1. Apa hubungan trauma dan minum jamu disangkal dengan keluhan?

Herbal Medicines During Pregnancy

While herbal medications are commonly thought of as "natural" alternatives to
other medicines, they can be just as potent as some prescription medications.
Many herbs contain chemicals that will cross the placenta to your baby if taken
while you are pregnant. Some herbs have been known to cause premature
contractions if taken during pregnancy. Generally, the use of medicinal drugs
(including herbal tea) is best avoided altogether, particularly during the first
trimester. You should always talk to your health care provider before taking any
herb during pregnancy.

http://umm.edu/health/medical/pregnancy/staying-healthy-during-
pregnancy/medicines-and-herbal-remedies-during-pregnancy
 http://ejournal.litbang.depkes.go.id/index.php/MPK/article/viewFile
/1038/771

Know the no-nos. There are many herbs and supplements that benefit
pregnant women, but science has also shown us that many should not be used
during pregnancy at all.
1. Pennyroyal is a good plant to use in the garden to repel bugs, but because it
can induce abortion, pregnant women should stay away from it.
2. Saw palmetto is usually used by men, but pregnant women should be sure to
avoid it because it induces testosterone activity.
3. Black cohosh (used for menstrual problems) and blue cohosh (used for
arthritis) can induce uterine cramps and labor, and can cause premature birth.
4. Red yeast rice can lower your cholesterol, but because it boasts some of the
same properties (minus the side effects) of the pharmaceutical drug Lipitor,
pregnant women should stay off of it. Lipitor has been shown to cause problems
during pregnancy.
5. Vitex, also an herb known as chasteberry, is used by a lot of women for PMS
symptoms, and by some for treatment of infertility. Its potential effects on
hormones make it a no-go for pregnant women.
6. Red clover. This herb is commonly used during menopause to deal with hot
flashes, but it can have estrogenic effects and should be avoided during
pregnancy. Note: Tea tree oil and lavender have also been shown to have mild
estrogenic effects, but Dr. McKee says occasional use for aromatherapy or in
natural bath products shouldn't be a problem, as long as you're not ingesting
them. Do not ingest any pure essential oils, and never apply them undiluted to
your skin.
7. While these aren't supplements, Dr. McKee also instructs her patients to avoid
dying their hair and using other everyday products containing harmful
chemcials. "We absorb about 60 percent of the chemicals we use topically—dyes,
soaps, shampoos, lotions," she says. "I would be really careful about what even a
nonpregnant person should be washing with," says Dr. McKee. An easy way to
avoid some harmful chemicals is to stop using personal-care products, laundry
products, and cleaners containing synhthetic fragrances.
http://www.rodalenews.com/supplements-during-
pregnancy?page=0,1

The major problem with retrospective studies on spontaneous abortion and

general anesthesia is selection bias among cases and controls (selected for
baseline rate of spontaneous abortion). The pathologic process that warranted
surgery may have increased the patient's risk of spontaneous abortion. The
selection of control patients may be biased by the timing and sensitivity of the
pregnancy test. The risk of spontaneous abortion varies considerably by
gestational age. The earlier the patient is tested, the higher the risk of
spontaneous abortion. Most studies have not adequately matched patients by
gestational age.
The sensitivity of pregnancy tests varies considerably (eg, serum human
chorionic gonadotropin versus home urine pregnancy test). The period of
greatest discordance between serum and urine pregnancy tests is 3-6 weeks
after the first day of the last menstrual period, and this is also the period of
greatest risk of spontaneous abortion after a positive test result. Most studies
have not evaluated timing and technique of pregnancy diagnosis.
The lessons of the thalidomide and diethylstilbestrol tragedies raise concerns
about teratogenic effects of anesthetic agents. Risk may be species-agent specific
(eg, humans and thalidomide), or effects may be manifested years after exposure
(eg, genital tract abnormalities and diethylstilbestrol). Many different anesthetic
agents are used alone and in combination. Although many of the most common
agents (eg, N20, diazepam [Valium], isoflurane) have demonstrated species-
specific teratogenic risk, these results have been neither reproduced consistently
nor easily translated to the human experience. Among 8000 women who
underwent surgery during pregnancy, no increased incidence of congenital
abnormalities in the offspring was demonstrated.
After 13 weeks' gestation, the major organ systems of the fetus are developed.
The risk of congenital malformation is minimal. Between 13 and 23 weeks'
gestation, the uterus is less sensitive to the stimulating effects of surgery, and
minimal risk of preterm labor exists. In addition, should a preterm delivery occur
as the result of surgery, heroic methods, such as cesarean delivery, rarely are
considered because no chance of neonatal survival exists. Therefore, if trauma
surgery must be performed during pregnancy, the period between 13 and 23
weeks' gestation is optimal.
After 24 weeks' gestation, trauma surgery can produce 3 complications—supine
hypotension, neurodevelopmental delay in the offspring, and preterm birth.
After 16 weeks' gestation, when the uterus becomes an extra pelvic organ, the
enlarging uterus has an increasing potential to obstruct return venous flow in
the inferior vena cava when the pregnant woman is supine. In the late third
trimester, symptomatic hypotension (characterized by syncope, nausea, and
vomiting) occurs in 10% of healthy pregnant women. This risk is higher when
the patient's cardiovascular system is challenged further by sepsis (eg,
appendicitis), hypovolemia (eg, trauma), or sympathetic blockage (eg, epidural
analgesia). After 16 weeks' gestation, place all patients undergoing surgery in the
left lateral tilt position to reduce venous and arterial compression by the
pregnant uterus.
A significant proportion of fetal neurodevelopment occurs in the third trimester.
Insult through the primary disease process, surgical complications, anesthetic
agents, or anesthetic management (eg, respiratory support) has the potential to
affect neonatal and childhood neurodevelopment. Animal models have been used
to investigate whether anesthetic agents can cause neurodevelopmental
handicap. Exposure to local anesthetic or inhalation of anesthetics has been
associated with neurodevelopmental deficits in rodents. Transfer to the human
experience is fraught with error. The few studies that have been performed on
children exposed to general anesthesia in utero have yielded conflicting data.
http://emedicine.medscape.com/article/435224-overview#showall

