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IMLE Preparatory Course

Lecture 53
Obstetrics and Gynecology

Medical and Obstetric


Complications of Pregnancy
Medical Complications of Pregnancy
Hyperemesis Gravidarum
Gestational Diabetes
Hypertension
Preeclampsia and Eclampsia
Antepartum Hemorrhage
Hyperemesis Gravidarum
 Persistent vomiting not related to other causes, acute
starvation (usually large ketonuria), and weight loss
(usually at least a 5% ↓ from prepregnancy weight).
 Occurs in 0.5–2.0% of pregnancies.
 More common in first pregnancies, multiple
gestations, and molar pregnancies.
 ↑ β-hCG and ↑ estradiol have been implicated in its
pathophysiology
Hyperemesis Gravidarum Diagnosis
 Distinguish from “morning sickness,” acid reflux,
gastroenteritis, hyperthyroidism, and neurologic
conditions.

 Rule out molar pregnancy: Check β-hCG level


and ultrasound.

 Determine severity: Evaluate for ketonemia,


ketonuria, hyponatremia, and hypokalemic,
hypochloremic metabolic alkalosis. Measure liver
enzymes, serum bilirubin, and serum amylase/lipase.
Hyperemesis Gravidarum Treatment
 First step: Administer vitamin B6.
 Second step: Doxylamine (an antihistamine) PO.
 Third step: Promethazine or dimenhydrinate
PO/PR.
 If severe: Metoclopramide, ondansetron,
prochlorperazine, or promethazine IM/PO.
 If dehydrated: IV fluids, IV nutritional
supplementation, and dimenhydrinate IV.
Diabetes during pregnancy
 One of most common medical problems seen in OB
 Pre-gestational Diabetes
 White Classification
 Increased risk for end-organ damage
 Gestational Diabetes
 Affects 3-5% of gravidas
 Accounts for 90% of diabetic pregnancies
 Defined as carbohydrate intolerance with its initial onset or
recognition during pregnancy
 > 50% develop overt diabetes later in life
White Classification
Class Onset Duration Vascular Disease
A Any Any None
B > 20 yrs < 10 yrs None
C 10-19 yrs 10-19 yrs None
D < 10 yrs > 20 yrs Benign Retinopathy
F Any Any Nephropathy
R Any Any Proliferative Retinopathy
H Any Any Heart Disease
RT Any Any Renal Transplant
Diabetes-Related Pregnancy
Complications
Non-diabetic % Diabetic (GDM) %

Pre-eclampsia 8 12
Stillbirth 5.7 10.4 (4.7)
Neonatal mortality 4.7 12.2 (3.3)
Macrosomia 10 25-42
Shoulder Dystocia 5-7 31
Anomalies 2-3 7-9
Diabetic Embryopathy
 Incidence 6-10% (vs 3% in general population)
 Related to HbA1c

Anomaly Risk Ratio Percent Risk


Cardiac Defects 18x 8.5%
VSD
Transposition of great vessels
Hypoplastic left heart
CNS Anomalies 16x 5.3%
Anencephaly 13x
Spina Bifida 20x
Holoprosencephaly
Caudal Regression
All Anomalies 8x 18.4%
Diabetic Embryopathy

Major congenital
Initial Maternal
Malformations
HbA1c
(%)

≤ 7.9 3.2

8.9 - 9.9 8.1

≥ 10 23.5
Screening for Gestational Diabetes
 Screening Criteria
 1 hour glucose with 50-g load
 140 mg/dl: 10-15% need 3 hour, 80% sensitivity
 135 mg/dl: 20-25% need 3 hour, 98% sensitivity

 High risk population


 Obesity
 Personal history of GDM
 FMHx of Diabetes
 Prior macrosomic infant
 High ethnic prevalence
Diagnosis
 First step: One-hour 50-g glucose
challenge test; venous plasma glucose is
measured one hour later (at ).
 Values ≥ 140 mg/dL are considered
abnormal.
 Next step: Confirm with an oral three-
hour (100-g) glucose tolerance test
showing any two of the following: fasting >
95 mg/dL; one hour > 180 mg/dL; two
hours > 155 mg/dL; three hours > 140
mg/dL
At what gestational age should laboratory
testing for gestational diabetes (50 Gr glucose
challange test) be performed?

