian follicle
Corpus luteum
Corpus albicans
II. OVARY: NON-NEOPLASTIC AND FUNCTIONAL CYSTS
Cystic Follicle- physiologic, up to 2 cm
Follicular Cyst
Usually greater than 2 cm
May cause pelvic pain
Lined by granulosa cells
Luteinized theca may be estrogenic with associated endometrial abnormalities
Luteal Cyst
Normal
Lined by luteinized granulosa cells
May rupture and cause peritoneal reaction
Back to Top

III. OVARY: POLYCYSTIC OVARIAN DISEASE (PCOD)
Histopathology
Gray white large ovaries(twice normal)
Numerous subcortical follicular cysts(0.5-1.5 cm)with follicular hyperthecosis
Thickened white superficial cortex
Corpora lutea are frequently absent
Pathogenesis
Ovarian and hormonal changes are due to the unbalanced or asynchronous release of LH by the pituitary owing to disruption of hypothalamic control of pituitary secretion
Hyperprolactinemia may be the cause in 25% of cases
Treatment- regulation of menstrual cycle or induction of ovulation
IV. OVARY: STEIN-LEVENTHAL SYNDROME
The Clinical Syndrome Associated with PCOD
Oligomenorrhea
Persistent Anovulation
Obesity (40%)
Hirsutism (50%)
Virilism (rare)
V. OVARY: STROMAL HYPERTHECOSIS
Usually seen in post-menopausal women
Uniform enlargement of ovaries, bilateral - up to 7 cm
White, tan cut surface
Hypercellular stroma with luteinization of stromal cells
Similar clinical presentation and effects on endometrium as PCOD; however, virilization may be striking
Back to Top

VI. OVARY: NEOPLASMS
Common
80% are benign and usually occur between 25 and 45 years of age
May be asynptomatic and incidental findings
20% are malignant and usually occur between 40 and 65 years of age
Usually non-functional and produce mild symptoms - often present at a late stage
Symptoms- abdominal pain, distension, urinary of GI symptoms, vaginal or abdominal bleeding
VII. OVARY: CANCER
Relative Incidence of Cancer: endometrium>cervix>ovary
Ovarian cancer--6% of cancers in women (exclude skin)
Cause of up to 50% of cancer deaths of the FGT--usually discovered late
Risk Factors
Nulliparity
Family history
Gonadal dysgenesis
Genetic and Candidate Host Genes
BRCA1--associated with breast cancer-chr 17q21
30% of ovarian carcinomas express high levels of HER-2/neu oncogene--poor prognosis
Mutations in p53-suppressor gene seen in 50% of ovarian carcinomas
Back to Top

VIII. OVARY: TUMORS
Classification- based on most probable tissue of origin
Ovarian surface coelomic epithelium-the source of mullerian epithelium
Germ cells
Stroma and sex cords
Metastatic- common site for metastases
Surface Epithelial Tumors
65-70% of ovarian cancer
20+ years
Types: serous, mucinous, endometrioid, clear cell, brenner
Benign/borderline/malignant
Prognosis depends on grade (degree of differentiation) and stage (extent of spread)
Ascites, peritoneal spread (implants)
50% of carcinomas have metastases to contralateral ovary
Cystadenofibroma
Benign
Pronounced fibrous stroma associated with epithelium
Brenner Tumor
Adenofibroma in which the epithelial component is transitional epithelium, sometimes with mucinous glands in the center
Associated with mucinous cystadenomas
90% are unilateral
Benign/borderline/malignant
Serous Papillary Tumors
Resembles tubal epithelium
Most common malignant ovarian tumor
Bilaterality common-up to 65%
Mucinous Tumors
25% of ovarian tumors, 10% of ovarian cancers
15% are malignant
Up to 20% are bilateral
Resembles endocervical or intestinal (goblet cells) epithelium
May be associated with pseudomyxoma peritonei--collection of extensive mucinous material resembling cystic contents within the peritoneal cavity
Endometrioid Tumors
Most are carcinomas
20% of all ovarian cancers
15-30% are associated with carcinoma of the endometrium-synchronous primaries
15% coexist with endometriosis
Clear Cell Adenocarcinoma
Aggressive tumor with spread beyond the ovary
May be associated with endometriosis ore endometrioid carcinoma
Histology- sheets, tubules, papillae of cells with clear cytoplasm, high grade nuclei and hobnail nuclei (protrude into lumen of gland)
Germ Cell Tumors
15-20% of all ovarian tumors--most are benign cystic teratomas
Classification
Dysgerminoma- no differentiation
Embryonal carcinoma- poorly differentiated
Extraembryonic tissue- endodermal sinus tumor (yolk sac)
Trophoblast- choriocarcinoma
Embryonic tissue- teratoma
Back to Top

IX. OVARY: MATURE CYSTIC TERATOMA
Cystic, mostly mature (adult)
Predominantly ectodermal differentiation (skin, brain)
Young women
15% are bilateral
1% undergo malignant transformation, most commonly squamous cell carcinoma, less commonly thyroid carcinoma and melanoma
X. OVARY: IMMATURE MALIGNANT TERATOMA
Solid, component tissues resemble that of the fetus or embryo
Prepubertal adolescents and young women, mean age 18
Grade based on proportion of immature tissue-predictive of extraovarian spread
Most recurrences occur within two years
XI. OVARY: MONODERMAL TERATOMA
Rare, Unilateral
Struma Ovarii- mature thyroid tissue, may be hyperfunctional
Carcinoid
Neuroendocrine tumor, less than 2% are malignant
Histology- nests and cords of small, bland, round to oval cells with coarsely granular chromatin ("salt and pepper")
May be functional- carcinoid syndrome
If bilateral, probably metastatic intestinal carcinoid
Back to Top

XII. OVARY: DYSGERMINOMA
Counterpart of seminoma in testis
2% of all ovarian cancers and 50% of malignant germ cell tumors
75% occur in second and third decades
80-90% are unilateral
Gross--solid, fleshy
Histology--sheets and cords of large vesicular cells with clear cytoplasm and well defined borders
Admixed lymphocytes, granulomas and syncytiotrophoblasts
Radiosensitive with good prognosis
XIII. OVARY: ENDODERMAL SINUS TUMOR (YOLK SAC TUMOR)
Rare, but second most common germ cell malignancy
Children, young women with pain and rapidly enlarging pelvic mass
Histology
Schiller-Duval body--glomerulus-like structure composed of a central blood vessel enveloped by germ cells within a space lined by germ cells
Hyaline droplets--positive for alpha-fetal protein
XIV. OVARY: CHORIOCARCINOMA
Pure forms are rare, usually mixed with other germ cell tumors
Metastasize widely to lungs, liver, bone, other viscera
Histology-avillous atypical cyto and syncytotrophoblast
Elevated HCG
Unresponsive to chemotherapy and highly fatal
Back to Top

XV. OVARY: EMBRYONAL CARCINOMA
Highly malignant tumor of primitive embryonal elements
XVI. OVARY: POLYEMBRYOMA
Malignant Tumor Containing Embrioid Bodies
XVII. OVARY: SEX CORD- STROMAL TUMORS
Granulosa-Theca Cell Tumors
Thecoma-Fibroma
Sertoli-Leydig Cell Tumors
Hilus Cell Tumors
Pregnancy Luteoma
Gonadoblastoma
XVIII. OVARY: GRANULOSA- THECA CELL TUMORS
5% of ovarian tumors
Two-thirds in postmenopausal women
Unilateral
Histology- cell-exner bodies-small gland-like structure mimicking immature follicles
May be estrogenic, occasionally androgenic
10-15% of functional tumors develop endometrial carcinoma
Indolent course, late recurrences
Back to Top

XIX. OVARY: THECA- FIBROMAS
4% of ovarian tumors
Unilateral, solid
Histology- fibroblasts and plump spindle cells with lipid droplets (theca)
Meigs' syndrome- ascites, right sided ovarian tumor
Association with the basal cell nevus syndrome
Fibrosarcomas are rare
XX. OVARY: SERTOLI-LETDIG CELL TUMORS
Recapitulate the cells of the testis
Commonly androgenic, rarely estrogenic
Second and third decades
Histology-tubules and eosinophilic leydig cells with varying degress of differentiation
<5% recurrences or metastases
XXI. OVARY: HILUS CELL TUMOR
Unilateral
Androgenic
Benign
Histology- large lipid laden cells with distinct borders
Reinke crystalloids (leydig cells) may be seen
XXII. OVARY: PREGNANCY LUTEOMA
Resembles corpus luteum and may be virilizing
Back to Top

XXIII. OVARY: GONADOBLASTOMA
Uncommon
Germ cells + sex cord-stroma
Abnormal sexual development
50% have coexistant dysgerminoma
Excellent Prognosis
XXIV. OVARY: METASTASIS
Usually Mullerian
Breast
Stomach
Bilary tract
Pancreas
Krukenberg's Tumor- bilateral metastases composed of mucin-producing signet-ring cancer cells, most often of gastric origin




GYNECOLOGIC PATHOLOGY- FALLOPIAN TUBE

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I. FALLOPIAN TUBE: HISTOLOGY
II. FALLOPIAN TUBE: NON-NEOPLASTIC
III. FALLOPIAN TUBE: PELVIC INFLAMMATORY DISEASE (PID)
IV. FALLOPIAN TUBE: TUMORS


I. FALLOPIAN TUBEL HISTOLOGY
Mucosa has numerous delicate folds (plicae)
Three Epithelial Cell Types
Ciliated columnar cell
Non-ciliated secretory columnar cell
Intercalated cell
Smooth Muscle Wall
II. FALLOPIAN TUBE: NON-NEOPLASTIC
Suppurative Salpingitis (part of pelvic inflammatory disease) Endometriosis
Tuberculous Salpingitis- uncommon in US, associated with infertility
Cysts
Paratubal cysts--0.1 to 2 cm translucent cysts filled with serous fluid
Hydatids of morgagni--large cysts found near fimbriated end or broad ligament
III. FALLOPIAN TUBE: PELVIC INFLAMMATORY DISEASE (PID)
Symptoms- pain, adnexal tenderness, fever, vaginal discharge
Pathology- acute salpingitis, salpingo-oophoritis,tubo ovarian abscesses, pyosalpinx
Infectious Etiologies
Gonorrhea (gram negative diplococci) > Chlamydia-ascending infection resulting in pelvic inflammatory disease (PID) a major cause of infertility
Puerperal infections-usually polymicrobial-staph,strep, coliforms, Clostridium perfringens-spread via lymphatics or venous channels
Complications
Peritonitis
Intestinal obstruction secondary to adhesions
Infertility
Treatment- antibiotics or surgery if there is little improvement
Back to Top

IV. FALLOPIAN TUBE: TUMORS
Uncommon
Adenomatoid Tumor (mesothelioma)- benign
Adenocarcinoma, serous papillary type
Poor prognosis
Bulk of tumor must be involving tube to distinguish from ovarian or endometrial primary

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Pelvic Inflammatory Disease (PID)

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WHAT IS PELVIC INFLAMMATORY DISEASE?