Trauma has become the most frequent cause of maternal death in the United
States of America. Although maternal mortality due to other causes such as
infection, hemorrhage, hypertension, and thromboembolism, has declined over
the years, the number of maternal deaths due to penetrating trauma, suicide,
homicide and motor vehicle accidents has risen steadily. Accidental injuries
occur in 6 to 7 % of all pregnant patients. Penetrating trauma accounts for as
many as 36 % of maternal deaths. In the case of gunshot wounds to the pregnant
abdomen, overall maternal mortality is low ( 3.9 % ). Fetal mortality, on the
other hand, is high, ranging between 40 and 70 %.

Although the initial assessment and management priorities for resuscitation of

the injured pregnant patient are the same as those for other traumatized
patients, the specific anatomic and physiologic changes that occur during
pregnancy may alter the response to injury and hence necessitate a modified
approach to the resuscitation process. The main principle guiding therapy must
be that resuscitating the mother will resuscitate the fetus.

Fetal Physiology
The effect of trauma on pregnancy depends on the gestational age of the fetus,
the type and severity of the trauma, and the extent of disruption of normal
uterine and fetal physiology. The survival of the fetus depends on adequate
uterine perfusion and delivery of oxygen. The uterine circulation has no
autoregulation which implies that uterine blood flow is related directly to
maternal systemic blood pressure, at least until the mother approaches
hypovolemic shock. At that point, peripheral vasoconstriction will further
compromise uterine perfusion. Once obvious shock develops in the mother, the
chances of saving the fetus are about 20 %.

If fetal oxygenation or perfusion are compromised by trauma, the response

of the fetus may include bradycardia or tachycardia, a decrease in the
baseline variability of the heart rate, the absence of normal accelerations
in the heart rate, or recurrent decelerations. It should be noted that an
abnormal fetal heart rate may be the first indication of an important
disruption in fetal homeostasis. During trauma resuscitation, evaluation of
the fetus should begin with auscultation of heart tones and continuous
recording of the heart rate.

Trauma to the uterus (direct or indirect) can also injure the myometrium
and destabilize decidual lysosomes, releasing arachidonic acid that can
cause uterine contractions, and perhaps inducing premature labor.

Maternal Physiology
Increases in cardiac output and blood volume begin early in the first trimester
and are 30-40% above the nonpregnant state by 28 weeks. This relative
hypervolemic state and hemodilution is protective for the mother because fewer
red blood cells are lost during hemorrhage. The hypervolemia prepares the
mother for the blood loss that accompanies vaginal delivery (500 ml) or
cesarean section (1000 ml). However, almost 40% of maternal blood volume
may be lost prior to the manifestation of signs of maternal shock.

Despite the increase in blood volume and cardiac output, the parturient is
susceptible to hypotension from aortocaval compression in the supine
position. Only about 10% of pregnant patients at term develop symptoms
of shock in the supine position, but fetal compromise can be occurring even
in the asymptomatic mother. Left uterine displacement increases cardiac
output by 30% and restores circulation. Uterine displacement must be
maintained at all times during resuscitation, transport and perioperatively
for nonobstetrical surgery.

As the uterus enlarges, the diaphragm rises about 4 cm and the diameter of
the chest enlarges by 2 cm, increasing the substernal angle by 50%. Care
should be taken to consider these anatomic changes when thoracic
procedures such as thoracostomies are being performed. The most
important respiratory change during pregnancy is the decrease in
functional residual capacity (FRC). Beginning in the second trimester, there
is a 20% decrease in FRC coupled with a 20% increase in oxygen
consumption. In addition, 30% of parturients have airway closure during
normal tidal ventilation in the supine position. All these changes
predispose to rapid falls in PaO2 during periods of apnea or airway
obstruction. Hence, supplemental oxygen is always indicated for these
patients in the resuscitation room. Minute ventilation increases at term by
50% due to an increase in tidal volume, so normal PaCO2 falls to 30-32
mmHg with a slight compensatory decrease in plasma bicarbonate levels.

