Gynecology Enhancement

Maribee T. Espiritu, RN, MD

BLEEDING IN PREGNANCY

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Spontaneous abortion

• is the termination of pregnancy resulting in

expulsion of an immature, nonviable fetus
• Occurs in 50 to 75% of all pregnancies
• Most are unrecognized because they occur
before or at the time of the next expected
menses.
• 15 to 20% of clinically diagnosed pregnancies
are lost in T1 or early T2.

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• Sixty percent of spontaneous abortions in
the first trimester are a result of chromosomal
abnormalities.

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• Top etiologies of spontaneous abortion:
1) Chromosomal abnormalities
2) Unknown
3) Infection
4) Anatomic defects
5) Endocrine factors

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ETIOLOGIES

• Chromosomal Abnormalities
– Majority of abnormal karyotypes are numeric
abnormalities as a result of errors during
gametogenesis, fertilization, or the first division of
the fertilized ovum.

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• Infectious Agents
– Infectious agents in cervix, uterine cavity, or
seminal fluid can cause abortions.

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• These infections may be asymptomatic:
– Toxoplasma gondii
– Herpes simplex
– Ureaplasma urealyticum
– Mycoplasma hominis

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Uterine Abnormalities

• Septate/bicornuate uterus—25 to 30%

• Cervical incompetence
• Leiomyomas (especially submucosal)
• Intrauterine adhesions (i.e., from curettage)

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Endocrine Abnormalities

• Progesterone deficiency
• Polycystic ovarian syndrome (POS)—
hypersecretion of luteinizing hormone (LH)
• Diabetes—uncontrolled

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Immunologic Factors

• Lupus anticoagulant
• Anticardiolipin antibody (antiphospholipid
syndrome)

Environmental Factors
• Tobacco––≥ 14 cigarettes/day increases
abortion rates
• Alcohol
• Irradiation
• Environmental toxin exposure
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THREATENED ABORTION

• vaginal bleeding that occurs in the first 20

weeks of pregnancy
• without the passage of products of
conception (POC) or rupture of membranes
• Pregnancy continues, although up to 50%
result in loss of pregnancy.

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• DIAGNOSIS
– Speculum exam reveals blood coming from a
closed cervical os, without amniotic fluid or
POC in the endocervical canal.

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• MANAGEMENT
– Bed rest with sedation and without intercourse
– Twenty to 50% of threatened abortions lead
to loss of pregnancy.

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INEVITABLE ABORTION

• vaginal bleeding, cramps, and cervical

dilation
• Expulsion of the POC is imminent.

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• DIAGNOSIS
– Speculum exam reveals blood coming from an
open cervical os
– Menstrual-like cramps typically occur

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• MANAGEMENT
– Surgical evacuation of the uterus
– Rh typing—D immunoglobulin (RhoGAM) is
administered to Rh negative, unsensitized patients
to prevent isoimmunization.

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• Inevitable abortion is different from
threatened
abortion because it has cervical dilation.

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INCOMPLETE ABORTION

• passage of some, but not all, POC from the

cervical os

• DIAGNOSIS
– Cramping and heavy bleeding
– Enlarged, boggy uterus
– Dilated internal os with POC present in the
endocervical canal or vagina

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MANAGEMENT

• Stabilization
– IV fluids and oxytocin if heavy bleeding is present
• Blood typing and crossmatching for possible
transfusion
• Rh typing
• POC are removed from the endocervical
canal and uterus with ring forceps.
• Suction dilation and curettage (D&C)

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COMPLETE ABORTION

• complete passage of POC

• DIAGNOSIS
– Uterus is well contracted.
– Cervical os may be closed.
– Pain has ceased.

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• MANAGEMENT
– Examine all POC for completeness and
characteristics.
– Between 8 and 14 weeks
• curettage is necessary
• large possibility that the abortion was incomplete.
– Observe patient for further bleeding and fever.

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MISSED ABORTION

• POC are retained after the fetus has expired

• DIAGNOSIS
– pregnant uterus fails to grow, and symptoms of
pregnancy have disappeared.
– Intermittent vaginal bleeding/spotting/brown
discharge and a firm, closed cervix
– Decline in quantitative beta-hCG
– US confirms lack of fetal heartbeat.