Pelvic inflammatory disease (PID) is an infection of the upper part of the female reproductive organs, especially the tubes "(salpingitis)". It is a result of sexually transmitted diseases (STDs) such as gonorrhea and chlamydia. These germs first infect the cervix but then go up to infect the uterus and tubes. Other bacteria from the vagina can then follow and make the infection worse. Sometimes PID is a complication of surgery to the uterus (such as an abortion) or the presence of an intrauterine device (IUD).


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WHO CAN GET PID?

Any woman who is sexually active may get PID. However, most cases are seen in women who are between the ages of 15 and 25.


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WHAT ARE THE SYMPTOMS OF PID?

This infection causes lower abdominal (pelvic) pain and pain during sex. It can also cause bleeding between periods or after sex. There is sometimes a yellow or greenish vaginal discharge that may have a foul odor. If the infection is severe, it also causes fever, chills, nausea and vomiting.


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WHAT ELSE CAN HAPPEN AS A RESULT OF PID?

Infections that are not treated or not completely treated can damage the tubes. The damage can block the tubes, making the woman unable to have babies in the future. It can also cause long-term pain. Some severe infections cause abscesses (pus pockets) on the ovaries. It may require surgery to drain the pus or to remove the organs.


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CAN A WOMAN GET PID MORE THAN ONCE?

Yes. Women may get PID after each STD. The more infections a woman gets, the higher her risk of not being able to have babies and/or having chronic pain.


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WHAT IS THE TREATMENT FOR PID?

If the infection is not too severe, antibiotics by mouth and by an injection (shot) can be given. However, if there is no relief within 48 hours, then the woman needs to go to a hospital to receive medicine by vein. Since most cases of PID are caused by STDs, the woman should avoid having sex while being treated. The partner should also be checked and treated for STD. If the partner is not treated, the woman may get PID again, especially if condoms are not used while having sex.


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WHAT SHOULD I DO IF I HAVE SYMPTOMS OF PID?

You should get medical care immediately. PID is a serious disease that requires immediate care. Furthermore, other serious conditions need to be ruled out. You should avoid having sex while you have symptoms since most cases of PID are caused by STDs.


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WHAT CAN BE DONE TO PREVENT PID?

Preventing STDs is the most important way to protect against PID. You should avoid sex with infected partners, and use protection like condoms every time you have sex. Try to limit your exposure to STDs. Unprotected sexual activity increases you chance of exposure and infection. If you have more than one partner or your partner has other sexual partners this may increase your chances of getting an STD if you think you may have come in contact with or may be infected with an STD, you should visit a local STD clinic, Family Planning clinic, hospital or doctor to get tested and treated before PID occurs. Your sex partner(s) also should get tested and treated.


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Physiology of the Menstral Cycle
I. Overview
A. Major glands/organs: hypothalamus, anterior pituitary, ovary, uterus (draw on board).

B. Hormone- a substance made in 1 place that works (or has an effect) in another place. travels through blood.

(write on board)


GnRH- gonadotropin releasing hormone

FSH- follicle stimulating hormone

LH- luteinizing hormone

estrogen

progesterone

testosterone

HCG (human chorionic gonadotropin)

C. "Ideal" cycle length is 28 days, range is 20-36 days, typically 26-32

D. Only 10% of women have 28 day cycle

E. Typical flow 2-7 days with wide var. in duration, amt of flow, pattern of flow

F. Normal to have variation in length of cycle at diff times of life

G. Pheromones- synchronicity of cycles in women living together, also dominance effect(?)

H. Convention to count 1st day of bleeding as day 1 in menstrual cycle (emphasize)

II. Phases (point of view of ovary)
A. Follicular phase

1. hypothalamus secretes GnRH (1x/hr to 1x/1.5 hr)-->ant. pit.

2. ant. pit. secretes FSH & LH-->ovary.

3. ovary- FSH stimulates follicles to begin to develop. Born c/ all follicles present (over 400,000), only about 500 will actually mature

4. developing follicle secretes estrogen- causes:

a. follicle to continue to develop

b. increased # of FSH receptors

c. neg. feedback to GnRH

d. neg. feedback to FSH

e. pos. feedback to LH

(NOTE: negative feedback means to turn down production, positive feedback means to increase production.)

5. 1 follicle becomes dom. (FSH levels drop, but # recept. increases), but in fraternal twins, 2 follicles become dominant.

B. Ovulation- release of egg from follicle-->corpus luteum

1. estrogen peaks 1-1.5 days before ovulation

2. ovulation is a response to LH surge and maybe prostaglandins (infert. patients advised no ibuprofen)

3. corpus luteum-->progesterone ("for life")-->thermogenic-->bbt record (draw on board)

4. progesterone neg. feedback to LH, neg. feedback to GnRH.

5. regressing follicles-->testosterone-->further regression, increase libido

6. mittelschmerz- pain of ovulation in some women

7. egg-->fimbria, moved along by cilia and motility of tube itself.

8. egg viable ~36 hrs, sperm viable ~ 3-5 days, therefore preg. can occur from 5 days prior to ~ 1.5-2 days after ovulation.

C. Luteal phase- consistently the last 14 days of the cycle (life of corpus luteum)

1. corpus luteum- left over follicle, yellow ("yellow body")

2. produces lots of progesterone as well as estrogen and testosterone

3. progesterone suppresses growth of new follicles (ovulate from alternate ovaries)

4. corpus luteum degenerates-->corpus albicans, white ("white body") if not preg.-->levels of progesterone and estrogen fall -->menstruation

5. if preg.-->devel. embryo produces HCG- human chorionic gonadotropin--> maintains corpus luteum-->keeps producing progesterone-->keep uterus quiescent & maintain preg.

III. Phases (point of view of uterus and cervix)
A. Proliferative phase (= follicular phase in ovary)- endometrium thickens, glands and blood vessels grow in response to estrogen. In cervix, estrogen causes cervical mucus to become thinner, clearer & stretchier, more of it (to facilitate passage of sperm)--> spinnbarkeit, ferning. Cervix may feel softer and more open

B. Ovulation-

C. Secretory phase (= luteal phase in ovary)- glands and blood supply mature, ready to secrete glycogen--> nutritive for egg. Maintained by progesterone. Increasing levels of progesterone cause cervical mucus to become sticky, thick, less and less is produced.

D. Menstruation (if no fert.)- progesterone and estrogen levels fall, causing blood vessels to constrict--> glands to lose blood supply and begin to be shed, etc., until whole lining is shed. Menstrual flow is some tissue and blood. Cramps result from lack of progesterone and presence of prostaglandins secreted in uterus. Warmth, relaxation techniues, exercises.

IV. Hypothalamus-pituitary-ovary axis
A. As progesterone and estrogen levels fall, GnRH secretion by hypothalamus increases (GnRH inhibited by progesterone and estrogen)

B. Ant. pit. starts producing FSH & LH as response to GnRH

C. FSH causes ovary to start to produce estrogen

D. estrogen turns down (inhibits) production of GnRH

E. hypothalamus is affected by starvation, stress, illness, travel, etc. so all these things can affect menstrual cycle

V. Onset of puberty- requires mature h-p-o--> increasing sensitivity to hormones, esp. estrogen which promotes maturation of 2o sex. char.
A. Stages

1. breasts

2. pubic hair

3. axillary hair

4. growth spurt a. last ~ 1.5 years, self-limited due to closure of long bones in response to estrogen

5. menses

a. usu. c/in 2.5 yrs of breast devel

b. critical body wt ~ 100 lbs d. minimal body fat ~ 16-20 %

c. younger ages- nutrition? faster to critical body wt?

VI. Toxic Shock Syndrome - affects men and non-menstruating women as well as menstruating women.
A. Caused by a new (since ~1975) Staphylococcus aureus strain, is resistant to penicillin and related antibx. grows 100 - 2500x faster than normal Staph.

1. Bacteria colonize and begin to grow on a mucosal area (e.g. the vagina).

2. Bacteria secrete toxins, toxins enter bloodstream.

3. First time you are exposed to the toxin, have a mild flu-like disease, which sensitizes you to the toxin.

4. Recover. Bacteria still present.

5. after 2nd or 3rd exposure to the toxin, your own immune system goes into an "autodestruct" mode. Toxic Shock Syndrome Toxin-1 is a "superantigen."

B. Menstrual cycle is "ideal vehicle" for this mechanism.

1. The sensitizing exposure occurs during one menstrual peroid, after which the patient recovers but the bacteria still remain in the vagina.

2. Then during the next or the next menstral period, the bacterial population skyrockets and a huge amount of toxin is produced, causing the immune system to self-destruct.

C. Highest incidences of TSS:

1. in U.S.: occur in people of Scandinavian and German extraction.

2. worldwide: in Sweden, Denmark and Germany.

3. presumably some genetic susceptibility to staph infections in these populations.

D. Symptoms of disease

1. high fever (102+).

2. a scarlet fever-like rash on chest and neck.

3. peeling skin on palms of hands and soles of feet.

4. radically lowered blood pressure.

5. at least 3 of the following:

a. diarrhea and vomiting.

b. muscle aches.

c. vaginal or throat infection.

d. kidney malfunction.

e. liver failure.

f. disorientation or confusion.

6. There are milder, more flu-like forms of the disease.

E. Prevention

1. change tampons frequently (every 3 - 4 hours). Do not leave a tampon in the vagina for more than 8 hours.

2. use the lowest absorbancy tampon you can, or use pads, clothes, etc., OR use both a low absorbancy tampon and a pad.

3. be aware of the symptoms and get medical attention ASAP if you develop them.


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Cancer
I. Vocabulary
benign tumor (benign neoplasm)- remains confined to its original location, neither invades surrounding tissue nor spreads to other body sites.
malignant tumor (malignant neoplasm)- capable of both invading surrounding tissue and spreading to other body sites. Cancer.
metastasize- spread throughout the body.
dysplasia- precancerous changes, but not yet cancer.
metaplasia- growing.
carcinoma- 90% of cancers, cancer of the epithelial cells that cover the surface of the body and line the internal organs.
sarcoma- rare, solid cancers of connective tissue (bone and muscle).
leukemia- cancer of the blood. Together with lymphoma, account for about 8% of cancers.
lymphoma- cancer of the lymph.
grade- how bad the cells and cellular architecture look, (grades 1, 2 and 3, higher is worse).
stage- how far the cancer has already spread (I, II, III and IV, higher is worse, meaning the cancer has spread further).
carcinoma in situ- small tumor that has not yet invaded adjacent tissue.
II. WHAT IS CANCER?
A. Abnormal, uncontrolled or unregulated cell proliferation. It is a disease at the level of the cell. If unchecked, cancer cells will invade surrounding tissue, enter the circulatory or lymphatic system, and spread to other parts of the body, where they can interfere with the function of normal cells, and eventually lead to death.

B. Cancer is the 2nd most common killer of people in the U.S., killing about 1 in every 4. Heart disease kills about 1 in every 3 Americans, AIDS, accidents and murder each account for about 5% of deaths in this country.

C. Caused by multiple genetic alterations in a cell. May take many years to accumulate the alterations that are necessary for a cell to become cancer (that's why chances of developing cancer increase with age). A little bit about the genetics of breast cancer: several genes seem to be involved: BRCA (BReast CAncer) 1, 2 and 3, p53, HER-2/neu. Focus on BRCA1.