Increased levels of progesterone and estrogen inhibit gastrointestinal

motility. In addition, there is a decrease competency of the
gastroesophageal sphincter, which increases the potential for aspiration.
As the uterus enlarges, it displaces the intestines upward and laterally,
stretching the peritoneum and making the abdominal physical
examination unreliable.

To accommodate both maternal and fetal metabolic and circulatory

requirements, renal blood flow increases by 25 to 50% during gestation.
Blood urea nitrogen (BUN) and serum creatinine are reduced. Also, the
kidneys enlarge by hypertrophy and hyperemia as early as the 10th week
of gestation secondary to hormonal and mechanical factors.

The neurologic changes of pregnancy include a 25 to 40% decrease in

anesthetic requirements. This means that loss of consciousness can occur
even at "sedative" doses.

Management of the Injured Pregnant Patient. Georges Desjardins MD

FRCPC, Assistant Professor of Anesthesiology
University of Miami, Miami, FL

http://www.trauma.org/archive/resus/pregnancytrauma.html

2. Mengapa pasien mengeluarkan darah sedikit2 dan nyeri perut bagian

bawah 1 minggu yll?

Vaginal bleeding during pregnancy has many causes. Some are serious, and many
aren't.

1st trimester

Possible causes of vaginal bleeding during the first trimester include:

 Miscarriage — the spontaneous loss of pregnancy before the 20th week

 Implantation bleeding — which occurs about 10 to 14 days after
conception
  Problems with the cervix, such as a cervical infection, inflamed cervix or
growths on the cervix
 Ectopic pregnancy
 Molar pregnancy — a rare occurrence in which an abnormal mass —
instead of a baby — forms inside the uterus after fertilization
2nd or 3rd trimester

Possible causes of vaginal bleeding during the second or third trimester include:

 Miscarriage (before the 20th week) or intrauterine fetal death

 Placental abruption
 Placenta previa
 Incompetent cervix — Premature opening of the cervix — which can lead to
preterm birth
 Problems with the cervix, such as a cervical infection, inflamed cervix or
growths on the cervix
 Preterm labor — which might result in light bleeding — especially when
accompanied by contractions, dull backache or pelvic pressure
 Uterine rupture, a rare but life-threatening occurrence in which the uterus
tears open along the scar line from a prior C-section
Normal vaginal bleeding near the end of pregnancy

Light bleeding, often mixed with mucous, near the end of pregnancy could be a
sign that labor is starting. Vaginal discharge that is pink or bloody is known as
the bloody show.
http://www.mayoclinic.org/symptoms/bleeding-during-
pregnancy/basics/causes/sym-20050636

Breakthrough bleeding, which happens when pregnancy hormones cover up

your usual menstrual cycle, but that cycle continues for a while. You may have
this bleeding more than once.
Implantation bleeding, which may happen when the fertilised egg implants in
your uterus (womb). It's thought that this is less common than breakthrough
bleeding.
Your softening cervix and a raw area that forms (cervical erosion or
ectropion). Bleeding can also be linked to vaginal or cervical infection, or a
harmless growth (polyp). These three conditions could all result in bleeding if
your cervix has been chafed, for example, during sex.

http://www.babycentre.co.uk/x2313/why-do-i-have-light-bleeding-in-early-
pregnancy#ixzz3IH9T0Zz9
 3. Mengapa didapatkan konjungtiva palpebra anemis?

Physiologic anemia in pregnancy is due to a dilutional effect of plasma volume

increasing by 50% but red blood cell volume increasing by only 18-30%. Thus,
the average hematocrit level is 32-34% and is at its nadir around the 30th to
34th week of gestation. Because the average estimated blood loss is
approximately 500 mL for a vaginal delivery and 1000 mL for a cesarean
delivery, no change in hemodynamic parameters occurs because of these
preemptive adaptations. The uterus, which grows from 70 g to 1000 g, enlarges
into the peritoneal cavity after the 12th week of pregnancy. Although it now
becomes more susceptible to injury, it also provides protection for other
maternal abdominal organs such as the small bowel. The bladder is also moved
into the abdomen by the uterus in the second and third trimesters, and the
ureters become dilated (right > left). Gastrointestinal tract motility decreases.

http://emedicine.medscape.com/article/796979-overview#showall
 http://ceaccp.oxfordjournals.org/content/3/3/65.full.pdf+html