A. 10-16 weeks
B. 20-24 weeks
C. 24-28 weeks
D. 33-36 weeks
At what gestational age should laboratory
testing for gestational diabetes (50 Gr glucose
challange test) be performed?

A. 10-16 weeks
B. 20-24 weeks
C. 24-28 weeks
D. 33-36 weeks
A pregnant woman not previously known to be diabetic,
who is at 26 weeks’ gestation, had a routine 50-g (GTT)
with a 1- hour blood glucose value of 144 mg/dL. A
follow-up 100-g, 3-hour oral GTT revealed plasma values
of fasting blood sugar of 102; 1 hour, 180; 2 hours, 162;
and 3 hours, 144.You should do which of the following?

a.begin American Diabetes Association (ADA) diet and


daily glucose monitoring
b.repeat the OGTT in early or mid-third trimester
c.start oral hypoglycemic agents in the diet
d.treat the patient as one with normal gestation.
A pregnant woman not previously known to be diabetic,
who is at 26 weeks’ gestation, had a routine 50-g (GTT)
with a 1- hour blood glucose value of 144 mg/dL. A
follow-up 100-g, 3-hour oral GTT revealed plasma values
of fasting blood sugar of 102; 1 hour, 180; 2 hours, 162;
and 3 hours, 144.You should do which of the following?

a.begin American Diabetes Association (ADA)


diet and daily glucose monitoring
b.repeat the OGTT in early or mid-third trimester
c.start oral hypoglycemic agents in the diet
d.treat the patient as one with normal gestation.
Goals for Treatment
 Maintain euglycemia:
 FBS < 95 mg/dL, 2hr PP < 120 mg/dL or 1hr PP <140 mg/dL
 HBA1c < 6.0
 TX: Diet and Exercise
 Insulin
 Minimize fetal effects
 Prevent associated pregnancy complications
 Prevention of DKA
 Prevent long-term complications
 Childhood obesity
 Diabetes
 Cardiovascular disease
Prenatal Diagnostic Testing Schedule
Delivery
 White Class A2-R or Type I or II: Between 38-40 weeks
 Good dating & Document fetal lung maturity
 IOL if not in labor by 39 weeks (up to 40 weeks if cervix not
favorable)
 Maintain euglycemia during labor
 May need insulin gtt
 GDMA1: Can go to 41 weeks
 DKA: stabilize mother, finding inciting factor, do not deliver
emergently
 Cesarean Section
 Macrosomia, with EFW ≥4500
 History of shoulder dystocia
Gestational Hypertension
 Formerly known as pregnancy-induced
hypertension: Idiopathic hypertension without
significant proteinuria (<300 mg/L) that
develops at > 20 weeks gestation.

 As many as 25% of patients may go on to


develop preeclampsia.
Chronic Hypertension
 Present before conception and at < 20
weeks gestation, or may persist for > 12
weeks postpartum.

 Up to one-third of patients may develop


superimposed preeclampsia.
Gestational and Chronic Hypertension
Treatment
 Monitor BP closely and treat with appropriate
antihypertensives (e.g., methyldopa, labetalol,
nifedipine).

 Do not give ACEIs or diuretics, as


ACEIs are known to lead to uterine ischemia,
and diuretics can aggravate low plasma volume to
the point of uterine ischemia.
Before we continue….
what is the most common cause of acute
renal failure in pregnancy?

a. drug abuse
b. systemic lupus erythematus
c. preeclampsia or eclampsia
d. sickle-cell disease
e.dehydration
Before we continue….
what is the most common cause of acute
renal failure in pregnancy?

a. drug abuse
b. systemic lupus erythematus
c. preeclampsia or eclampsia
d. sickle-cell disease
e.dehydration
Preeclampsia and Eclampsia
 Preeclampsia: New-onset hypertension (SBP ≥
140 mmHg or DBP ≥ 90 mmHg) and proteinuria (>
300 mg of protein in a 24-hour period) occurring at >
20 weeks’ gestation.

 Eclampsia: New-onset grand mal seizures in


women with preeclampsia.