Normal BRCA1 gene thought to carry instructions for making a protein that suppresses tumor growth.
More than 60 different mutations found so far for this gene--> less functional, or maybe no protein at all--> tumor growth.
Presence of a mutated form of this gene is a strong predictor of breast cancer and ovarian cancer. A mutated form of BRCA1 now thought to be present in most women /c breast cancer, whether they have a family history or not.
Commercial tests for BRCA1 now available. May be offered to all women /c a suggestive family history if they meet criteria:
family history of breast, ovarian or other cancers.
tumor specimens from affected family members must be available for study.
must participate in genetic counseling program.
must have financial resources to pay cost of test ($670 for 1st family member, $250 for each subsequent family member).
test is 85 - 90% effective in detecting mutations.)
Specific BRCA1 mutation may be a freq cause of breast cancer in women /c Ashkenazi Jewish ancestry (~1% of U.S. women of this ethnicity, if have this particular mutation these women have 80 - 90% chance of breast cancer and a 40 - 50% chance of ovarian cancer). Follow-up studies on Ashkenazi Jewish populations being set up in Washington DC and on Long Island.
D. Cure: cancer cells are our own cells "turned against us." Therefore it is difficult to develop a cure that would only affect cancer cells, not our own normal cells. Current work is to discover how normal cell growth and division is regulated, try to use that information to design new treatment strategies.

E. Changes in cancer rates over time: lung, uterus, stomach.

F. Early screening- example: The Pap smear/pelvic exam (the "annual")- exam that looks for infection, abnormal cells, or cancer. Partially consists of Pap smear specimen (using Pap stick and/or the cervical brush) taken from cervix and inside the cervical canal. Specimens are sent to lab for reading and evaluation. Pap smear results have a false negative rate of 15%! This is why many clinicians recommend all women have yearly Pap smears. Results can be grouped into several classes:

Pap class I- benign (assume everything is ok).

Pap class II- inflamed or atypical (anemia, infection, vitamin deficiency, genital warts).

Pap class III- mild (Cervical Intraepithelial Neoplasia I) cervical dysplasia (an abnormality in the pattern of growth in the epithelial layer, a precancerous condition) or moderate (CIN II) cervical dysplasia.

Pap class IV- severe (CIN III) cervical dysplasia or cervical carcinoma in situ (cancer, localized, has not spread).

Pap class V- very suggestive of invasive cervical cancer (invading other nearby tissues).)

In 1992 only 63% of women between the ages of 50 and 64 had a Pap smear in the previous 3 years, and only 35% of women over the age of 50 had annual mammograms.

G. Development of cancer: multistep process. (colorectal cancer example)

Start with a single proliferative cell.
Increased proliferation of cells.
Eventually gives rise to a small benign tumor (adenoma).
Many rounds of selection for increased cell growth leads to larger and larger adenomas.
Malignant cells develop from the benign tumor cells.
Invasion of surrounding tissue.
Metastasis to other body sites.
H. Grade and stage: used to describe different the cancer cells are from normal cells, and how far the cancer has spread. grade- how bad the cells and cellular architecture look, (grades 1, 2 and 3, higher is worse). stage- how far the cancer has already spread (I, II, III and IV, higher is worse, meaning the cancer has spread further). Important to know if cancer has spread, so will assess tumor size and will look at lymph nodes in surrounding area for presence of cancer cells.

III. TREATMENTS-
treat both locally and systemically (to destroy any malignant cells that may have escaped and spread to other parts of body. Surgery, radiation, chemotherapy, hormonal therapy.

A. Surgery- (local) removes tumor and some normal tissue around it.

B. Radiation- (less local) designed to kill any cancer cells that were not removed by surgery, try to give it very locally, and try to avoid exposure of other organs.

C. Chemotherapy- (systematic) 4 commonly used drugs (1 is methotrexate), given in combinations of 2 or 3 drugs over 4 - 6 months. Side effects: nausea, vomiting, hair loss. Will give other drugs to reduce nausea and vomiting. Many insurance cos. cover cost of wig, hair always grows back after chemotherapy finished. Taxol- new drug esp. used in treating ovarian cancer, received lots of press, still in experimental stages of determining which drugs to combine it with, when and how long to use it.

D. Hormone therapy- (systematic) if it is a type of cancer that grows more in response to estrogen, will reduce levels of circulating estrogen.

in pre-menopausal women-->remove or radiate ovaries. Side effects: hot flashes, vaginal dryness, increased risk of osteoporosis, increased risk of heart disease (all are menopausal problems).
in postmenopausal women-->use tamoxifen (Nolvadex) to block estrogen. Side effects: hot flashes, prevents bone loss, reduces LDL (bad) cholesterol, increases HDL (good) cholesterol, increases risk of endometrial cancer so must have annual checks of endometrium.
E. Other approaches- (all currently experimental)

"Teach" or trick the immune system to attack tumor cells, disappointing early results, but as we learn more about cancer and the immune system, there is more optimism that this approach could be useful in treating some kinds of cancer.
Angiogenesis inhibitors: cancers must have blood to grow, so cause blood vessels to grow to supply themselves. These drugs would inhibit this process.
Remove some stem cells (which give rise to all types of blood cells) and culture them with growth factors to speed production of new cells. Then give massive doses of chemotherapy-->kills cancer cells and infection-fighting cells. Replace cultured stem cells into circulation. May increase 5 yr survival, but also carries 5 - 10% chance of dying from infection.
Gene therapy: transferring genes to correct a mutation or to enhance the cancer-fighting ability of cells. By the end of 1996, there had been 79 c linical trials of several of these approaches approved in the U.S., most still in the very earliest stages of testing.
G. Complementary approaches:

Support groups: breast cancer patients who participated in support groups during their treatments live longer than those who did not participate in support groups.
For the following, there is no evidence of extended survival, but they don't hurt, and are helpful supplements to conventional therapy.
relaxation.
biofeedback.
massage.
macrobiotic diet.
herbal remedies.
visualization.
Important to take care of self and be involved in treatment decisions as much as you want to be.
IV. Cervical Cancer (squamous intraepithelial lesion)-
A. regular screening (via Pap smear) of all women could prevent 90% of deaths from cervical cancer. Screening is responsible for reduction of mortality by 75% since 1940.

Advantages of Pap smear as an early detection tool:
safe, reliable, inexpensive, minimal discomfort.
very early stages of disease (dysplasia and in situ) can be detected reliably.
detection of very early stages makes treatment easier and almost 100% effective.
Suggestive Pap smear results often followed up with colposcopy- using a magnifying lens to look at suspicious areas on the cervix, often used with vinegar (acetic acid) which makes suspicious cells turn white (making them more obvious).
Risk factors:
sexual practices (having multiple sex partners) that increase the chance of HPV transmission.
age at first intercourse (connected with the size of the transition zone (T-zone).
the glandular, columnar cells of the inner cervix (the cells that line the cervical canal), are more exposed in young women.
the glandular, columnar cells of the inner cervix (the cells that line the cervical canal) seem to be more susceptible to infection /c HPV.
as women age, T-zone migrates towards the cervical canal, and thus shrinks.
younger women may be more at risk.
cigarette smoking.
symptoms of cervical cancer: cervix bleeds easily with intercourse or other jostling, can cause renal failure due to close proximity of ureters, leading to coma and death.
B. Treatments and 5 year survival rates: up to 60% of cases of mild dysplasia will regress spontaneously. Only 10-15% will progress to a more serious form, so we need to be cautious about overtreatment.

cryotherapy, Loop Electrosurgical Excision Procedure (LEEP), laser therapy, cone biopsy for early disease. LEEP and cone biopsy have the added advantage of providing tissue that can be used to evaluate the dysplasia or cancer further. Cryotherapy and laser therapy destroy the cells, thus making them unavailable for further evaluation. Cone biopsy (or conization)- remove dysplastic cells from cervix in a cone shaped piece of tissue. This technique has been replaced by cryosurgery, laser therapy, and LEEP.
radical hysterectomy- removal of uterus and other tissue (blood vessels, lymph nodes) for more advanced disease, tissue can be removed clear out to body wall or bone.
lymph nodes checked to see how far cancer has spread.
ovaries are usually not involved in cervical cancer.
radiation therapy for metastatic cervical cancer (when the cancer has already spread to distant locations) works well.
5 year survival rates:
in situ = ~100%, localized = 90%, regional spread = 50%, distant metastasis = <20%.
D. Post treatment follow-up is important, as can recur in small percentage of women.

E. 1996 report of efforts to develop a vaccine, still in very early stages of development.

V. Endometrial Cancer (Adenocarcinoma)
A. early detection:

Pap smears pick up endometrial problems only 15% of the time.
most common symptom is bleeding that has no pattern and does not respond to progesterone treatment (remember that endometrial hyperplasia is overgrowth of the endometrium, causing irregular bleeding, but can be treated with progesterone) or unexplained post- menopausal bleeding.
most common in women 55 - 70; women /c increased risk, or on unopposed ERT should have endometrial biopsies.
B. risk factors:

high estrogen exposure increases chances of uterine cancer, examples:
delayed menopause.
early menarche.
hypertension (HTN, high blood pressure).
diabetes.
obesity (estrogen production by fat cells).
positive family history.
high doses of unopposed estrogen replacement therapy (in the absence of progesterone). [Hormone replacement therapy (HRT), where woman takes estrogen and progesterone, not assoc. /c endometrial cancer. Progesterone has protective effect on endometrium.]
cigarette smoking.
C. Protective factors: low estrogen exposure decreases chances of uterine cancer, examples:

late menarche.
pregnancy.
birth control pills (low dose, contain progesterone as well as estrogen).

D. diagnosed by:

endometrial biopsy- like a mini-D & C (dilation and curettage).
hysteroscopy- uses an instrument with a scope and a light that is placed up through the cervix to look inside the uterus. Cancer looks fleshy, glandular, has blood vessels.
E. cancer of uterus usually doesn't spread because the uterus has a thick muscular wall that apparently helps contain the cancer.

F. Usually surgery alone is effective, usually don't need radiation therapy for early stages of disease.

G. 5 year survival rates: in situ and localized = 90 - 95%, regional spread ~ 65%, distant metastasis = can prolong survival in ~1/3 of patients, but not cure. Overall survival rate ~85%.

H. Post treatment surveillance is controversial.

VI. Ovarian Cancer
A. In 1996, estimates are that 26,700 women diagnosed with ovarian cancer, and that 14,400 of them will die from it. There is no good screening test for women at large, means this cancer is usually diagnosed late (after it is already very advanced and probably has already spread), which means long term survival is low. Most women (60-70%) are diagnosed at stage III or IV, 5 year survival rate is less than 40%. Usually affects women in their 50s and 60s.

B. risk factors: average risk, general pop. of women in U.S. = 1.4%.

family history of ovarian or breast cancer.
carrying a mutation of the BRCA1 gene (increases risk to between 10 and 40%)
never being pregnant, first pregnancy after 30
ovulating for more than a total of 40 years
risk is one third lower in African-American women, one study says that's because they are more likely to have at least 4 children and to have breastfed for a total of at least 6 months.