During pregnancy, your body produces more blood to support the growth of
yourbaby. If you're not getting enough iron or certain other nutrients, your body
might not be able to produce the amount of red blood cells it needs to make this
additional blood.
It's normal to have mild anemia when you are pregnant. But you may have more
severe anemia from low iron or vitamin levels or from other reasons.
Anemia can leave you feeling tired and weak. If it is severe but goes untreated, it
can increase your risk of serious complications like preterm delivery.
Iron-deficiency anemia. This type of anemia occurs when the body doesn't
have enough iron to produce adequate amounts of hemoglobin. That's a protein
in red blood cells. It carries oxygen from the lungs to the rest of the body.
In iron-deficiency anemia, the blood cannot carry enough oxygen to tissues
throughout the body.
Iron deficiency is the most common cause of anemia in pregnancy.
Folate-deficiency anemia. Folate, also called folic acid, is a type of B vitamin.
The body needs folate to produce new cells, including healthy red blood cells.
During pregnancy, women need extra folate. But sometimes they don't get
enough from their diet. When that happens, the body can't make enough normal
red blood cells to transport oxygen to tissues throughout the body.
Folate deficiency can directly contribute to certain types of birth defects, such as
neural tube abnormalities (spina bifida) and low birth weight.
Vitamin B12 deficiency. The body needs vitamin B12 to form healthy red blood
cells. When a pregnant woman doesn't get enough vitamin B12 from her diet, her
body can't produce enough healthy red blood cells. Women who don't eat meat,
poultry, dairy products, and eggs have a greater risk of developing vitamin B12
deficiency, which may contribute to birth defects, such as neural tube
abnormalities, and could lead to preterm labor.
Blood loss during and after delivery can also cause anemia.
http://www.webmd.com/baby/guide/anemia-in-pregnancy

4. Interpretasi dari hb? Klasifikasi dan nilai normal dari HB?

http://www.who.int/vmnis/indicators/haemoglobin.pdf

http://cghealth.nic.in/ehealth/2013/QA_website/5StandardTreatme
ntGuidelines/Anaemia.pdf

5. Apa hubungan darah tidak disertai gelembung berisi cairan dan

riwayat pingsan (-) dengan keluhan? Apa perbedaan perdarahan
fisiologis dan patologis?
 Bleeding in the First Trimester

About 20% of women have some bleeding during the first 12 weeks of
pregnancy. Possible causes of first trimester bleeding include:
Implantation bleeding. You may experience some normal spotting within the
first six to 12 days after you conceive as the fertilized egg implants itself in the
lining of the uterus. Some women don't realize they are pregnant because they
mistake this bleeding for a light period. Usually the bleeding is very light and
lasts from a few hours to a few days.
Miscarriage. Because miscarriage is most common during the first 12 weeks of
pregnancy, it tends to be one of the biggest concerns with first trimester
bleeding. About half of women who bleed in pregnancy eventually miscarry, but
that doesn't necessarily mean that if you're bleeding you've lost the baby,
especially if you don't have any other symptoms.
Other symptoms of miscarriage are strong cramps in the lower abdomen and
tissue passing through the vagina.
Ectopic pregnancy. In an ectopic pregnancy, the fertilized embryo implants
outside of the uterus, usually in the fallopian tube. If the embryo keeps growing,
it can cause the fallopian tube to burst, which can be life-threatening to the
mother. Although ectopic pregnancy is potentially dangerous, it only occurs in
about 2% of pregnancies.
Other symptoms of ectopic pregnancy are strong cramps or pain in the lower
abdomen, and lightheadedness.
Molar pregnancy (also called gestational trophoblastic disease). This is a very
rare condition in which abnormal tissue grows inside the uterus instead of a
baby. In rare cases, the tissue is cancerous and can spread to other parts of the
body.
Other symptoms of molar pregnancy are severe nausea and vomiting, and rapid
enlargement of the uterus.
Additional causes of bleeding in early pregnancy include:

 Cervical changes. During pregnancy, extra blood flows to the cervix. Intercourse
or a Pap test, which cause contact with the cervix, can trigger bleeding. This type
of bleeding isn't cause for concern.
 Infection. Any infection of the cervix, vagina, or a sexually transmitted infection
(such as chlamydia, gonorrhea, or herpes) can cause bleeding in the first
trimester.

Bleeding in the Second and Third Trimesters

Abnormal bleeding in late pregnancy may be more serious, because it can signal
a problem with the mother or baby. Call your doctor as soon as possible if you
experience any bleeding in your second or third trimester.
Possible causes of bleeding in late pregnancy include:
 Placenta previa. This condition occurs when the placenta sits low in the uterus
and partially or completely covers the opening of the birth canal. Placenta previa
is very rare in the late third trimester, occurring in only one in 200 pregnancies.
A bleeding placenta previa, which can be painless, is an emergency requiring
immediate medical attention.
Bleeding in the Second and Third Trimesters continued...