 HELLP syndrome (hemolytic anemia, elevated liver


enzymes, and low platelets): A variant of preeclampsia
with a poor prognosis.
Which of the following will decreased in pregnant
woman with severe preeclampsia, as compared
with pregnant women without preeclampsia?
a.response to pressor amines
b.plasma volume
c.total body sodium
d.uric acid
e.serum liver functions
Which of the following will decreased in pregnant
woman with severe preeclampsia, as compared
with pregnant women without preeclampsia?
a.response to pressor amines
b.plasma volume
c.total body sodium
d.uric acid
e.serum liver functions
Mild Preeclampsia
 Usually asymptomatic.
 BP ≥ 140/90 on two occasions > 6 hours apart.
 Proteinuria (> 300 mg/24 hrs or 1–2 positive urine
dipsticks).
 Edema.
Severe Preeclampsia
 BP > 160/110 on two occasions > 6 hours apart.
 Renal: Proteinuria (> 5 g/24 hrs or 3–4 positive
urine dipsticks) or oliguria (< 500 mL/24 hrs).
 Cerebral changes: Headache, somnolence.
 Visual changes: Blurred vision, scotomata.
 Hyperactive reflexes/clonus.
 RUQ pain.
 Hemolysis, elevated liver enzymes, thrombocytopenia
(HELLP syndrome)
Eclampsia
 The most common signs preceding an eclamptic
attack are headache, visual changes, and
RUQ/epigastric pain.

 Seizures are severe if not controlled with


anticonvulsant therapy.
Preeclampsia and Eclampsia Treatment
The only cure for preeclampsia/eclampsia is
delivery of the fetus.

Preeclampsia:
 If the patient is close to term or preeclampsia worsens, induce
delivery with IV oxytocin, prostaglandin, or amniotomy.

 If far from term, treat with modified bed rest and


expectant management.
Preeclampsia and Eclampsia Treatment
Severe preeclampsia:
 First step: Control BP with labetalol and/or hydralazine
(goal < 160/110 with a DBP of 90–100 to maintain fetal blood
flow).
 Second step: Prevent seizures with continuous
magnesium sulfate drip. Watch for signs of magnesium
toxicity (loss of DTRs, respiratory paralysis, coma). Continue
seizure prophylaxis for 24 hours postpartum.
 Treat magnesium toxicity with IV calcium gluconate.
 Third step: Deliver by induction or C-section when
mother is stable.
A woman with severe preeclampsia was given MgSO4. How is
the magnesium excreted from the body?

A. By diffusion through the lungs


B. By conjugation in the liver
C. In the urine through the kidneys
D. By secretion into the gastrointestinal tract
A woman with severe preeclampsia was given MgSO4. How is
the magnesium excreted from the body?

A. By diffusion through the lungs


B. By conjugation in the liver
C. In the urine through the kidneys
D. By secretion into the gastrointestinal tract
Preeclampsia and Eclampsia Treatment
Eclampsia:
 First step: ABCs with supplemental O2.
 Second step: Seizure control/prophylaxis with magnesium.
 If seizures recur, give IV diazepam.
 Monitor magnesium blood levels and magnesium toxicity; monitor fetal
status.
 Control BP (labetalol and/or hydralazine). Limit fluids.
 Third step: Initiate delivery if the patient is stable and convulsions
are controlled.
 Postpartum management is the same as that for preeclampsia.
 Seizures may occur antepartum (25%), intrapartum (50%), or
postpartum (25%); most occur within 48 hours after delivery
Complications
 Preeclampsia: Prematurity, fetal distress, stillbirth,
placental abruption, seizure, DIC, cerebral
hemorrhage, serous retinal detachment,
fetal/maternal death.

 Eclampsia: Cerebral hemorrhage, aspiration


pneumonia, hypoxic encephalopathy,
thromboembolic events, fetal/maternal death.
Antepartum Hemorrhage
 Defined as any bleeding that occurs after 20 weeks
gestation.

 Complicates 3–5% of pregnancies (prior to 20 weeks,


bleeding is referred to as threatened abortion).

 The most common causes are placental abruption and


placenta previa.