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• MANAGEMENT
– Although most women will spontaneously deliver a
dead fetus within 2 weeks
– psychological stress imposed by carrying a dead
fetus
– dangers of coagulation defects favor the practice
of labor induction and early delivery

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• Check fibrinogen level, partial thromboplastin
time (PTT), antibody screen, and ABO blood
type.
• Evacuate the uterus (suction D&C in first
trimester)
• induce labor with IV oxytocin and cervical
dilators or prostaglandin E2 suppositories.
• Administer RhoGAM to Rh-negative,
unsensitized patients 

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PRETERM LABOR

• after 20 weeks AOG and before 37 completed

weeks AOG.
• Contractions less than 10 mins apart
• progressive cervical dilatation of 2cm
• effacement of 75%

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Risk Factors

• Multiple gestation
• History of previous labor &/or delivery
• Abdominal surgery during current pregnancy
• Uterine anomaly
• History of cone biopsy
• History of abortion
– >2 1st trimester abortions or
– >1 2nd trimester abortion
• Fetal/maternal malformation

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• Maternal age
• Poor nutritional status
• Poor, irregular pre-natal care
• Smoking
• Drug use

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Nursing Management
• Provide accurate information on the
status of the fetus and labor
• Encourage visits from family
especially other children and
friends
• Plan for a daily rest period

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Medical Management
• Goal is to prevent the delivery of a preterm infant
– Bed rest in a left lateral position
– Hydration with IVF
– Tocolytic therapy (Ritodrine, Isoxuprine, Terbutaline)
– Side effects
• ↑ PR and Blood volume
• ↓BP

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Medical Management
• Laboratory exam done before giving the meds
– CBC
– Electrolytes
– Glucose
– BUN, Crea
– PT, PTT

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PREMATURE RUPTURE OF
MEMBRANES
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• spontaneous rupture of fetal membranes
before the onset of labor
• can occur at term (PROM) or preterm
(PPROM).

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• multiple pregnancy
• Chorioamnionitis
• breech presentation
• fetal distress in labor

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Etiology

• Unknown but hypothesized:

– Vaginal and cervical infections
– Incompetent cervix
– abnormal membranes
– nutritional deficiencies

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Risks

• Prolonged rupture of membranes:

– The rupture of membranes > 18 to 24 hours
before labor
– Patients who do not go into labor immediately will
have prolonged rupture of membranes
– at increasing risk of infection as the duration of
rupture increases

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Complications:

• Chorioamnionitis and other infections

• Neonatal infection
• Umbilical cord prolapse

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if preterm PROM

• Prematurity
• Oligohydramnios
– occurs at < 24 weeks
– risk of oligohydramnios
– may cause pulmonary hypoplasia
– Survival at this age is low

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Diagnosis of Rupture of Membranes
(ROM)
• A digital exam should not be performed, as it
increases the risk of infection:
• Sterile speculum examination:
– Visualize extent of cervical effacement and dilation
– exclude prolapsed cord or protruding fetal
extremity.

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• Pool test
– Identify fluid coming from the cervix or pooled in
the posterior fornix of the vagina → supports
diagnosis of PROM.
• Nitrazine test
– Put fluid on nitrazine paper, which turns blue if
fluid is alkaline
– Alkaline pH indicates fluid is amniotic.

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• Ferning test
– A swab from the posterior fornix is smeared on a
slide, allowed to dry, and examined under a
microscope for “ferning”
– + for amniotic fluid.

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Management of All PROM Patients

• Evaluate patient for chorioamnionitis

– common etiology of PROM
• Fever > 38 °C
• leukocytosis
• maternal/fetal tachycardia
• uterine tenderness
• malodorous vaginal discharge

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Management of All PROM Patients

• Gram stain and culture of amniotic fluid to

assess for chorioamnionitis
– If positive, delivery is performed despite GA
– antibiotics are initiated (ampicillin, gentamicin)

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• begin ampicillin and/or erythromycin
prophylaxis.
• Amniotic fluid assessment of L:S ratio
– for lung maturity
• Perform ultrasound to assess
– gestational age
– position of baby
– Level of fluid.