C. protective factors:

pregnancy (more pregnancies, less risk).
breastfeeding
birth control pills (as /c endometrial cancer).

D. symptoms are extremely vague (from common to rare)- abdominal swelling, abdominal pain, gas, indigestion, nausea, urinary frequency, weight change, diarrhea or constipation.

Normally, post-menopausal ovaries shrink until can no longer be felt on bimanual exam. If ovary can be felt on bimanual exam in a post-menopausal woman, it needs to be checked for cancer.
can use vaginal probe ultrasound to check for size of ovary, presence of tumor.
CA 125 is a tumor marker (blood test). It seems to be valuable for detecting a recurrence of the cancer (as CA 125 levels rise, resurgence of cancer is more likely). It is not a good screening test, especially for premenopausal women, since increased levels of CA 125 can be caused by many other conditions (endometriosis, fibroids, pregnancy, ovarian cysts, etc.)
E. lots of kinds of ovarian tumors, not all are cancer.

benign (not cancerous) cystic teratoma- most common ovarian tumor in young women, has lots of cell types present (teeth, hair, bone, etc.).
granulosa tumor- causes precocious (too early) development of 2o sexual characters in girls.
benign solid tumors- like fibroids on the ovary.
serous cystadenoma- this is the bad one. It is the most common kind of ovarian tumor (85-90%). It is epithelial in origin, is papillary (has lots of little bumps that can easily break off and cause spreading), and spreads easily to the bowels, lymph nodes, liver, diaphragm, chest, and can go to the brain.
Gilda Radnor Tumor Registry- tries to identify families where women are at high risk of developing this kind of tumor. High risk families are those that have histories of breast and ovarian cancer. Once identified, these women should be encouraged to undergo regular screening starting at age 35. Some experts recommend prophyllactically removing the ovaries from women from high risk families as soon as they are finished with childbearing to prevent them from getting ovarian cancer.
F. Treatment:

Surgery.
Radiation.
Chemotherapy- new drug in testing stages is paclitaxel (taxol from Pacific yew tree). Data indicate patients' cancers respond to taxol therapy better (there is longer time of progression-free survival by 6 mos, and the overall survival rate was longer by 14 mos) when used with standard chemotherapy drugs than when standard chemotherapy drugs used alone. Side effects of taxol were more toxic to patients. However, the results of a study published in 1996 indicate that most patients value survival over the quality of life during chemotherapy. Currently, the dosage, schedule and use of other drugs to alleviate taxol side effects are not clearly worked out. And as with any new drug, we don't know if the 5 or 10 year survival will be longer with taxol than with other drugs.
an even newer drug is topotecan (Hycamtin), which inhibits the production of topoisomerase I, an enzyme essential for DNA replication.
trying to introduce the drugs more locally (via catheter) which allows use of increases dose of drugs by 6020 times without increaseing the complication rates.
G. 5 yr survival:

in situ and localized: >80%.
regional spread: 45%
distant metastasis: <20%.

Overall: ~38%.

H. Ovarian stimulation: few data so far,

what we do have indicates no increased risk of ovarian cancer for women who used fertility drugs (Clomid, Pergonal).
more and larger studies are being mounted.
VII. Lung Cancer

A. no early screening, difficult to detect in early stages.

B. Risk factors

CIGARETTE SMOKING. 75 - 80% of all cases of lung cancer due to cigarette smoking--> preventable.
excess radon in home.
exposure to asbestos particles.
C. Symptoms are persistent cough, chest pain, sputum streaked /c blood. Symptoms usually don't appear until cancer is advanced and good chance it has already metastasized.

D. Treatment:

Surgery.
Radiation.
Chemotherapy.
Lung cancers are not very responsive to treatment.
E. Overall 5 year survival rate is ~13%.

F. est. # cases est. # deaths %

(1991) (1991) mortality
Lung 60,000 51,000 85%
Breast 175,000 44,500 25%

VIII. Skin Cancer
A. Basal cell and Squamous cell carcinoma extremely common, seldom lethal. Caused by UV radiation. Metastasize very slowly, easily cured by surgery or radiation. Est 750,000 cases/yr of basal cell carcinoma, result in ~2,500 deaths, cure rate of >99.5%. Assoc /c frequent exposure to sun over many years.

mutations of patched, a gene active in a key developmental control pathway in fruit flies (where it was first found) that helps determine how different tissues are laid out in embryoes. In mammals is now thought to be a new tumor suppressor gene. It is located on the long arm of chromosome 9, and is part of a pathway which contains other genes already implicated in other kinds of cancer (e.g. hedgehog).
B. Melanoma- carcinoma arising from the pigment-producing cells of skin. Incidence has been increasing worldwide for 40 years.

Risk factors: Major risk factor is UV radiation. 10x more frequent in Caucasians than in African Americans. Some rare types of inherited susceptibility.
light, fair skin, blonde or red hair.
living in a sunny climate.
sunburn episodes in childhood.
personal or family history of melanoma.
presence of many moles or of large irregularly shaped moles.
Early detection by self-examination of skin. May develop /cin mole, or as new mole-like growth.
Treatment: surgical removal, possibly including removal of surrounding lymph nodes.
5 yr survival rates:
in situ and localized: ~90%.
metastatic disease not responsive to therapy.
risk factors associated with less favorable prognosis:
being male.
a thicker lesion.
ocation of the lesion on the trunk of the body.
age over 60.
Melanomas metastasize very quickly, early detection is major element determining survival.
Prevention:
use sunscreen with SPF <15.
wear protective clothing and hats.
do regular thorough examination of skin, looking for:
a mole shaped asymmetrically.
ia mole with scalloped or irregular edges.
a mole that is dark or irregular in color.
a mole larger than a pencil eraser.
a mole that changes in appearance, bleeds or is painful.
vaccine currently in final stages of testing to see if it is effective in preventing recurrenes in patients at high risk. But will be 4-5 more years before enough people have been included in these trials before we know for sure whether it will work.

Contraception II: Progesterone methods, Sterilization, Emergency Contraception, Abortion
I. Progesterone-dominant methods
A. General comments- work by preventing ovulation and by thickening cervical mucus to make sperm penetration more difficult.

B. Mini-pill- Micronor and Ovrette. daily pills. approved by FDA in 1973. a good method for women that want to use an oral contraceptive but shouldn't use estrogen, (lactating, HTN, E sensitive migraines, etc).

1. (0.35 mg norethindrone/tablet of Micronor, 0.075 mg norgestrel/tablet of Ovrette.) Take 1 pill/day, imp to take consistently. there are no placebos, take hormone-containing tablets continuously, even through menstrual period.

2. Failure rate is 3%.

3. side-effects and risks include: lighter periods, fewer PMS symptoms, unpredictable bleeding, higher risk of ectopic preg, the same women that shouldn't take bcps shouldn't take mini-pills (not because of known problems but because there isn't enough data to know if there are problems or not). No STD or HIV protection.

4. return to fertility is similar to that for BCPs.

5. reduces risk of endometrial and ovarian cancers.

C. Depo-provera (DMPA)- an injection, used by >9 x 106 women around the world for decades, approved by the U.S. FDA in late 1992. A good method for women who have trouble c/ other methods, women done c/ babies but not ready for sterilization, women close to menopause, women who should not take estrogen or BCPs, women who have chronic medical problems (sickle cell disease, HTN, diabetes, etc), women on teratogenic meds or antiseizure drugs. $25 - $50/3 mos (compared to $20 - $25/1 mo for bcps).

1. Shot in either shoulder or hip. Lasts 3 mos (once it's in, it's there for all 3 months, no way to remove it). imp to return for next shot on time.

2. Most women experience change in menstrual cycle, irreg. spotting and bleeding. Most will eventually have amenorrhea.

3. women who do not want amenorrhea or irregular spotting or bleeding may be poor candidates for this method. women who have thrombotic (blood clot) problems, active liver disease, undiagnosed vaginal bleeding, known or suspected preg, and hx of stroke, heart attack, or breast cancer all should not use this method.

4. Other side-effects- weight gain (4 lbs/yr), change in hair pattern (loss or growth), nausea, dizziness, headaches, mood changes (esp depression), decreased libido, decreased HDL and increased LDL. May increase the risk of cervical cancer (prob. because many of these women are not using condoms), IMP to have regular pap smears. No STD or HIV protection.

5. Non-contraceptive benefits- decreased risk of ovarian and endometrial cancers.

6. Return to fertility- good, usually c/in 9-10 mos of last injection (70% preg c/in 1 yr of last use). women who want to get preg c/in 6 mos-1 yr of DMPA are not good candidates.

7. Can use DMPA if breastfeeding, seems to be no bad side-effect on breast milk quantity or quality.

8. Effectiveness similar to sterilization (99.7%).

D. Norplant- levonorgestrel implant. Approved by FDA in Dec. 1990. Used by 2 x 106 women worldwide. A good method for the same kinds of women as DMPA.

1. 6 capsules, each c/ 36 mg of levonorgestrel, placed just under the skin. Lasts 5 yrs, costs $450 - 750/5 yrs ($8 - 13/ mo) but have to pay up front. May cost extra to have it removed earlier. Among users, about 1/3 actually keep implant for 5 yrs, & 1/4 of all users ask for a second set of implants (BUT one MD told me that except for 1 woman, every other woman in her practice that had Norplant had asked to have it removed [weren't comfortable with the irregular bleeding, weight gain and mood swings]).

2. Same affects on menstrual cycle as DMPA for 1st yr., after that most women return to a predictable pattern of bleeding. No STD or HIV protection. Chloasma at insertion site.

3. Implants must be inserted and removed by trained clinician. Have been lawsuits over the problems with breakage and scar tissue associated with removal. Implants may be visible, can feel them.

4. Return to fertility is rapid or immediate upon removal.

5. Women who would be poor candidates for Norplant are similar to those who would be poor candidate for DMPA.

6. Effectiveness similar to that for sterilization and DMPA (99.7%). NOTE: If you are interested in using either Depo-provera or Norplant, consider using Mini-pills for a while first, to see how the side effects are. With Mini-pills, hormone will be cleared from your system in a day, with Depo-provera it's 3 months. Norplant has to be removed by a trained and experienced clinician, but once it's out the hormone is cleared from the system rapidly (a day or so).

II. Sterilization
A. Bilateral tubal ligation- female sterilization. Almost as effective as abstinence (99.7%). Safe (death rate is 3/100,000). EXPENSIVE $3,000-4,000. PERMANENT. PROVIDES NO STD OR HIV PROTECTION.

1. through the abdomen, using laparoscopy (the preferred technique in the U.S., uses either a local or a general anesthetic), mini-laparotomy (very small abdominal incision, commonly uses local anesthesia, can be on outpatient basis or very short hospital stay, very few complications, rapid recovery, not commonly done in U.S.) or laparotomy (abdominal incision, requires hospitalization of 5 - 7 days).

a. tubes are picked up, and then either tied, clipped, ringed, cut, fimbria removed or cauterized.

b. all methods cause damage to the tubes, some cause more damage than others. Those that cause less damage may allow more successful reversal. Ranked from least amount of damage to most, Pomeroy (tie & cut), clip, ring, cautery, fimbria removed.

c. can be done post-partum, c/in 48 hrs of full term delivery, at the same time as C-section, etc.