 Other causes include other forms of abnormal placentation (e.g.,


placenta accreta), ruptured uterus, genital tract lesions, and
trauma.
Obstetric Complications of Pregnancy

Ectopic Pregnancy
Placenta Previa, Abruptio Placentae
Intrauterine Growth Restriction
Polyhydramnios, Oligohydramnios
Rh Incompatibility
Gestational trophoblastic disease
Ectopic Pregnancy
 Any pregnancy that occurs outside of the uterine cavity

 Tubal
 Ampulla (55%)
 Isthmus (25%)
 Fimbria (17%) 97%

 Cervical
 Ovarian
 Abdominal 3%
Ectopic Sites
Ectopic Pregnacy
 1.9% of reported pregnancies

 Leading cause of pregnancy-related death in the


first trimester
 Ruptured ectopic pregnancy accounts for 10-15%
of all maternal deaths
Ectopic Pregnancy Risk Factors
 Previous tubal surgery HIGH
 Previous ectopic pregnancy
 In utero DES exposure
 Previous genital infections
 Infertility
 Current smoking
 Previous IUD use
Ectopic Pregnancy Most Common
Presentation

 Woman of reproductive age

 Abdominal pain

 Vaginal bleeding
 Approx 7 weeks after amenorrhea
Ectopic Pregnancy
Differential Diagnosis

 Acute appendicitis
 Miscarriage
 Ovarian torsion
 Pelvic inflammatory disease
 Ruptured corpus luteum cyst or follicle
 Tubo-ovarian abcess
 Urinary calculi
Ectopic Pregnancy Exam Findings

 Normal or slightly enlarged uterus

 Vaginal bleeding

 Pelvic pain with manipulation of the cervix

 Palpable adnexal mass (fallopian tube)


Ectopic Pregnancy Suspected Rupture
 Approach a woman of reproductive age
presenting with abdominal pain as a
ruptured ectopic pregnancy until proven
otherwise.

 Proceed as follows:
 First step: + pregnancy test and a
transvaginal ultrasound showing an empty
uterus.
 Second step: Confirm with a serial hCG without
appropriate hCG doubling.
Ectopic Pregnancy Diagnositc Tests
 Ultrasound (test of choice)
 No intrauterine gestational sac
 bHCG
 Do not increase appropriately
 Urine pregnancy test
 Pregnant / not pregnant
 Progesterone level (less reliable)
Ectopic Pregnancy Treatment

 Medical treatment (methotrexate) is


sufficient for small, unruptured tubal
pregnancies.

 Surgical options for salpingectomy or


salpingostomy with evacuation (laparoscopy
vs. laparotomy).
Ectopic Pregnancy Complications
 ~30% have later difficulty conceiving
 No difference between treatment options

 5-20% rate of recurrence


 32% risk of recurrence if she’s had 2
consecutive ectopic pregnancies
Placenta Previa
 Implantation of the placenta over or
near the internal os of the cervix
 Vaginal bleeding in the 2nd and 3rd
trimesters

 5/1,000 deliveries
 Maternal mortality rate of 0.03%
Placenta Previa
 Total placenta previa
 internal os is completely covered by the placenta
 Partial placenta previa
 internal os is partially covered by the placenta
 uterus enlarges, placental site moves cephalad
 Marginal placenta previa
 placenta is at the margin of the internal os
 Low-lying placenta previa
 placenta is implanted in the lower uterine segment
 edge of the placenta is near the internal os but does not reach it
Placenta Previa Risk Factors

 Prior previa
 Multiparity
 Multiple gestations
 Advanced maternal age
 Previous cesarean delivery
 Prior induced abortion
 Smoking
Placenta Previa Presentation
 History  Exam Findings
 Vaginal bleeding  Profuse hemorrhage
 Bright red and painless  Hypotension
(recurrent)  Tachycardia
 Occurs on average at 27-
 Soft and nontender uterus
32 weeks' gestation
 Normal fetal heart tones
 Contractions may or may
not occur simultaneously (usually)
with the bleeding
Placenta Previa Differential
 Abruptio Placenta
 Disseminated Intravascular Coagulation
 Pregnancy, Delivery
 Vasa previa
 Infection
 Vaginal bleeding
 Lower genital tract lesions
 Bloody show
Placenta Previa Diagnosis
 Ultrasound

 Management
 <37 weeks without hemorrhage
 expectant management
 Hemorrhage or >37 weeks and in labor
 delivery
 C-section
 trial of labor may be considered for anterior
marginal previa
Abruptio Placentae
 Separation of the normally located placenta
after the 20th week of gestation (prior to birth)