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• If < 34 weeks
– give steroids to decrease incidence of RDS

• Expectant management

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Terms:

• ROM:
– Rupture of membranes
• PROM:
– Premature rupture of membranes (ROM before the
onset of labor)
• PPROM:
– Preterm (< 37 weeks) premature rupture of
membranes
• Prolonged rupture of membranes:
– Rupture of membranes that lasts for 18 hrs
Management
• Tocolytic therapy
– used until fetal lungs have
– 2 doses of Betamethasone given
– delivery is delayed for at least 24hrs
– Evaluate amount and odor of amniotic fluid
– Do not perform internal examination

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• Place patient on disposal pad
– to collect leaking fluid
– Change pads every 2 hrs or more
frequently as needed
– fetal heart rate q2
– maternal temperature q2
– PR, RR, BP, and uterine tenderness
every 4 hrs
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PREGNANCY INDUCED HYPERTENSION

– PIH
– Toxemia of pregnancy

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PREGNANCY-INDUCED HYPERTENSION
(PIH)

• hypertension during pregnancy in a

previously normotensive woman
– normal blood pressure prior to 20 weeks’
gestation
• Mild:
– Systolic ≥ 140 mm Hg and/or diastolic ≥ 90 mm
Hg
• Severe:
– Systolic > 160 mm Hg and/or diastolic > 110 mm
Hg (same as chronic HTN)
PREGNANCY-INDUCED HYPERTENSION
(PIH)

• Subsets of PIH
1. Preeclampsia
- Renal involvement leads to proteinuria
- Hypertension
- edema
2. Eclampsia
CNS involvement leads to seizures.
PREGNANCY INDUCED HYPERTENSION

• Actual cause is UK
• Theory :
– exposure to chorionic villi for the first
time
– large amounts of chorionic villi

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CONTRIBUTING FACTORS

• nulligravida
• adolescents and women over 35
• Multigravida with multiple gestations
• Multigravida with history of chronic
hypertension, DM, renal disease

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CLINICAL MANIFESTATIONS
• Hypertension
– BP of 140/90 mmHg or greater
• Proteinuria
– 300mg or more in 24 hr
• Edema
– non-dependent
– present after 8-12 hrs of bed rest
• Weight gain
– more than 2 lb in 1 week or
– 6 lbs in 1 month
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MANAGEMENT

• Evaluate BP in sitting and left lateral position

• Check the protein level of urine
• Evaluate edema after 12 hrs or more of bed
rest

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MANAGEMENT

• Evaluate presence of:

– epigastric pain
– visual changes
– level of consciousness
– headache
• Evaluate weight gain

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• Evaluate for signs of abruptio placenta
• Urine output at least 300ml or more/ voiding
• Position patient to left lateral position
• Magnesium sulfate
– to prevent and treat convulsions
– decreases the neuromuscular irritability
– depresses the CNS

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• MgSO4 is administered IV with a
LD of 3-4 gm
– followed by hourly doses of 1-4 gm
– irritating to the veins

– IM administration
• 5 gm in each hip every 4 hrs
• z-tract

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• Urine output monitored
– to avoid toxicity
• Deep Tendon Reflexes (DTR)
should be evaluated

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• Magnesium level should be 4-7.5 mEq/L
• Calcium gluconate- antidote
• Hydralazine (Apresoline)
– relaxes the arterioles and stimulates cardiac
output
– Drug of choice for hypertension

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ANTIHYPERTENSIVE AGENTS USED IN
PREGNANCY

• Short-Term Control
– Hydralazine: IV or PO
– vasodilator
– SE: headache, palpitations

– Labetalol: IV or PO
– nonselective beta-1 and alpha-1 blocker
– SE: Headache and tremor
ECLAMPSIA

Management
• Long-Term Control
– Methyldopa:
• sympatholytic
• SE: fluid retention

– Nifedipine:
• calcium channel blocker

– Atenolol:
• PO
• selective beta-1 blocker
• Diazepam may be used if
convulsions occur
• Severe complication of PIH is the
HELLP syndrome
– Hemolysis
– Elevated Liver enzymes
– Low Platelet

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RH INCOMPATIBILITY AND
PREGNANCY
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What Is Rh?