2. Through the vagina, using incision just below the cervix. Usually the Pomeroy done or fimbria removed. Recovery is rapid, but infection rates are higher. Investigating the use of a polymer glue injected into tubes to block the whole tube, not widespread.

3. Complications and risks (as with all surgery):

a. anesthesia

b. bleeding or damage to other internal organs (rare), requires further surgery to correct damage or stop bleeding (symptoms are abdominal pain, faintness or weakness, heavy bleeding from vagina).

c. infection (symptoms are pain, fever, unusual vaginal discharge), treated with antibiotics.

4. Women who should not undergo tubal ligation:

a. active or previous pelvic infection with adhesions & scarring.

b. are preg. and plan to continue preg.

c. cardiovascular problems.

d. very over- or underweight.

B. Hysterectomy- removal of the uterus /c or /s removal of ovaries (usually for reason other than sterilization).

C. Vasectomy- male sterilization.

1. Cost ~$500, PERMANENT. Provides no STD/HIV protection.

2. Best candidate- 21 yrs or +, in a stable long term relationship, both partners agree that family is complete.

3. Most freq regrets in men who remarry or experience the death of a child. Maturity or age can help offset these unpredictable life events. (freq of regret is low).

4. Effectiveness is 95 to 99.85%.

5. Urologist makes small incisions in scrotum, lifts vas out, cuts and ties vas on each side. Must have ~10 ejaculations after procedure to use up sperm already produced. Want a sperm count with no sperm. (Preg can occur after vasectomy if live sperm still somewhere in the system).

6. Complications:

a. vas can reopen or reconnect (rare).

b. a duplicate vas is present and was missed during the procedure and is still functional (rare).

c. swelling, discomfort or pain, discoloration or bruises, blood clots, infection, granulomas (buildup of small lump of tissue), epididymitis (inflammation/infection in upper tract) (all rare).

d. connection with cancer of the prostate?

e. Can produce anti-sperm antibodies (33-50%), which attack and kill sperm. Therefore, if a man wanted to reverse the vasectomy, while the physical connections could be repaired, the presence of anti-sperm antibodies can cause continued sterility.

7. No change in testosterone, FSH, LH or other hormone levels.

8. No change in sexual function.

D. General comments on reversibility- reversals of tubal ligations and vasectomies are possible, but success rates are low (only up to ~50%), and the procedures are expensive since it entails very delicate work on a very small scale.

III. Morning-after pill (aka day-after pill)- better known as EMERGENCY CONTRACEPTION,
can be used after a birth control method fails (condom breaks, discover a hole in you diaphragm, etc), unprotected intercourse, rape, etc.

A. Timing- c/in 72 hrs, prefer 48 hrs. Dosage- 2 (50 ug EE, 500 ug norgestrel) pills, then repeat in 12 hrs.

B. About 25% of patients vomit after taking 2nd dose. If vomit c/in 3 hrs of taking second dose, need to tell clinician, and either repeat 2nd dose /c something to prevent vomiting or have IUD inserted (have up to 5 days after unprotected intercourse to have IUD inserted for emergency contraception).

C. Mechanism: we think that this big dose of hormones alters the endometrium and makes it inhospitable to implantation.

D. A woman who has taken emergency contraception should expect a period c/in 3 weeks. If no period in that time, follow up with a preg test.

E. Should either abstain from sex during that time or use a barrier method.

F. Effectiveness is ~97%. The affects of emergency contraception (that didn't work and women decided against abortion) on the resulting babies (in English work): 45 total, 42 ok, 1missing a kidney, 2 c/ minor abnormalities.

G. BCP ALTERNATIVE, consult with clinician for dosage, risks, side-effects, etc, (Ovral, contains 50 ug estrogen: 2 pills, and repeat in 12 hours, or use a 35 ug pill (like Ortho-novum 1/35) and take 4 pills and repeat in 12 hours.

H. Who shouldn't use this treatment? Women c/ past hx of throbosis (blood clots), women who are breastfeeding, women who get E-sensitive migraines and are having an attack at the time of treatment.

IV. Abortion-
surgical evacuation of the products of conception from the uterus

A. Has been legal since Roe vs Wade 1973, are very strong feelings on all sides of the issue. We want to present the facts so students can make an informed decision based on facts as well as on moral beliefs.

B. Counselling- about options available, feelings of you and your partner, understand what the procedure will entail, what to watch for post-operatively, birth control, etc.

C. First trimester vacuum abortion- the most common surgical abortion procedure performed in U.S. used for preg 4 - 12 wks gestation.

1. Procedure-

a. do pelvic exam to determine size & position of uterus.

b. insert speculum, disinfect vagina and cervix.

c. tenaculum to steady cervix.

d. anesthesia- in cervix.

e. dilation of cervix with metal rods, or may have inserted laminaria or dilating rods at a previous visit which are now removed. Purpose is to open cervix enough for vacuum tube.

f. vacuum tube is inserted and vacuum created by either an electric pump or large syringe. amount of tissue that needs to be removed depends on the length of preg.

g. some surgeons then use a curet to explore uterus to make sure all material has been removed.

h. remove tenaculum and speculum, total time for the procedure is only a few minutes.

i. may get a Rx for an antibiotic to prevent infection, may also get counselling or Rx for BCPs if you want to start a new birth control method.

2. May have some strong cramping, like the very worst menstrual cramps, and subsequent symptoms of possible complications.

3. Safety of procedure- safer than full term preg (abortion deaths 5 or 6/1,000,000 abortions, preg deaths 80/1,000,000 pregs). infection and incomplete abortion are the most common complications. also possible for hemorrhage, injury to uterus, cervix or other abdominal organs.

4. Subsequent fertility usually not impaired, but infection can cause scarring with subsequent effects on fertility.

D. Other surgical abortion methods

1. Dilation & Evacuation (D&E)- 13 - 16 wks of preg. similar to vacuum aspiration except requires more dilation and surgical instruments to help remove the larger volume of tissue since the pregnancy has had more time to develop. safer than amniocentesis abortion.

2. Amniocentesis abortion (saline, prostaglandin or urea). used at 15 - 24 wks of preg. insert a needle into the fluid-filled sac that surrounds the fetus. Through the needle the clinician inserts saline, prostaglandin or urea to induce premature labor. Woman may be given oxytocin to strengthen contractions. Uterine contractions expel the preg through the vagina. Requires hopitalization for at least 2 days.

E. Rh test for the presence of a factor called Rh. If present = Rh+, if absent = Rh-. Rh- women will be given Rhogam c/in 36 - 72 hrs of delivery, miscarriage or abortion to prevent production of antibodies that could harm future embryos.

V. Chemical options for abortion
A. RU 486- pill, makes operation unnecessary, invented in France in 1982.

1. Antiprogesterone- blocks the progesterone effect on the endometrium (prevents the endometrium from being secretory and stabilized), and blocks implantation. Is in clinical trials in the U.S., the U.S. license holder is the U.S. Population Council (a non-profit organization) as the company that holds the patent did not want to be involved in U.S. abortion debate.

a. If given alone within 10 days of missed period it is 85% successful at preventing implantation of an embryo.

b. dosage- 600 mg of RU 486 (three pills, each with 200 mg).

c. effectiveness increases when given with prostaglandin pills (Cytotec), dosage of prostaglandin- 2 (200mg) pills taken 48 hours after RU 486. The prostaglandin causes cramping and helps evacuate the uterus. Using the prostaglandin increases the effectivenes to 96.9%, and speeds the procedure up (bleeding begins within 4 hours of prostaglandin dose in 61% of cases).

2. Safety of drug- info is from French data, based on thousands of women who have taken the drug.

a. Risks & side-effects.

nausea and diarrhea (from prostaglandin).

prolonged bleeding (> 1 week), uncommon.

incomplete abortion, recheck 10 days after treatment.

not effective for preg past 12 weeks, after 12 weeks need to use a different method (D & E).

b. RU 486 as compared to first trimester vacuum abortion is less painful, less risk of infection, and gives women a greater amount of privacy and control over the process than a surgical procedure.

c. As of 1993, no birth defects had been found in the small number of babies born to women known to have taken RU 486.

d. RU 486 is not recommended for women who are heavy smokers, or who are 35 years old or older.

3. Subsequent fertility not impaired.

4. Non-contraceptive benefits- RU 486 potentially can be used to treat:

a. endometriosis

b. fibroids

c. maybe Cushing's syndrome (a life-threatening metabolic disease)

d. maybe breast cancer.

5. FDA approval is expected soon.

B. Methotrexate

1. Attacks rapidly dividing cells, has already been approved by the FDA for use as an anti-cancer drug, also used for ectopic preg.

2. Also used with a prostaglandin (Cytotec) to improve efficacy and speed.

3. Results from small clinical trials look promising, good efficacy, few serious side-effects. Now in larger clinical trials.

4. As with RU 486, provides women with a safer alternative, more privacy and control than with a first trimester vacuum abortion.



Disorders of the Menstral Cycle
I. Overview
A. Some of the most common reasons for visits to clinicians.

B. Sometimes "disorders" ar expected, or aren't really disorders.

1. 1st year of periods after menarche are usually anovulatory --> normal.

2. peri-menopausally

3. lactating

4. cramps aren't really a disorder.

C. Reassuring to know that:

1. effect on future fertility is usually slight.

2. chance of the cause being cancer is slight, esp if <40

D. Break problems in to categories based on symptoms:

1. painful periods = dysmenorrhea.

2. periods very heavy and/or too frequent = menometrorrhagia.

3. periods too few or too light = oligomenorrhea.

4. periods absent completely = amenorrhea.

5. learn the roots of these words:

a. meno = menstrual.

b. metro = time.

c. oligo = few.

d. a = without or none.

e. rhagia = excess or abnormal.

f. dys = not or pain.

g. rrhea = flow.

h. osis - disease.

i. plasia = growth.

II. Painful menstruation or dysmenorrhea
A. Primary or functional dysmenorrhea = painful periods / s underlying pathology.

1. due to increased amount of uterine cramping and/or increased amounts of prostaglandins present as endometrium sheds.

a. prostaglandins known to cause cramps, nausea, diarrhea (e.g., when used to induce abortion).

2. may or may not be assoc / c increased flow.

3. will usually respond to:

a. anti-prostaglandins (ibuprofen Advil, Motrin, etc.).

b. aerobic exercise and some yoga postures.

c. acupressure/acupuncture.

d. diet changes:

i. reduce the intake of meat and dairy products (substitute leafy green begies, legumes and carrots to maintain Ca intake).

ii. increase intake of fish, fruits, vegies, whole grains, legumes, raw seeds and nuts.

iii. decrease salt intake (helps decrease bloating, as does eating lots of fruits and vegies).

iv. Vitamin B6 100-200mg/day (higher doses can cause nerve problems, such as numbness in hands and feet).

v. 1000 mg/day of Ca and 400-500 mb/day of Mg (both promote muscle relaxation).