 1% of all pregnancies

 Results in compromised blood supply to the fetus


 Severity of fetal distress correlates with the degree
of placental separation
Abruptio Placentae Presentation
 Vaginal bleeding (80%)
 Abdominal or back pain and uterine
tenderness (70%)
 Fetal distress (60%)
 Abnormal uterine contractions (35%)
 Idiopathic premature labor (25%)
 Fetal death (15%)
Abruptio Placentae Diagnosis
 Severe uterine pain and tenderness
 Mild vaginal bleeding
 Hypertension (HTN)

 Difficult to identify on ultrasound


 Can help differentiate from other causes of
bleeding (i.e. placenta previa)
Abruptio Placentae (Class 0-3)

 Class 0
 Asymptomatic
 Diagnosis is made retrospectively
 organized blood clot or a depressed area
on a delivered placenta
Abruptio Placentae (Class 0-3)
 Class 1
 Mild
 ~48% of all cases
 Characteristics :
 No vaginal bleeding to mild vaginal bleeding
 Slightly tender uterus
 Normal maternal BP and heart rate
 No coagulopathy
 No fetal distress
Abruptio Placentae (Class 0-3)
 Class 2
 Moderate
 ~27% of all cases
 Characteristics:
 Vaginal bleeding: none to moderate
 Moderate-to-severe uterine tenderness with
possible tetanic contractions
 Maternal tachycardia with orthostatic changes in BP
and heart rate
 Fetal distress
 Hypofibrinogenemia (ie, 50-250 mg/dL)
Abruptio Placentae (Class 0-3)
 Class 3
 Severe
 ~24% of all cases
 Characteristics:
 vaginal bleeding: none to heavy
 Very painful tetanic uterus
 Maternal shock
 Hypofibrinogenemia (ie, <150
mg/dL)
 Coagulopathy
 Fetal death
Abruptio Placentae Causes
 Sudden decompression of
 Maternal hypertension
(44%) the uterus
 Maternal trauma (1.5-  premature rupture of
9.4%) membranes, delivery of first
 MVA, assaults, falls twin
 Cigarette smoking  Retroplacental bleeding
 Alcohol consumption from needle puncture
 Cocaine use  postamniocentesis
 Short umbilical cord  Idiopathic
 Advanced maternal age  probable abnormalities of
 Retroplacental uterine blood vessels and
fibromyoma decidua
Abruptio Placentae Complications
 Maternal  Fetal complications
complications  Hypoxia
 Hemorrhagic shock  Anemia
 Coagulopathy/DIC
 Growth retardation
 Uterine rupture
 CNS anomalies
 Renal failure
 Fetal death
 Ischemic necrosis of
distal organs (eg, hepatic,
adrenal, pituitary)
Intrauterine Growth Restriction (IUGR)
 Defined as an EFW less than the 10th percentile
for GA.

 Affected infants are commonly born to women with


systemic diseases that lead to uteroplacental insufficiency
(intrauterine infection, hypertension, anemia).

 Other risk factors include maternal substance abuse,


placenta previa, and multiple gestations.
IUGR Diagnosis
 First step: Diagnose by confirming serial fundal
height measurements with ultrasound.

 Second step: Ultrasound the fetus for EFW


(although as pregnancy advances, ultrasound fetal
weight estimates become increasingly unreliable).
IUGR Treatment
 First step: Explore the underlying etiology and
correct if possible.
 If near due date: Administer steroids (e.g.,
betamethasone) to accelerate fetal lung maturity.
 Then: Perform fetal monitoring with NST, CST,
BPP, and umbilical artery Doppler velocimetry.
 A nonreassuring status near term may prompt
delivery.
Polyhydramnios
 Abnormally high level of
amniotic fluid
 >2000 mL of fluid
 Normal: peaks at 800-
1000mL at 36-37 weeks'
gestation
 1% of pregnancies

 20% are born with


congenital anomalies
Polyhydramnios Risk Factors
 Multiple gestations
 twin to twin transfusion
 Maternal diabetes
 Fetal anomolies
 Gastrointestinal system (most common)
 Central nervous system
 swallowing dysfunction
 Cardiovascular system
 Genitourinary system
 Chromosomal abnormalities
Polyhydramnios Presentation
 Rapidly enlarging uterus
 Difficulty identifying fetal parts (Leopold’s)
 Fetal ballottement is easier
Polyhydramnios Complications
 Preterm labor and delivery (26%)
 Premature rupture of the membranes
(PROM)
 Abruptio placenta
 Malpresentation
 Cesarean delivery
 Postpartum hemorrhage
Polyhydramnios Treatment
 Etiology Specific