• The surface of the human red blood cell

(RBC) may or may not contain a Rhesus (Rh)
antigen
• Rhesus +
• Half of all antigens in a fetus come from the
father, and half come from the mother

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• Hemolytic Disease of the Newborn (HDN)
• Erythroblastosis Fetalis

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The Problem with Rh Sensitization

• The parental combination you must worry

about:
– Mother Rh− and father Rh+
• If the pregnant female
– Rh−
– fetus is Rh+
– may become sensitized to the Rh antigen and
develop antibodies
– These antibodies cross the placenta and attack
the fetal RBCs → fetal RBC hemolysis.

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Sensitization

• Amniocentesis
• Miscarriage/threatened abortion
• Vaginal bleeding
• Placental abruption/previa
• Delivery
• Abdominal trauma
• Cesarean section
• External version

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Screening

• indirect Coombs’ test

• RHOGAM: TREATMENT FOR EXPOSURE

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Screening

• If the Rh− mother is exposed to fetal blood,

RhoGAM is given

• RhoGAM
– is RhIgG
– IgG that will attach to the Rh antigen
– prevent immune response by the mother

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Maternal Antibodies causes:

• Fetal RBC hemolysis

• Anemia
• Fetal hyperbilirubinemia
• Kernicterus
• Heart failure
• Edema
• ascites

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Managing the Unsensitized Rh−

• Antibody screen should be done at 0, 24 to

28 weeks.
• If negative
– give 300 μg of RhIgG to prevent maternal
development of antibodies
– 28 weeks AOG
• At birth
– determine if baby is Rh+
– if so, give postpartum RhIgG

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Management of the Sensitized Rh−
Patient
• Perform antibody screen at 0, 12 to 20
weeks.
• Check the antibody titer.
– If titer remains stable at < 1:16, the likelihood of
HDN is low.
– If the titer is > 1:16 and/or rising, the likelihood of
HDN is high.

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• Amniocentesis begins at 16 to 20 weeks’ GA
• Fetal cells are analyzed for Rh status.

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Cardiac disease

– as a complication in about 1% of all

pregnancies
– outcome of the pregnancy depends
on the functional capacity of the
maternal heart

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NEW YORK HEART ASSOCIATION FUNCTIONAL
CLASSIFICATION OF CARDIAC DISEASE

CLASS I No functional limitation of activity.

No symptoms of cardiac
decompensation with activity.

CLASS II Mild amount of functional limitation.

Patients are asymptomatic at rest.
Ordinary physical activity
results in symptoms.

CLASS III Limitation of most physical activity.

Asymptomatic at rest
Minimal physical activity results in
symptoms.

12/08/21 79
NEW YORK HEART ASSOCIATION FUNCTIONAL
CLASSIFICATION OF CARDIAC DISEASE

CLASS IV Severe limitation of physical activity

results in symptoms.
Patients may be symptomatic at rest
heart failure at any point of pregnancy.

CLASS V If patient is on ionotropic support,

ventilator, Assisted circulation or having
comprised renal or pulmonary function
necessitating dialysis/EMCO to maintain
vital signs.

The criteria committee of the New York Heart Association, Nomenclature and criteria for diagnosis of diseases of heart and
great vessels, Edi 8, New York Association,1979.

12/08/21 80
– most women in class 1 and 2
• able to handle the physiologic demands of pregnancy
– cardiac status is carefully monitored throughout pregnancy
– monitor for signs of cardiac decompensation
• crackles at lung base
• cough
• hemoptysis
• dyspnea on exertion
• cyanosis
• labored respiration
• increased pulse
• edema of face, ankles and hands
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Management

– Class 1 and 2
• 10 hrs of rest at night
– 30 mins after every meal
• Weight gain limited to 24 lb
• Diet: high in iron, low sodium
• No heavy work permitted
• Medications are used as needed
– to control symptoms
• Relief of pain and anxiety
– primary goal during labor
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– Class 1 and 2
• Vaginal delivery
– delivery method of choice
• During the postpartum
– VS are closely monitored for signs of CHF
• Contraception is stressed

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– Class 3
• 1st trimester
– counseled regarding a therapeutic abortion
• if the pregnancy continues
– Treatment with class 1 and 2 +
– hospitalization with strict bed rest for most of the
duration of the pregnancy
• vaginal delivery is preferred
• VS closely monitored for signs of CHF