4. see article on reserve: Lark, S., 1991. Managing primary dysmenorrhea. Today's Woman February: 6-8.

B. Secondary dysmenorrhea can be cause by:

1. Cervical stenosis - cervical os is so tightly closed that menstrual blood can't escape (may be due to some trauma). Treated by slowly dilating the cervix. NOT COMMON.

2. Pelvic infection - (to be covered in STD lectures).

3. Endometriosis - presence of endometrial tissue outside the uterine cavity.

a. formation of endometriomas (or implants) typically occurs on outside of uterus, surface of ovaries, fallopian tubes, bladder, rectum, ligaments, and even intestines. Responds to hormones of menstral cycle (estrogen --> implants grow, progesteron --> stabilizes. loss of estrogen and progesterone causes shedding and bleeding).

i. closely related condition is adenomyosis = endometriosis into the wall of the uterus (myometrium).

b. theories of cause include retrograde menstruation, and embryological placement of primordial endometrial cells.

c. effect is pain, mild to severe b/c cyclic bleeding into a closed space (BLOOD WHERE IT DOESN'T BELONG HURTS.) and release of prostaglandins to neighboring tissues. Pain is assoc /c period.

i. symptoms usually begin a few years after menarche.

ii. pain and cramps get worse as woman ages. may not be controlled by anti-prostaglandins, may need narcotics.

iii. may also cause irr. menstrual bleeding, but less typical.

iv. symptoms eventually burn out, may subside /c decreased hormonal cycles (pregnancy, perimenopause)

d. a potential for decreased fertility. structural problems /c advanced disease, but even mild to moderate dz can cause infertility (but we don't know why).

e. Diagnosis: biopsy after suspected hisory. Usually laparascopy. Chocolate cysts (old blood turns brown).

f. Treatment:

i. hormones including BCPs (to reduce hormomal stimulation of implants), GnRH agonist (Danazol/Danocrine, estrogen look-alike, fools pituitary gland into decreasing production of FSH --> no cycling. = chemical menopause). Drugs only work while you take them, symptoms often reappear when discontinue drugs.

ii. surgery to remove implants.

g. Frequency: 5 - 15% of menstruating women (40% of infertility patients). May have a genetic component as higher rates among family members.

THE ENDOMETRIOSIS ASSOCIATION
8585 N. 76th Place
Milwaukee WI 53223
(a self-help group for women with endometriosis. publications available, has chapters, groups and networks across the U.S.)

III. Menometrorrhagia = heavy and/or frequent periods. All of the following may or may not cause menometrorrhagia.
A. Anatomical:

1. Fibriods = growths of uterine tissue in irr. pattern on uterus. Called "tumors" but rarely become cancerous. Leiomyomata.

a. cells contain high levels of enzyme hydroxyl CoA dehydrogenase which increases fatty acids in cells and promotes faster growth. Increased # of estrogen receptors accounts for increased growth during preg, shrinkage after menopause.

b. position may be submucosal, intramural, or subserosal.

c. May cause no sx. Subserosal may cause pressure on other organs. Submucosal fibroids may cause bleeding (may be heavy and inter-menstrual). May cause infertility.

d. COMMON, 30% of women over 35. only about 30% of those women have sx.

e. Cause unknown, previously very common cause for hysterectomy. accounted for ~30% of the 650,000 hysterectomies each year in U.S.

f. Diagnosis:

i. irr. enlarged uterus on physical exam (described as # wks gestation).

ii. ultrasound.

iii. confirmed on hysteroscopy or laparoscopy.

g. Treatment:

i. do nothing if sx not too bad, will shrink with menopause.

ii. if bleeding severe, can be shrunk /c GnRH agonist/antagonist which induces chemical menopause, usu as prep for surgery.

iii. hysteroscopy (remove fibroid and leave uterus intact) if possible.

2. Cancer of cervix, <3%, bleeding results from a structural lesion (erosion, bleeding esp. if irritated by intercourse. (more in cancer lecture).

3. Cancer of uterus (adenocarcinoma) rare if under 40, usually found in >50 year old women. Often has inter-menstrual bleeding. (more in cancer lecture).

B. Endocrine/metabolic

1. Thyroid dysfunction (esp hypothyroidism). need to r/o bleeding disorders (e.g. hemophilia), iron deficiency (esp. in teens) and out of control diabetes (rare).

2. Dysfunctional uterine bleeding (DUB) = bleeding in absence of tumor, inflammation or preg. (may be the most common menstrual cycle disorder diagnosis that a physician makes).

a. Cause: "hormonal imbalance", depends on age.

i. Teens - immature hypothalamus-pituitary-ovary (h-p-o) axis, may have insuff. estrogen, progesterone or both.

ii. Ages 20 - early 40s - emotional or physical factors disrupt h-p-o axis, usu /c decreased progesterone (estrogen levels usu. ok). cycles usu anovulatory, endometrium sheds asynchronously.

iii. Ages 40 - 50s - peri-menopausal, more anovulatory cycles due to ovarian shut-down.

b. Sx: frequent and irr bleeding, may or may not be heavy.

c. uterus may show:

i. hyperplasia = overgrowth of endometrium with little secretory pattern due to lack of progesterone. can be precancerous.

ii. "raw spots" if not enough estrogen to build up endometrium.

iii. dyssynchronous pattern of shedding, as areas of uterus build and shed "out of sync" with each other.

d. Treatment is PROGESTERONE to stabilize the endometrium (Provera and others). Occasionally estrogen is also needed. BCP can be used to cycle endometrium for 1 - 3 cycles.

i. Typically give 10 days of Provera, then wait for a period. May then use BCPs for regularity.

ii. If suspicious of other cause, or if not responding as expected to progesterone, do endometrial biopsy.

iii. uterine ablation - new technique where lining is destroyed /c lasers.

IV. Oligomenorrhea = infrequent and/or light periods. Grades into amenorrhea.
A. Menopause or premature menopause (more in menopause lecture).

B. H-P-O dysfunction caused by:

1. Rapid weight loss (dieting or illness).

2. High levels of exercise (training athlete).

3. Anorexia or anorexia-bulimia.

4. Illicit drugs, esp. heroin (usu weight loss too). LOSS OF CRITICAL WEIGHT

5. Certain other drugs (BCPs cause lighter periods).

6. Polycystic Ovarian Syndrome (PCOS)

a. may be several causes that result in same clinical picture: multiple cysts on ovaries, amenorrhea or very irr periods, sometimes infertility, overweight and hirsutism (increased hair growth).

i. all have lack of LH surge, though LH levels may be increased.

ii. all have lack of H-P-O rhythm. Initial defect may be an abnormal conversion of an androgen (like testosterone) into a weaker form of estrogen (called estrone), or there may be an abnormal feedback of estrogen on the pituitary, or ?

(in ovary, some of testosterone produced is converted to estrone which doesn't turn down FSH as effectively as estrogen) (Peripheral fat also converts estrogen and androgens into estrone, therefore heavier women may have high levels of estrone, abnormal feedback loops, anovulatory cycles or PCOS.)

iii. result is ovaries have follicular cysts in arrested development, "twilight ovaries", have thickened fibrous capsule on ovary, can lead to infertility.

iv. FSH and testosterone levels are high.

b. Clinical picture:

i. typical pt has had trouble since teens "periods have always been irr"

ii. most show signs of increased androgens: increased body hair, acne, some PCOS cases discovered because the pt initially requests treatment for increased body hair.

iii. may have difficulty conceiving when interested, though most able to eventually conceive.

c. Diagnosis: made clinically, confirmed /c lab tests (elevated but not surging LH, reversal of usual FSH:LH, high testosterone) and by ultrasound.

d. Treatment: none needed unless:

i. pregnancy desired.

ii. PROGESTERONE.

iii. to protect ovaries and heart from continuous high levels of testosterone and LH, many women cycle /c BCPs, shuts down both LH and testosterone.

C. Functional ovarian cysts

1. Common for a woman to have at least one during lifetime.

2. Result of abnormal feedback loop, follicular cyst that does not rupture.

3. Name "functional" is misnomer, since they are really dysfunctional.

4. Can get to be 2 - 3", feel quite painful or no sx.

5. Usu assoc /c irr (esp late) cycle, as that cycle is anovulatory.

6. Diagnosed on exam or by ultrasound.

7. Treatment: none unless recurring, then BCPs to shut down cycle.

V. Amenorrhea = lack of periods.
A. Primary = no menses by age 17 - 18. freq. assoc /c athletes, dancers, anorexics: some "constitutional".

B. Secondary = no menses for 6 months after previous regular periods. Causes include:

1. Most frequent cause of secondary amenorrhea is pregnancy.

2. PCOS.

3. Pituitary tumors = microadenomas.

a. assoc /c breast discharge due to presence of high levels of prolactin.

b. prolactin interferes in an unknown way with rest of H-P-O axis.

c. treatment necessary if pregnancy desired and/or tumor enlarging.

d. frequently assoc /c low estrogen levels, so may need estrogen supplementation.


Female Sexual Response
I. Overview
A. Approached from biological basis. Landmark physiological work done by Masters and Johnson in 1950s and 60s, further sociolocigal work done by Kinsey.

B. No single normal or typical response; humans have wide diversity. Since multiple sex partners carries higher risk for HIV/AIDS and other STDs, more people experimenting with new positions, fantasies, sex toys, locations, etc to keep sex /c same partner interesting.

C. Physiological response usually occurs in predictable sequence, whether young or old, hetero or homosexual orientation.

D. Some aspects of response are under involuntary nervous system control, some under voluntary control.

II. Lesbian and bisexual sexuality
A. Biological issues in women having sex /c women aren't much different than what will be mentioned for heterosexuals. (/c obvious exception of penis-related issues)

B. Can have problems /c insufficient lubrication, vaginismus, decreased libido, sexual addiction, etc.

C. Some statistics - may or may not be reliable.

1. Masters and Johnson found 5% of U.S. population self-identified as bisexual (sexual activity /c a man and a woman within the last year), although most reported a preference.

2. Kinsey found 2 - 3% of women were exclusively homosexual (vs 4% of men), and 20% of women have had a lesbian encounter by age 40 (vs 33% of men).

III Phases of sexual response
A. Excitation - generally under voluntary control as we pay attention to internal or external stimuli (e.g. thoughts, fantasies, five senses)

1. in both women and men, artieries dilate. In women, see engorgement of labia majora and labia minora, increased size of clitoris (comes out from under its hood), nipples may become erect, breast veins engorge, and breasts may swell.

a. vaginal lubrication begins as vaginal cells secrete clear discharge.

b. may see flushing of chest, sometimes face (more typical of orgasm).

2. In men, under influence of prostaglandin E, corpus cavernosum becomes engorged /c blood --> erection, . Note: tiny drop of semen on tip of penis contains sperm even this early in response.

3. Increased heart rate, blood pressure and muscle tone result from autonomic nervous system response ("automatic" or involuntary).

4. Portions of the excitation phase can be an involuntary response e.g. from vibrator or forced sexual contact.

B. Plateau

1. In women: clitoris retracts under hood, draws back against the pubic bone; outer opening of vagina engorges, upper vagina increases in length and diameter by 1 - 2"; labia continue to engorge, become deep pink before orgasm.