 Steroid therapy
 enhance fetal lung maturity if preterm labor is
expected
 Genetic counseling
 if congenital anomaly is present
Oligohydramnios
 Inadequate levels of amniotic fluid
 results in poor development of the lung
tissue and can lead to fetal death

 Affects ~4% of pregnancies


Oligohydramnios Causes
 Fetal urinary tract  Maternal problems
anomalies  Placental
 Renal agenesis insufficiency
 Polycystic kidneys  Premature rupture of
 Obstructive urinary membranes
lesion  Chronic leakage of
the amniotic fluid
 Postmaturity syndrome
 Possibly caused by a decline in
placental function
Oligohydramnios
 Fetal mortality rate is high (5-6%)

Increased risk of
 Pulmonary hypoplasia
 Meconium staining of the amniotic fluid
 Fetal heart conduction abnormalities
 Poor tolerance of labor
 Lower Apgar scores
 Fetal acidosis
 Intrauterine growth restriction (IUGR)
Oligohydramnios Complications
 Fetal distress before or during labor
 Meconium
 potential for aspiration

 Fetal infection
(prolonged rupture of the membranes)
Oligohydramnios Management
 Rule out inaccurate gestational dates.

 Treat the underlying cause if possible.

 Maternal bed rest and hydration


 promote the production of amniotic fluid
Rh Incompatibility and Sensitization
 In this condition, fetal RBCs leak into the maternal
circulation, and maternal anti-Rh IgG antibodies
form that can cross the placenta, leading to
hemolysis of fetal Rh RBCs (erythroblastosis fetalis).

 There is an ↑ risk among an Rh negative women who


have had a previous SAB or TAB as well as among those
who have undergone a previous delivery with no
RhoGAM given
Rh Incompatibility and Sensitization
 Sensitized Rh negative mothers with titers > 1:16
should be closely monitored with serial ultrasound and
amniocentesis for evidence of fetal hemolysis.

 In severe cases, initiate preterm delivery when fetal


lungs are mature.
 Prior to delivery, intrauterine blood transfusions may be
given to correct a low fetal hematocrit
Prevention
 If the mother is Rh negative at 28
weeks and the father is Rh positive
or unknown, give RhoGAM (Rh
immune globulin).
 If the baby is Rh positive, give
RhoGAM postpartum.

 Give RhoGAM to Rh negative mothers


who undergo abortion or who have had
an ectopic pregnancy, amniocentesis,
vaginal bleeding, or placenta
previa/placental abruption.
Pregnancy: Rh + fetus
Sensitization
Sensitization
Subsequent Rh + Pregnancies
Gestational Trophoblastic Disease
 A range of proliferative trophoblastic abnormalities that
can be benign or malignant.

 Complete moles: Usually result from sperm fertilization


of an empty ovum. 46,XX (paternally derived).

 Incomplete (partial) moles: Occur when a normal ovum


is fertilized by two sperm (or a haploid sperm that
duplicates its chromosomes); usually 69,XXY and
contain fetal tissue.
Gestational Trophoblastic Disease
 Presents with first-trimester
uterine bleeding (most common),
hyperemesis gravidarum,
preeclampsia/eclampsia at < 24
weeks, and uterine size greater
than dates.

 Risk factors include extremes of age (<


20 or > 40 years) and a diet deficient
in folate or beta-carotene.
GTD Diagnosis
 No fetal heartbeat is detected. Pelvic exam may reveal
enlarged ovaries (bilateral theca-lutein cysts) or expulsion of
grapelike molar clusters into the vagina.

 Labs show markedly ↑ serum β-hCG (usually > 100,000


mIU/mL), and pelvic ultrasound reveals a “snowstorm”
appearance with no gestational sac or fetus present.

 CXR may show lung metastases; D&C reveals “cluster-of-


grapes” tissue.
Transvaginal ultrasound shows a large, complex
intrauterine mass with cystic regions that have
the characteristic appearance of grapes
Gross specimen of hydatidiform mole
GTD Treatment
 Evacuate the uterus and follow with
weekly β-hCG.

 Treat malignant disease with


chemotherapy (methotrexate or dactinomycin)
and residual uterine disease with
hysterectomy.
 Chemotherapy and irradiation are highly effective
for metastases.