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– Class 4
• same care with the preceeding class
• woman has CHF for most of the
pregnancy and is treated as such
• delivery and postpartum periods
– especially critical

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• Semi-fowler’s position
• Left side lying position
• evaluate fetal growth weekly
• measure the fundal height
• evaluate FHR daily
• evaluate weight weekly

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GESTATIONAL DIABETES

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DIABETES MELLITUS
• Gestational DM
• Body unable to produce enough insulin
to meet the needs for glucose
metabolism
• pregnancy is diabetogenic state

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• Pregestational diabetes—patient had DM
before pregnancy

• Gestational diabetes—patient develops

diabetes only during pregnancy.
– classified as type A according to White
classification.
– White classification A1—controlled with diet
– White classification A2—requires insulin

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Screening

• Screening is controversial, but tests often

used are:
• Glucose challenge test
– at 26 to 28 weeks:
– Give 50-mg glucose load (nonfasting state).
– Draw glucose blood level 1 hour later
– > 140 is high (a 3-hour glucose tolerance test is
then required to diagnose GDM).
– If ≥ 200, patient is diagnosed with GDM type A1
and a diabetic diet is initiated.

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• 3-Hour glucose tolerance test
– if glucose challenge test is > 140 and < 200
– Draw fasting glucose level
• norma l(n) < 95
– Give 100-g glucose load.
– Draw glucose levels at
• 1 hour (n < 180)
• at 2 hours (n < 155)
• at 3 hours (n < 140)
– Positive for gestational diabetes if 2/4 high values

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Risk Factors

• Be extra careful to test:

– Previous or family history of gestational diabetes
– Obesity
– History of large babies
– History of full-term stillbirth or child with cardiac
defects

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Effects of Gestational Diabetes

• Maternal Effects
– Four times increased risk of preeclampsia
– Increased risk of bacterial infections
– Higher rate of C-section
– Increased risk of polyhydramnios
– Increased risk of birth injury

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• Fetal Effects
– Increased risk of perinatal death
– Three times increased risk of fetal anomalies
(renal, cardiac, and CNS)
– Two to three times increased risk of preterm
delivery
– Fetal macrosomia increases risk of birth injury.
– Metabolic derangements (hypoglycemia,
hypocalcemia)

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Management

• Good glucose control:

• Prepregnancy glucose levels should be
maintained during pregnancy with insulin.
• Glucose control should be checked at each
prenatal visit.

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Starting at 32 to 34 weeks:

• Fetal monitoring:
– Ultrasonography at 16 to 20 weeks’ GA
– For fetal growth, GA, amniotic fluid volume
• Nonstress test and amniotic fluid index
testing weekly to biweekly
• Biophysical profile

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Starting at 32 to 34 weeks:

• Contraction stress test

– oxytocin challenge test
• Early elective delivery:
– Fetal macrosomia must be ruled out with
ultrasonography.

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• If fetal weight is > 4,500 g
– elective cesarean section should be considered to
avoid shoulder dystocia
– Unless there is an obstetric complication, induction
of labor and vaginal delivery are done.

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• Onset during pregnancy
– second or third trimester
– Due to hormones secreted by the placenta that
inhibit the action of insulin

100
DIABETES MELLITUS

• Clinical Manifestations
– 3 p’s and weight loss
– blood glucose level >140 mg/dl at 24-28 wks
– glucosuria
– urine positive for ketones
– history of monilial infection
– GCT with 50gm glucose
– re-evaluating after 1 hr (24th-28th AOG)

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DIABETES MELLITUS

• Management
– aim is to control the glucose level
• maintain a state of euglycemia
– diet, exercise and insulin
– insulin administration in the morning

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DIABETES MELLITUS

– wear cotton underwear

– wipe the perineal area from front to back
only
– report any symptoms such
• vaginal burning or itching
• burning or pain on urination

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ECTOPIC PREGNANCY
(EXTRAUTERINE PREGNANCY)
• implantation of the blastocyst anywhere other
than the endometrial lining of the uterine
cavity
• It is a medical emergency

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• Ectopic pregnancy is the leading cause of
pregnancy-related death during T1

Diagnose and treat before tubal rupture occurs

to decrease the risk of death!