2. In men: testicles increase in size (up to 50%) and draw up toward abdomen.

3. both excietment and plateau under control of parasympathetic nervous system, (vs sympathetic control for orgasm). Means it is possible to have disruption of one pathway and still have other pathway working (e.g. spinal cord injuries).

4. increased respiratory rate.

C. Orgasm pleasurable sensation under sympatheic control, "a cortical-sensory event" means it uses both the brain and the body.

1. Western concept of "coming," vs Eastern concept of "going."

2. sensation described by women and men similar in written descriptions.

3. In women: sequential enhancement of "intense clitoral-pelvic awareness", a "suffusion of pelvic warmth", and finally pelvic throbbing as involuntary pelvic contractions occur at about 0.8 second intervals, from 4 - 10 contractions.

4. In men: semen is propelled into urethra as prostate gland and seminal vesicles contract = emission, a feeling of the inevitablity of orgasm. Ejaculation is the expulsion of semen (sperm + alkaline substances + fructose). Also contractions about every 0.8 seconds.

5. Both women and men report orgasm experienced as strongest /c masturbation, but not necessarily "more pleasurable."

6. In women: no incontrovertible evidence of orgasm.

7. No lab. evidence for "more than one kind" of orgasm. Only clitoral orgasm is validated (makes sense, glans of clitoris is homolog and analog of glans of penis). Some women report difference in experience of orgasm after primarily vaginal vs clitoral stimulation.

8. above may relate to the G-spot (Grafenberg spot), located in anterior (nearest bladder) vaginal wall, along urethra near where it joins bladder. Tissue engorges /c arousal, pleasurable to touch. Others besides Grafenberg have noticed clear secretions from female urethra /c orgasm that are not urine.

9. Time to orgasm may differ for women and men, and different at diff. stages of life.

D. Resolution

1. "Genital hypersensitivity" when clitoris or glans of penis too sensitive to touch.

2. General feeling of well-being, intimacy, "love" --> ?role of oxytocin (present in sperm) as "love hormone?"

3. Rapid opening of veins, and engorgement subsides, clitoris returns to unretracted postion.

4. Vaginal tissue may appear engorged if actual abrasions (overvigorous penetration) occurred.

5. In men: true resolution, e.g. must go through excitement to plateau phases to reach orgasm, while women may return directly to plateau phase, thus have potential for multiple orgasms in relatively short period.

6. Sequence is obviously not inevitable.

IV. Masturbation - a self-stimulation or "self-pleasuring": is a normal, healthy sexual practice. Valuable in learning what is pleasurable, where erogenous zones are, etc.
A. A learned behavior, may be more common for boys to learn at an earlier age in our society than girls.

B. may be difficult for some to learn due to certain religious teachings or due to strong negative conditioning.

C. Good section in OBOS.

D. Masturbation is not healthy if it is draining energy away from the primary relationship.

V. Fantasy - normal, generally non-threatening to relationship.
VI. Some common sexual problems
A. Decreased libido or sex drive will affect excitement phase.

1. Fatigue - incredibly common. Helped by getting regular exercise.

2. Stress - including stress about family, kids, division of energies in too many directions, acute or chronic disease, relationship problems, problems in school or at work, when trying to conceive including performance anxiety. In some people, or at other times in your life, stress may actually increase libido.

3. Depression - An almost universal sign of depression is decreased libido.

4. Anger - esp if unidentified or simmering toward partner.

5. Drugs - including alcohol, opiates (codeine, heroin, etc), marijuana (regular use decreases testosterone levels), and prescription drugs (esp. drugs for high blood pressure, anti psychosis drugs, etc)

6. Fear of pregnancy

7. Previous history of sexual trauma or abuse.

8. History of negative messages about sex.

9. Pregnancy and/or post-partum, nursing - may or may not decrease libido.

10. After hysterectomy - esp if ovaries taken, or blood supply to ovaries compromised (testosterone gone).

B. Vaginismus - much less common than decreased libido. Condition of involuntary spasm of vaginal muscles around introitus with attempt at vaginal entry.

1. May be due to current or past pelvic infection or to healing stitches (after episiotomy).

2. May be due to previous sexual trauma, including rape, abuse or incest.

3. Burning vulva syndrome - exquisitely sensitive perineum, esp in area of Bartholin's glands ("vestibulitis" or "vulvodynia" infection).

4. Treatment involves identifying and treating the underlying cause. May involve medications, therapy (psychological and/or sexual), including progressive vaginal dilation (starting with fingers, progressing to dildos).

C. Anorgasmia

1. Primary = never had one. Very common in women. Partner may not be aware due to "faking". Better term may be pre-orgasmia. "Treatment" is education, progressive exercises esp in self-stimulation, making transition to partner. Strong need for communication with partner.

a. ~ 2/3 of women need extra clitoral stimulation in addition to penetration to achieve orgasm (education and communication).

2. Secondary = previously could have orgasms, now can't. May relate more to performance anxiety, or to relationship problems (esp around issues of control).

D. Dyspareunia = painful intercourse. May affect excitement or plateau phase.

1. Location of pain is key to identifying the cause. Is there pain on entry? with deep thrusts? in certain positions?

2. Insufficient lubrication if insufficient arousal. Can be caused by certain drugs (cocaine, anti-histamines, anti-depressants), nursing, aging, immediately after tampon use. Can use water-based lubricants (contraceptive foam or jelly, K-Y jelly), estrogen-containing creams, Estrogen/Hormone Replacement Therapy.

3. Infection - vaginal or cervical. (yeast -->external or entry discomfort vs pelvic inflammatory disease (PID) if pain is deep or cervical).

4. Cervical stimulation /c deep penetration, certain positions.

5. History of sexual trauma.

E. Other relationship problems, including differences in expectations of frequency, length of intercourse, differences in libido, different circadian rhythms, double career couples, etc.

1. Role of intimacy - esp talking, shared work, etc. Remember, a woman's most important sex organ is her brain.

F. Due to birth control method - improper fit of diaphragm, decreased sensation /c latex condom, need more lubrication /c condom. More on contraceptives in next two lectures.

G. Male problems

1. Inability to achieve erection (impotence)

a. first need to rule out medical conditions such as diabetes, or the effect of a medication.

b. Vast majority due to performance anxiety, with a possible vicious cycle developing if it is not overcome.

c. Frequently assoc. /c drugs, alcohol, depression, fatigue, fear of pregnancy, (etc, see list for decreased libido). Also /c history of sexual trauma (1 in 7 men).

d. Treatment is available.

2. Premature ejaculation - ejaculation occurs within 30 - 60 seconds of erection (or could be longer if man feels out of control)

a. Treatment is the "pause" or "squeeze" technique.

H. Sexual addiction

1. An addiction can be to a substance (alcohol, nicotine, cocaine, etc) or to a process (gambling, work, love or sex).

2. Person prob. has a problem /c a behavior if it causes trouble /c >1 of the following:

a. relationship

b. work or school

c. finances

d. the law

e. self-esteem

f. health

3. If cont' behavior in spite of problems, definitely have a problem.

4. Sexual addiction manifests differently in women and men:

a. In women: consequences are to relationship and self-esteem (engaging in sex acts that make her feel uncomfortable or promote self-loathing, having an affair /c adverse consequences to relationship /c primary partner).

b, In men: problems /c finances, the law, deviant behavior (using prostitutes, pedophile, masturbation to point of injury).

5. Set up in childhood as a learned way of dealing /c feelings of low self-esteem.

a. almost always has a component of sexual abuse or trauma.

b. "I'm not loveable unless I'm sexual."

6. In this era of STDs and HIV/AIDS, real possibility of adverse health consequences.



Childbirth
I. TERMS
Nullipara- a woman who has never had a vaginal delivery before.
Multipara- a woman who has had at least one vaginal delivery before.
Primagravida- a first pregnancy.
Multigravida- a second or subsequent pregnancy.
Oxytocin (natural form)/Pitocin (synthetic form)- a hormone that causes uterine contractions.

II. BEFORE LABOR STARTS
A. Settings for labor. important for woman to feel comfortable where ever she goes through labor and delivery.

Home- for early labor, or entire labor and birth.
Birthing center- intermediate to hospital and home birth. (Sutter Maternity and Surgical Hospital)
Hospital- previously were separate labor and delivery rooms, now often a woman labors and delivers in the same room (delivery room reserved for special situations, e.g. vacuum-assisted, forceps, c-section, or fetal problems).
B. Lightening or engagement- fetal head drops into woman's pelvis, woman feels like she can breathe again. Happens up to a couple of wks before labor begins (or just hours before labor begins).

C. Braxton-Hicks contractions

D. Triggers of labor- from research on non-human primates.

fetal brain (hypothalamus and pituitary) "instructs" fetal adrenal glands to produce a steroid androgen hormone (DHEAS).
DHEAS transported through fetus' bloodstream to placenta.
In placenta, DHEAS is converted into estrogen (specifically estradiol). Estrogen levels rise.
a. Increased estrogen levels (with a relatively constant progesterone level) stimulate:

i. increased maternal production of oxytocin, occurs at night (highest oxytocin concentrations seen between midnight and 3 am).

ii. increased numbers of oxytocin receptors on the muscle cells of the myometrium.

iii. increased prostaglandin production, which stimulates the muscle cells of the myometrium to contract.

1.                                                                                                                                                                                                        About 1 wk before delivery, the numbers of uterine contractions/hr start to increase (occurs at night) and every subsequent night there are more than the night before, until delivery occurs.

2.                                                                                                                                                                                                        Still don't know why or how the fetal brain "decides" that it's time for fetus to be born.

E. Passing mucus plug- indicates cervical softening, occurs up to 2 wks before birth.

III. STAGES OF LABOR
A. PRODROMAL LABOR (EARLY LABOR OR LATENT PHASE OF LABOR)

1. earliest stage, can last minutes - days. Usually irreg. pattern of contractions, become more reg. as contractions get longer, stronger, closer together.

2. burst of energy, "nesting", but need to conserve energy for later.

3. cervix softens, effaces (thins), dilates, fetus descends into pelvis.

4. generally cervix is relaxation. Continuous emotional support speeds labor.

Problem: if prodrom. goes on for days, can cause maternal fatigue, less ability to cope/c intense work of labor in later process.

a. Decision: accelerate labor? allow sleep by shutting down contrac'ns?

b. accelerate/augment by vigorous walking, nipple stimulation, breaking bag of waters (ROM/AROM), prostaglandin gel, pitocin.

c. sleeping done/c narcotc meds (Seconal, Nembutal etc.). Baby sleeps too, woman often wakes feeling rested and either in better more effective labor pattern or labor may not return until later.

B. STAGE ONE: ACTIVE LABOR (4-10 cm dilated, 10 = complete)

1. contrac'ns get longer, stronger, closer together /c freq of every 3 - 5 mins.

2. woman changes from excited to settling in to do work.

3. Friedman or labor curve - labor "should" progress at certain rate. Does not take allow for indiv. factors.

a. position - woman lying down (fetal monitoring) will progress slower than woman allowed to walk, change positions. Back labor.

b. woman threatened or afraid at this stage will have slower labor (Odent's animal model of protecting laboring female).

c. standing, walking, squatting, taking shower/bath all help speed/smooth labor.