Placental abruption. In about 1% of pregnancies, the placenta detaches from

the wall of the uterus before or during labor and blood pools between the
placenta and uterus. Placental abruption can be very dangerous to both the
mother and baby.
Other signs and symptoms of placental abruption are abdominal pain, clots from
the vagina, tender uterus, and back pain.
Uterine rupture. In rare cases, a scar from a previous C-section can tear open
during pregnancy. Uterine rupture can be life-threatening, and requires an
emergency C-section.
Other symptoms of uterine rupture are pain and tenderness in the abdomen.
Vasa previa. In this very rare condition, the developing baby's blood vessels in
the umbilical cord or placenta cross the opening to the birth canal. Vasa previa
can be very dangerous to the baby because the blood vessels can tear open,
causing the baby to bleed severely and lose oxygen.
Other signs of vasa previa include abnormal fetal heart rate and excessive
bleeding.
Premature labor. Vaginal bleeding late in pregnancy may just be a sign that
your body is getting ready to deliver. A few days or weeks before labor begins,
the mucus plug that covers the opening of the uterus will pass out of the vagina,
and it will usually have small amounts of blood in it (this is known as "bloody
show"). If bleeding and symptoms of labor begin before the 37th week of
pregnancy, contact your doctor right away because you might be in preterm
labor.
Other symptoms of preterm labor include contractions, vaginal discharge,
abdominal pressure, and ache in the lower back.
Additional causes of bleeding in late pregnancy are:

 Injury to the cervix or vagina

 Polyps
 Cancer

http://www.webmd.com/baby/guide/bleeding-during-
pregnancy?page=2

6. Mengapa dokter melakukan tes penunjang tes HCG?

HCG appears in the blood and urine of pregnant women as early as 10 days after
conception. Quantitative HCG measurement helps determine the exact age of the
fetus. It can also diagnose abnormal pregnancies, such as ectopic pregnancies,
molar pregnancies, and possible miscarriages. It is also used as part of a
screening test for Down syndrome.

This test is also done to diagnose abnormal conditions not related to pregnancy
that can raise HCG level.

 Normal Results

HCG level rises rapidly during the first trimester of pregnancy and then slightly
declines.

 What Abnormal Results Mean

 Higher-than-normal level may indicate:
1. Normal pregnancy
2. More than one fetus -- for example, twins or triplet
3. Choriocarcinoma of the uterus
4. Hydatidiform mole of the uterus
5. Ovarian cancer
6. Testicular cancer (in men)
 Lower-than-normal levels may indicate:
1. Fetal death
2. Incomplete miscarriage
3. Threatened spontaneous abortion (miscarriage)
4. Ectopic pregnancy

http://www.nlm.nih.gov/medlineplus/ency/article/003510.htm

7. Mengapa pasien mengeluh nyeri perut bagian bawah? Namun saat

dilakukan pemeriksaan nyeri tekan bawah (-)?

8. Apa kemungkinan etiologi pada skenario?

 http://repository.usu.ac.id/bitstream/123456789/23479/4/Chapter
%20II.pdf
9. Apa hubungan amenore 2 bulan dengan keluhan?
10. Apa hubungan keluhan dengan OUE yang masih tertutup?
 http://repository.usu.ac.id/bitstream/123456789/23479/4/Chapter
%20II.pdf

http://repository.usu.ac.id/bitstream/123456789/23479/4/Chapter
%20II.pdf

11. Fluxus +2 apa interpretasinya? Interpretasi lain?

 12. Mengapa dokter melakukan px USG?
Pemeriksaan USG (Ultrasonografi). Hal ini membantu dokter untuk
memeriksa detak jantung janin dan menentukan apakah embrio
berkembang normal.
http://repository.usu.ac.id/bitstream/123456789/23479/4/Chapter
%20II.pdf