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Etiology/Risk Factors

• Fallopian tube transport malfunction due

to:
– Infection such as Chlamydia and gonorrhea (50%)
– Previous ectopic pregnancy
– Previous tubal surgery
– Abdominal surgery resulting in adhesions
– Endometriosis
– Congenital abnormalities (often from
diethylstilbestrol [DES] exposure)
– Pregnancy with intrauterine device in place

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• Assisted reproduction:
– Ovulation-inducing drugs
– In vitro fertilization

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Symptoms and Diagnosis

• Amenorrhea
• irregular vaginal bleeding
• Adnexal tenderness or mass
• US evidence of an adnexal mass without
intrauterine gestation
• An adnexal gestational sac with a fetal pole
and cardiac activity

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• Less-than-normal increase in hCG
• A serum progesterone level lower than
normal for patients with an intrauterine
pregnancy (i.e., < 25 ng/mL)
• Laparoscopy shows an adnexal mass or
abdominal gestation.

110
• Signs of Rupture
– Shock
– Bleeding
– Increased abdominal pain

111
Management

• There are two options of treatment:

– Operative
• Laparoscopy or laparotomy with salpingostomy
• segmental resection if the tube is to be retained
• salpingectomy if the tube requires removal

112
• Medical
– Intramuscular methotrexate (prevents DNA
synthesis via its antifolate actions)
– Patient is monitored as an outpatient.
– 67 to 100% effective

113
• If ruptured, always stabilize with IV fluids,
blood replacement

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DISSEMINATED INTRAVASCULAR
COAGULATION (DIC)

• or consumptive coagulopathy
• pathological condition associated with
inappropriate activation of the coagulation
and fibrinolytic system.

117
DISSEMINATED INTRAVASCULAR
COAGULATION (DIC)

• Most commonly associated with one of the

following disease states:
– Fetal demise
– Amniotic fluid embolism
– Preeclampsia–eclampsia
– Placental abruption

118
Pathophysiology

• In pathologic states (i.e., via thromboplastin

production from dead POC), the coagulation
cascade is activated
• results in consumption of platelets and
coagulation factors.
• Fibrin deposition in small vessels results in
bleeding and circulatory obstruction.

119
Diagnosis

• Physical exam
– multiple bleeding points associated with purpura
and petechiae.

• Lab evaluation
– thrombocytopenia
– hypofibrinogenemia
– Elevated prothrombin time
– increased fibrin split products.

120
Management

• Supportive therapy
– to correct/prevent shock, acidosis, and tissue
ischemia
• prompt termination of pregnancy.

121
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Gestational Trophoblastic Neoplasias
(GTN)
• HYDATIDIFORM MOLE
• Complete Mole
• A placental (trophoblastic) tumor forms when
a maternal ova devoid of DNA
• is “fertilized” by the paternal sperm:

123
• Karyotype:
– Most have karyotype 46XX, resulting from sperm
penetration and subsequent DNA replication.
– Some have 46XY, believed to be due to two
paternal sperms simultaneously penetrating the
ova.

124
Partial Mole

• A mole with a fetus or fetal parts.

• Women with partial (incomplete) molar
pregnancies tend to present later than those
with complete moles:
• Karyotype:
– Usually 69XXY
– contains both maternal and paternal DNA

125
Invasive Mole

• A hydatidiform mole that invades the

myometrium
• It is by definition malignant
• treatment involves complete metastatic
workup and appropriate malignant/metastatic
therapy

126
• HISTOLOGY OF HYDATIDIFORM MOLE
– Trophoblastic proliferation
– Hydropic degeneration (swollen villi)
– Lack/scarcity of blood vessels

127
• SIGNS AND SYMPTOMS
– Passage of vesicles (look like grapes)
– Preeclampsia < 20 weeks
– Abnormal painless bleeding in first trimester

128
• DIAGNOSIS
– hCG > 100,000 mIU/mL
– Absence of fetal heartbeat
– Ultrasound- “snowstorm” pattern
– Pathologic specimen—grapelike vesicles

129
• Treatment of Complete or Partial Moles
– Dilation and curettage (D&C)
• to evacuate and terminate pregnancy
– Follow-up with the workup to rule out invasive
mole (malignancy)
– Chest x-ray (CXR) to look for lung mets
– Liver function tests to look for liver mets

130
• Weekly hCG level:
– hCG level should decrease and return to normal
within 2 months
– If the hCG level rises, does not fall, or falls and
then rises again
• molar pregnancy is considered malignant
• metastatic workup and chemotherapy is necessary.
• Contraception should be used during the 1-
year follow-up.