4. coping /c labor: focus, breathing, visualization --> relaxation. Continuous emotional support speeds labor.

5. fetus helps, pushes /c 1 foot, skull bones mold to fit through pelvis, predictable sequence of movements fetus goes through. to get through pelvis.

6. TRANSITION 7 - 10 cm dilation, most intense sensations, characterized by bizarre thoughts, actions by woman. contrac'ns strong, right on top of each other, no time to recover or regroup.

7. Monitoring

a. Maternal- BP hourly, proteinuria (both for pre-eclampsia), temp (esp if membranes have ruptured), uterine contrac'ns /c external belt or internal pressure monitors.

b. Fetal- intermittent (US or Doppler). Sometimes is continuous, esp if problem /c fetal coping is suspected. Internal monitoring /c fetal scalp probe (rarely used, only if suspect fetal distress).

8. Interventions in active labor:

a. AROM (Artificial Rupture of Membranes)- used to speed labor or if suspect fetal distress to look at color of fluid (meconium), or to place internal fetal scalp monitor.

i. Baby can be born /s bag rupturing, "born under the veil"

ii. Meconium- passage of fetal bowel movement, turns fluid greenish, indicates fetal distress.

b. Pitocin- to intensify contrac'ns. given in smaller amounts and more gradually than for induction.

9. Time frames vary, 1 cm/hr for primagravidas, 2x as fast for multis.

C. STAGE TWO: PUSHING

1. Time frame- up to 2 hrs in primas, multis high risk of maternal bleeding. Uterus will contract down to help stop bleeding, routinely do uterine massage, may give pitocin or other meds to help, nursing also helps since it stimulates secretion of mother's oxytocin.

2. Positions - squatting (opens pelvis more), birthing chair (like toilet), semi-reclining, left-side lying. May feel better (or not, multis).

3. Fetal ejection response - (Odent) in this stage, if threatened (either woman or baby) may see rapid ejection of baby (clang forceps).

4. Pelvic floor expands, stretches. massage /c hot oil, hot packs helpful to prevent tearing.

a. episiotomy controversy - to use or not? healing time seems to be faster /s epis and tear anyway.

b. need epis for rapid birth (if there is fetal distress). Done after local anesthesia on perineum (or to pudendal nerves for more complete block, not done much anymore).

c. if don't have epis, may still have tears that require stitches.

5. "Crowning" - head on perineum, intense burning/stinging (ring of fire). Some women fear expusion of baby will cause tearing/ripping.

6. with head out, baby rotates head either to R or L so shoulders are straight up and down. After delivery of shoulders, rest of body follows easily.

7. Immediately after birth - baby dried off, gently stimulated, Apgar score (at both 1 and 5 min after birth, bonding /c mother imp in first mins to hrs.)

a. Apgar score tells clinician if baby needs help (breathing, muscle tone, skin tome).

b. Bonding - based on infant's pre-existing reflexes: rooting, hand grasp, eye contact, baby knows mothers smell and voice, as well as voices of other household members.

G. STAGE THREE: EXPULSION OF PLACENTA

1. usually /cin 5-30 mins after birth, great relief after it's out.

2. occasionally need manual removal, rare complication is placenta accreta which may require hysterectomy.

3. After placenta delivered --> high risk of maternal bleeding. Uterus will contract down to help stop bleeding, routinely do uterine massage, may give pitocin or other meds to help, nursing also helps since it stimulates secretion of mother's oxytocin.

4. repair tears or epis. use sutures that dissolve.

5. cord blood sample to determine baby's blood type and Rh.

a. if mother is Rh- and baby is RH+, mother is given RhoGam.

b. baby may have jaundice, usually not a problem.

H. PROBLEMS IN LABOR

1. Failure to progress- many causes.

a. back labor- baby facing up (stargazer).

b. weak contrac'ns due to fatigue, may need to use acceleration techniques.

c. cephalo-pelvic disproportion (CPD)- baby can't fit even /c molding.

d. malpresentation- wrong part of head comes out 1st (face, brow).

2. Fetal intolerance of labor (a stress to distress continuum)

a. presence of meconium.

b. fetal heart tracing pattern.

3. Outlet difficulties, may be due to macrosomia-

a. vacuum extraction- useful if baby near enough to crowning.

b. forceps- if baby higher, may need rotation. may cause bruising, lacerations to baby's face, may or may not cause nerve damage (debated), may prevent c-section, must be done by experienced person.

c. shoulder dystocia- head out, shoulders retained, more freq /c larger babies, may result in fetal loss of O2 and death, injury to fetal collar bone or brachial plexus (nerves) leading to arm movement problems.

d. breech presentation.

I. CESAREAN SECTION- from Latin verb caesura (to cut).

1. Types- classical (vertical on uterus) or low transverse (horizontal on uterus).

2. Rates: 5% in Scotland, 18% in U.S.

3. Healing takes longer than normal vaginal delivery (major abdominal surgery).

4. Some women view it as imposed by doctors, some women as a personal failure.

5. VBAC (Vaginal Birth After Cesarean)

a. "Once a cesarean, always a cesarean" is a MYTH.

b. only absolute requirement is low transverse incision from previous c-section. Trend is to offer VBAC to most women. VERY SAFE, as safe for women carrying twins as for singleton. Needs closer monitoring since there is ~1% chance of rupture of scar.

c. "relative requirements"

i. has had previous vaginal delivery.

ii. has attended prenatal classes.

iii. fetus is estimated to weigh

J. INDUCTION OF LABOR

1. may be needed for postdates, if not enough fluid around fetus, if suspect baby will be huge if it goes to term.

2. elective for personal reasons.

3. synthetic oxytocin (pitocin)- IV infusion, requires constant monitoring, means woman's ability to walk, shower, change positions is limited.

4. prostaglandin gel (Prostin 32)- put on cervix, used to soften or ripen cervix, requires less monitoring, allows woman to move around, walk, change position, take shower, etc.

5. assoc /c higher rates of other interventions (any intervention seems to increase the risk that another intervention will be needed).

K. MEDICATIONS IN LABOR

1. early labor - "sleeping" meds if want mother to sleep, anti-nausea meds.

2. active labor - narcotics to "take edge off pain" (Demerol, Stadol), administered via IV or IM (injection into muscle)

3. Epidural anesthesia - catheter placed in space just outside spinal column to let anesthesia "marinate" the nerves. Want to block sensation, not prevent movement. Assoc /c risk of other interventions, useful to achieve relaxation, may prevent c-section.


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SHOULDER DYSTOCIA

A. Shoulder dystocia is an infrequent obstetric emergency associated with:

maternal morbidity (hemorrhage, soft tissue laceration and uterine rupture)
fetal morbidity (brachial plexus injury, fracture of humerus or clavicle and later hypoxic brain damage) and up to 8% fetal mortality.
B. Those complications can be greatly diminished by appropriate recognition of macrosomia and planning delivery procedures.

Incidence

       0.2-6 per 1,000 deliveries

Prevention

A. Risk Assessment

1. Historical

a. Previous delivery of large infant (over 4000 grams) or history of shoulder dystocia.

b. Maternal diabetes.

c. One half of all cases occur in babies under 4000 grams.

2. Clinical findings

a. Fetal weight over 4,000 grams.

b. Maternal obesity.

c. Maternal diabetes.

d. Gestational age over 41 weeks.

e. Mid-pelvic delivery after second stage of labor lasting more than two hours.

3. Ultrasound evaluation

a. All patients at risk for macrosomia should be scanned during the third trimester to better estimate fetal weight using standard ultrasound techniques.

b. Estimated Fetal Weight (EFW) at delivery can be approximated by adding 30 grams per day from the day the scan was performed to the day of delivery.

B. Recommendations based on EFW and knowledge of maternal diabetes

1. Estimated fetal weight and diagnosis of fetal macrosomia should be based upon clinical findings and ultrasound evaluation.

2. Avoid operative mid-pelvic delivery if EFW is over 4000 grams.

3. Cesarean delivery for non-diabetics with EFW over 4500 grams.

4. Cesarean delivery for diabetics with EFW over 4000 grams.

Diagnosis

A. There is recoil of the head back against the perineum caused by the impaction of the anterior shoulder behind the symphysis pubis, instead of rotation under the pubic ramus.

B. Restitution rarely occurs spontaneously.

C. Vaginal examination is done to rule out other causes of difficulty, such as:

1. Abdominal or thoracic enlargement of the infant (anasarca, congenitally anomalous infants, neoplasms)

2. Locked or conjoined twins

3. Uterine constriction ring

Management

A. Anticipate occurence and have an experienced team available for the delivery (when EFW is over 4000 grams). The team should include a(n):

1. anesthesiologist

2.pediatrician

3. another obstetrician

4. adequate nursing personnel

B. If shoulder dystocia occurs unexpectedly, call the above team.

C. Guidelines for delivery

1. Do not apply fundal pressure or apply traction on the head and neck.

These maneuvers only serve to waste precious time and to impact the shoulders more firmly in the inlet. Furthermore, they may result in uterine rupture or brachial plexus injury.

2. Cut a generous episiotomy or episioproctotomy. This will:

a. Reduce the incidence of major perineal lacerations.

b. Provide additional space for manipulation.

3. Ensure adequate anesthesia. General anesthesia may be required to obtain complete muscle relaxation.

4. McRoberts Maneuver

a. Remove the patient's legs from the stirrups and sharply flex them against her abdomen (knee-chest position).

b. Apply gentle traction to free the impacted anterior shoulder without further manipulation of the fetus.

5. Delivery of the anterior shoulder

a. Place the hand deeply in the vagina in front of, or behind the anterior shoulder

b. With the next contraction, rotate the axis of the shoulders into an oblique diameter of the pelvis.

c. Apply firm traction on the head, deflecting it toward the floor.

d. Exert suprapubic pressure

1) This usually succeeds in bringing the anterior shoulder into and through the pelvis.

2) Assistant should ask physician which direction to apply pressure.

6. If delivery of the anterior shoulder is unsuccessful, attempt delivery of the posterior arm.

a. The operator's entire hand is inserted along the hollow of the sacrum.

b. Reaching within the uterus, and with two fingers applying pressure to the mid-humerus, sweep the posterior arm across the fetal chest and deliver it.

c. Rotate the infant's trunk through a half-circle, if necessary, to accomplish delivery. Never apply excessive traction to the fetal head or neck.

7. Alternative maneuver (Zavanelli Maneuver)

a. If restitution has occurred following expulsion of the head, the head is first manually returned to its pre-restitution position, full extension in a direct occipito-anterior position.

b. The head is then manually flexed, recapitulating in reverse the birth of the head by extension.

c. Then upward pressure is applied to force the head into the vagina.

d. A ceserean delivery is then accomplished.

Complications

A. Maternal

1. Postpartum hemorrhage

a. Uterine atony

b. Vaginal and cervical lacerations

2. Ruptured uterus

B. Fetal/Neonatal complications

1. Fractures of clavicle or humerus

2. Brachial plexus or other nerve injuries

3. Asphyxial damage

4. Death