13. DD?

The pathophysiology of a spontaneous miscarriage may be suggested by its

timing. Chromosomal defects are commonly seen in spontaneous miscarriages,
especially those that occur during 4-8 weeks' gestation. Genetic etiologies are
common in early first-trimester loss but may be seen throughout gestation.
Trisomy chromosomes are the most common chromosomal anomaly. Insufficient
or excessive hormonal levels usually result in spontaneous miscarriage before
10 weeks' gestation. Infectious, immunologic, and environmental factors are
generally seen in first-trimester pregnancy loss. Anatomic factors are usually
associated with second-trimester loss. Factor XIII deficiency and a complete or
partial deficiency of fibrinogen are associated with recurrent spontaneous
miscarriage.[1]
A prospective study by Jayasena et al indicated that in in asymptomatic pregnant
women at 6 weeks’ gestation or more, low plasma levels of the hormone
kisspeptin are associated with an increased miscarriage risk.[2]
A spontaneous miscarriage is a process that can be divided into 4 stages, as
follows: threatened, inevitable, incomplete, and complete.
 Threatened miscarriage: Vaginal bleeding, abdominal/pelvic pain of any
degree, or both during early pregnancy represents a threatened miscarriage.
Approximately a fourth of all pregnant women have some degree of vaginal
bleeding during the first 2 trimesters. About half of these cases progress to an
actual miscarriage.[3] Bleeding and pain accompanying threatened miscarriage
is usually not very intense. Threatened miscarriage rarely presents with severe
vaginal bleeding. On vaginal examination, the internal cervical os is closed and
no cervical motion tenderness or tissue is found. Diffuse uterine tenderness,
adnexal tenderness, or both may be present. Threatened miscarriage is defined
by the absence of passing/passed tissue and the presence of a closed internal
cervical os. These findings differentiate threatened miscarriage from later
stages of a miscarriage.
 Inevitable miscarriage: Vaginal bleeding is accompanied by dilatation of the
cervical canal. Bleeding is usually more severe than with threatened
miscarriage and is often associated with abdominal pain and cramping.
 Incomplete miscarriage: Vaginal bleeding may be intense and accompanied by
abdominal pain. The cervical os may be open with products of conception being
passed, or the internal cervical os may be closed. Ultrasonography is used to
reveal whether some products of conception are still present in the uterus.
 Complete miscarriage: Patients may present with a history of bleeding,
abdominal pain, and tissue passage. By the time the miscarriage is complete,
 bleeding and pain usually have subsided. Ultrasonography reveals a vacant
uterus. Diagnosis may be confirmed by observation of the aborted fetus with
the complete placenta, although caution is recommended in making this
diagnosis without ultrasonography because it can be difficult to determine if
the miscarriage is complete.
 Patients with spontaneous miscarriage usually present to the ED with vaginal
bleeding, abdominal pain, or both.
 Vaginal bleeding may vary from slight spotting to a severe life-threatening
hemorrhage. The patient's history should include the number of pads or
tampons used. Hasan et al found that heavy bleeding in the first trimester,
particularly when associated with abdominal pain, is associated with higher
risk of miscarriage.[7]
 Presence of blood clots or tissue may be an important sign indicating
progression of spontaneous miscarriage.
 Abdominal pain is usually located in the suprapubic area or in one or both
lower quadrants.
 Pain may radiate to the lower back, buttocks, genitalia, and perineum.
 The patient's history should also include the following:
 Date of last menstrual period (LMP)
 Estimated length of gestation
 Sonogram results, if previously performed
 Bleeding disorders
 Previous miscarriage or elective abortions
 Other symptoms, such as fever or chills, are more characteristic of a septic
miscarriage or abortion.
 Consider any woman of childbearing age with vaginal bleeding pregnant until
proven otherwise.
Physical
 Pelvic examination should focus on determining the source of bleeding.
 Blood from cervical os
 Intensity of bleeding
 Presence of clots or tissue fragments
 Cervical motion tenderness (presence increases suspicion for ectopic
pregnancy)
 Status of internal cervical os: open indicates inevitable or possibly incomplete
miscarriage; closed indicates threatened miscarriage.
 Uterine size and tenderness, as well as adnexal tenderness or masses
 Signs of threatened miscarriage:
 Vital signs should be within reference ranges unless infection is present or
hemorrhage has caused hypovolemia.
 The abdomen usually is soft and nontender.
 Pelvic examination reveals a closed internal cervical os. The bimanual
examination is unremarkable.
 Signs of incomplete miscarriage:
 The cervix may appear dilated and effaced, or it may be closed.
 Bimanual examination may reveal an enlarged and soft uterus.
 On pelvic examination, products of conception may be partially present in the