131
• Metastatic Workup
– CXR
– computed tomography (CT) of brain, lung, liver,
kidneys

132
Treatment (For Nonmetastatic Molar
Pregnancies)

• Chemotherapy
– methotrexate or actinomycin-d (as many cycles as
needed until hCG levels return to normal)
or
• Total abdominal hysterectomy +
chemotherapy (fewer cycles needed)

• Treatment for metastatic molar pregnancy is

the same as for choriocarcinoma

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PELVIC INFLAMMATORY DISEASE
(PID)
• Inflammation of the female upper genital tract
(uterus, tubes, ovaries, ligaments)
• caused by ascending infection from the
vagina and cervix

138
• Common Causative Organisms
– Neisseria gonorrhoeae
– Chlamydia trachomatis
– Escherichia coli, Bacteroides

139
• Diagnosis
– Physical Exam
– Abdominal tenderness
– Adnexal tenderness
– Cervical motion tenderness

140
Lab Results and Other Possible Exam
Signs

• +/− Fever
• Gram-positive staining
• Pelvic abscess
• Elevated white count
• Purulent cervical discharge

141
Laparoscopy

• “gold standard” for diagnosis

• usually employed only in cases unresponsive
to medical treatment.

142
Risk Factors

• Multiple sexual partners

• New sex partner(s)
• Unprotected intercourse
• Concomitant history of sexually transmitted
disease

143
Criteria for Hospitalization

• Pregnancy
• Peritonitis
• Gastrointestinal (GI) symptoms
– nausea
– vomiting
• Abscess (tubo-ovarian or pelvic)
• Uncertain diagnosis

144
Treatment

• Inpatient
• Cefotetan + doxycycline
– preferred for chlamydia
• Clindamycin + gentamicin
– preferred for abscess

145
• Outpatient
• Ofloxacin + metronidazole
• Ceftriaxone + doxycycline
– preferred for chlamydia (because of doxycycline)
• Sexual partners are treated also

146
Infections during Pregnancy

Sexually Transmitted
Disease
CHLAMYDIA

• Frequently seen with gonorrhea

• May result to
– SGA
– low birth weight
– ectopic pregnancy
– PROM
– Preterm labor
– Amnionitis
• Effects :
– Neonatal Sepsis, conjunctivitis & Chlamydial pneumonia
148
CHLAMYDIA

• an infection of the genitourinary (GU) tract, GI

tract, conjunctiva, nasopharynx
• Chlamydia trachomatis, an obligate
intracellular bacteria.

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Clinical Manifestations

• Asymptomatic
• Mucopurulent discharge
• Cervicitis
• Urethritis PID
• Trachoma
– conjunctivitis resulting in eyelash hypercurvature
and eventual blindness from corneal abrasions
• Fitz-Hugh–Curtis syndrome

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• SEROTYPES L1–L3
– lymphogranuloma venereum.
• Primary lesion
– painless papule on genitals
• Secondary stage
– Lymphadenitis
• Tertiary stage
– rectovaginal fistulas
– rectal strictures

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Diagnosis

• Microimmunofluorescence test (MIF

– measures antichlamydia immunoglobulin
• M (IgM) titers
• Titer > 1:64 is diagnostic.
• Isolation in tissue culture
• Enzyme immunoassay

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Treatment

• Doxycyline or azithromycin/erythromycin
• CREDE’S PROPHYLAXIS
– newborn

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SYPHILIS

• Cause : Treponema Pallidum

• May result to
– fetal demise
– congenital malformation
– Hutchinson's triad
• deafness
• Hutchinson's teeth
– centrally notched
– widely-spaced peg-shaped upper central incisors
• interstitial keratitis (IK)
– inflammation of the cornea
– can lead to corneal scarring and potentially blindness.