uterus, may protrude from the external os, or may be present in the vagina.
Bleeding and cramping usually persist.
 Complete miscarriage: On pelvic examination, the cervix should be closed, and
the uterus should be contracted.
 Missed miscarriage:
 Vital signs usually are within reference ranges. Abdominal examination may or
may not reveal a palpable uterus. If palpable, the uterus usually is small for the
presumed gestational age.
 Fetal heart tones are inaudible or unseen on sonogram.
 The cervical os is closed upon pelvic examination. The uterus may feel soft and
enlarged.
Causes
Causes of first- and second-trimester miscarriage
 Embryonic abnormalities account for 80-90% of first-trimester miscarriages.
 Chromosomal abnormalities are the most common cause of spontaneous
miscarriage. More than 90% of cytogenic and morphologic errors are
eliminated through spontaneous miscarriage.
 Chromosomal abnormalities have been found in more than 75% of fetuses that
miscarry in the first trimester.
 The rate of chromosomal abnormalities increases with age, with a steep
increase in women older than 35 years.
 Trisomy chromosomes commonly are encountered, with trisomy 16 accounting
for approximately a third of chromosomal abnormalities in early pregnancy.
 Maternal factors account for the majority of second-trimester miscarriages.
 Chronic maternal health factors:
 Maternal insulin-dependent diabetes mellitus (IDDM): As many as 30% of
pregnancies in women with IDDM result in spontaneous miscarriage,
predominantly in patients with poor glucose control in the first trimester.
 Severe hypertension
 Renal disease
 Systemic lupus erythematosus (SLE)
 Hypothyroidism and hyperthyroidism
 Acute maternal health factors:
 Infections (eg, rubella, cytomegalovirus [CMV], and mycoplasmal,
ureaplasmal, listerial, toxoplasmal infections)
 Trauma
 Severe emotional shock
Other factors that may contribute to miscarriage
 Exogenous factors:
 Alcohol
 Tobacco
 Cocaine and other illicit drugs
 Anatomic factors: Congenital or acquired anatomic factors are reported to occur
in 10-15% of women who have recurrent spontaneous miscarriages.
 Congenital anatomic lesions include müllerian duct anomalies (eg, septate
uterus, diethylstilbestrol [DES]-related anomalies). Müllerian duct lesions
usually are found in second-trimester pregnancy loss.
 Anomalies of the uterine artery with compromised endometrial blood flow are
congenital.
  Acquired lesions include intrauterine adhesions (ie, synechiae), leiomyoma,
and endometriosis.
 Other diseases or abnormalities of the reproductive system that may result in
miscarriage include congenital or acquired uterine defects, fibroids, cervical
incompetence, abnormal placental development, or grand multiparity.
 Endocrine factors:
 Endocrine factors potentially contribute to recurrent miscarriage in 10-20% of
cases.
 Luteal phase insufficiency (ie, abnormal corpus luteum function with
insufficient progesterone production) is implicated as the most common
endocrine abnormality contributing to spontaneous miscarriage.
 Hypothyroidism, hypoprolactinemia, poor diabetic control, and polycystic
ovarian syndrome are contributive factors in pregnancy loss.
 Infectious factors:
 Presumed infectious etiology may be found in 5% of cases.
 Bacterial, viral, parasitic, fungal, and zoonotic infections are associated with
recurrent spontaneous miscarriage.
 Immunologic factors:
 Immunologic factors may contribute in up to 60% of recurrent spontaneous
miscarriages.
 Both the developing embryo and the trophoblast may be considered
immunologically foreign to the maternal immune system.
 Antiphospholipid antibody syndrome generally is responsible for more second-
trimester pregnancy losses than first-trimester losses.
Miscellaneous factors
Miscellaneous factors may account for up to 3% of recurrent spontaneous
miscarriages. Other contributing factors implicated in sporadic and recurrent
spontaneous abortions include environment, drugs, placental abnormalities,
medical illnesses, and male-related causes.
Gestational exposure to nonaspirin NSAIDs may increase the risk for
miscarriage. Nakhai-Pour et al identified 4705 women who had spontaneous
abortions by 20 weeks’ gestation. Each case was matched to 10 control subjects
(n=47,050) who did not have a spontaneous abortion. In the women who had a
miscarriage, 352 (7.5%) were exposed to a nonaspirin NSAID, whereas NSAID
exposure was lower (1213 exposed [2.6%]) in women who did not have a
miscarriage.[8]
On the other hand, a study by Daniel et al suggested that for the most part,
gestational exposure to nonaspirin NSAIDs does not increase the risk for
spontaneous miscarriage. In a study cohort that included 65,457 women who
conceived during the study period, a total of 6508 (9.9%) experienced
spontaneous miscarriage. Exposure to NSAIDs was not found to be an
independent risk factor for miscarriage, with the exception of indomethacin,
which, the study indicated, is significantly associated with spontaneous abortion
following first-trimester exposure.[9]
 KET