• Treatment : Penicillin
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Presentation

• Syphilis has various stages of manifestation

that present in different ways:
• Primary syphilis
– painless hard chancre of the vulva, vagina, or
cervix
– or even anus, tongue, or fingers
– usually appearing 1 month after exposure
– Spontaneous healing after 1 to 2 months

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• Secondary syphilis
– generalized rash (often palms and soles)
– condyloma lata
– mucous patches with lymphadenopathy
– fever
– Malaise
– usually appearing 1 to 6 months after primary
chancre
– Spontaneous regression after about 1 month

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• Tertiary syphilis
– presents years later
– with skin lesions
– bone lesions (gummas)
– cardiovascular lesions (e.g., aortic aneurysms)
– central nervous system (CNS) lesions (e.g., tabes
dorsalis)

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Diagnosis

• rapid plasma reagin (RPR) or Venereal

Disease Research Laboratory (VRDL)
– These are nonspecific and can give positive
results for many conditions

• Treponemal test (FTA-ABS)

– a very specific test, performed if RPR is positive.
– Visualization of spirochetes on darkfield
microscopy is an additional test available.

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Treatment

• Penicillin G for all stages, though in differing

doses
• Doxycycline, if penicillin allergic

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HUMAN PAPILLOMAVIRUS (HPV)

• causes genital warts

• condylomata acuminata
• Subtypes 6 and 11
– not associated with cervical or penile cancer.
• Subtypes 16, 18, 31, and 33
– associated with cervical and penile cancer.

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Presentation

• Warts of various sizes

– sometimes described as cauliflower-like
– external genitalia, anus, cervix, or perineum

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Diagnosis

• Warts are diagnosed by visualization.

• Cervical dysplasia caused by HPV infection is
screened via Pap smear.

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Treatment

• Condylomata acuminata
– Cryosurgery
– laser ablation
– trichloroacetic acid

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CHANCROID

• Presentation
– papule on external genitalia that becomes a
painful ulcer (unlike syphilis, which is painless)
– with a gray base
– Inguinal lymphadenopathy also is possible.

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Etiology

• Haemophilus ducreyi

• Diagnosis
– Gram stain of ulcer or inguinal node aspirate
showing gram-negative rods

• Treatment
– Ceftriaxone, erythromycin, or azithromycin

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VAGINITIS

• inflammation of the vagina

• often resulting in increased discharge and/or
pruritus
• usually caused by an identifiable microbe

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Etiology

• Antibiotics
– destabilize the normal balance of flora
• Douche
– raises the pH
• Intercourse
– raises the pH
• Foreign body
– serves as a focus of infection and/or inflammation

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Diagnostic Characteristics

• Clinical characteristics
• Quality of discharge
• pH
– secretions applied to test strip reveal pH of
discharge.
• “Whiff” test
– combining vaginal secretions with 10% KOH
– Amines released will give a fishy odor
– indicating a positive test.

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Bartholin’s Abscess

• occur when the main duct draining Bartholin’s

gland is occluded
• usually occurs due to infection
• Inflammatory symptoms generally arise from
infection and can be treated with antibiotics.

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• TREATMENT
– Incision and drainage and marsupialization
• suturing the edges of the incised cyst to prevent
reocclusion
– Or
– Ward catheter
• a catheter with an inflatable tip left in the gland for 10 to
14 days to aid healing

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GONORRHEA

• Most common STD in 15-24 age group

• Usually asymptomatic
• May result to :
– Chorioamionitis
– preterm delivery
– PROM
– IUGR
• Effects : sepsis & conjunctivitis

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GONORRHEA

• An infection of the urethra, cervix, pharynx, or

anal canal, caused by the
• gram-negative diplococcus, Neisseria
gonorrhoeae

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Presentation

• Asymptomatic
• Dysuria
• Endocervicitis
• Vaginal discharge
• Pelvic inflammatory disease (PID)

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Diagnosis

• Culture in Thayer–Martin agar (gold standard)

• Gonazyme (enzyme immunoassay)

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Treatment

• Ceftriaxone
or
• Ciprofloxacin + doxycycline
or
• Azithromax
• Treat partners.

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GOOD DAY!!!

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