Ectopic pregnancy is the result of a flaw in human reproductive physiology that

allows the conceptus to implant and mature outside the endometrial cavity,
which ultimately ends in the death of the fetus. Without timely diagnosis and
treatment, ectopic pregnancy can become a life-threatening situation.[1]
Signs and symptoms
The classic clinical triad of ectopic pregnancy is as follows:
 Abdominal pain
 Amenorrhea
 Vaginal bleeding
Unfortunately, only about 50% of patients present with all 3 symptoms.
Patients may present with other symptoms common to early pregnancy (eg,
nausea, breast fullness). The following symptoms have also been reported:
 Painful fetal movements (in the case of advanced abdominal pregnancy)
 Dizziness or weakness
 Fever
 Flulike symptoms
 Vomiting
 Syncope
 Cardiac arrest
The presence of the following signs suggests a surgical emergency:
 Abdominal rigidity
 Involuntary guarding
 Severe tenderness
 Evidence of hypovolemic shock (eg, orthostatic blood pressure changes,
tachycardia)
Findings on pelvic examination may include the following:
 The uterus may be slightly enlarged and soft
 Uterine or cervical motion tenderness may suggest peritoneal inflammation
 An adnexal mass may be palpated but is usually difficult to differentiate from
the ipsilateral ovary
 Uterine contents may be present in the vagina, due to shedding of endometrial
lining stimulated by an ectopic pregnancy
Diagnosis
Serum β-HCG levels
In a normal pregnancy, the β-HCG level doubles every 48-72 hours until it
reaches 10,000-20,000mIU/mL. In ectopic pregnancies, β-HCG levels usually
increase less. Mean serum β-HCG levels are lower in ectopic pregnancies than in
healthy pregnancies.
No single serum β-HCG level is diagnostic of an ectopic pregnancy. Serial serum
β-HCG levels are necessary to differentiate between normal and abnormal
 pregnancies and to monitor resolution of ectopic pregnancy once therapy has
been initiated.
The discriminatory zone of β-HCG (ie, the level above which an imaging scan
should reliably visualize a gestational sac within the uterus in a normal
intrauterine pregnancy) is as follows:
 1500-1800 mIU/mL with transvaginal ultrasonography, but up to 2300
mIU/mL with multiple gestates[2]
 6000-6500 mIU/mL with abdominal ultrasonography
Absence of an intrauterine pregnancy on a scan when the β-HCG level is above
the discriminatory zone represents an ectopic pregnancy or a recent abortion.
Ultrasonography
Ultrasonography is probably the most important tool for diagnosing an
extrauterine pregnancy.
Visualization of an intrauterine sac, with or without fetal cardiac activity, is often
adequate to exclude ectopic pregnancy.[3]
Transvaginal ultrasonography, or endovaginal ultrasonography, can be used to
visualize an intrauterine pregnancy by 24 days postovulation or 38 days after
the last menstrual period (about 1 week earlier than transabdominal
ultrasonography). An empty uterus on endovaginal ultrasonographic images in
patients with a serum β-HCG level greater than the discriminatory cut-off value
is an ectopic pregnancy until proved otherwise.
Color-flow Doppler ultrasonography improves the diagnostic sensitivity and
specificity of transvaginal ultrasonography, especially in cases in which a
gestational sac is questionable or absent.
Laparoscopy
Laparoscopy remains the criterion standard for diagnosis; however, its routine
use on all patients suspected of ectopic pregnancy may lead to unnecessary risks,
morbidity, and costs. Moreover, laparoscopy can miss up to 4% of early ectopic
pregnancies.
Laparoscopy is indicated for patients who are in pain or hemodynamically
unstable.
See Workup for more detail.
Management
Therapeutic options in ectopic pregnancy are as follows:
 Expectant management
 Methotrexate
 Surgery
Expectant management
 Candidates for successful expectant management should be asymptomatic and
have no evidence of rupture or hemodynamic instability. Candidates should
demonstrate objective evidence of resolution (eg, declining β-HCG levels).
Close follow-up and patient compliance are of paramount importance, as tubal
rupture may occur despite low and declining serum levels of β-HCG.
Methotrexate
Methotrexate is the standard medical treatment for unruptured ectopic
pregnancy. A single-dose IM injection is the more popular regimen. The ideal
candidate should have the following:
 Hemodynamic stability
 No severe or persisting abdominal pain
 The ability to follow up multiple times
 Normal baseline liver and renal function test results
Absolute contraindications to methotrexate therapy include the following:
 Existence of an intrauterine pregnancy
 Immunodeficiency
 Moderate to severe anemia, leukopenia, or thrombocytopenia
 Sensitivity to methotrexate
 Active pulmonary or peptic ulcer disease
 Clinically important hepatic or renal dysfunction
 Breastfeeding
 Evidence of tubal rupture
Surgical treatment
Laparoscopy has become the recommended surgical approach in most cases.
Laparotomy is usually reserved for patients who are hemodynamically unstable
or for patients with cornual ectopic pregnancies; it also is a preferred method for
surgeons inexperienced in laparoscopy and in patients in whom a laparoscopic
approach is difficult.
See Treatment and Medication for more detail.
Image library

An endovaginal sonogram demonstrates

an early ectopic pregnancy. An echogenic ring (tubal ring) found outside of the
uterus can be seen in this view.
Background
Ectopic pregnancy refers to the implantation of a fertilized egg in a location
outside of the uterine cavity, including the fallopian tubes (approximately
97.7%), cervix, ovary, cornual region of the uterus, and abdominal cavity. Of
tubal pregnancies, the ampulla is the most common site of implantation (80%),
followed by the isthmus (12%), fimbria (5%), cornua (2%), and interstitia (2-
3%). (See the image below.)

Sites and frequencies of ectopic

pregnancy. By Donna M. Peretin, RN. (A) Ampullary, 80%; (B) Isthmic, 12%; (C)
Fimbrial, 5%; (D) Cornual/Interstitial, 2%; (E) Abdominal, 1.4%; (F) Ovarian,
0.2%; and (G) Cervical, 0.2%.

In ectopic pregnancy (the term ectopic is derived from the Greek word ektopos,
meaning out of place), the gestation grows and draws its blood supply from the
site of abnormal implantation. As the gestation enlarges, it creates the potential
for organ rupture, because only the uterine cavity is designed to expand and
accommodate fetal development. Ectopic pregnancy can lead to massive
hemorrhage, infertility, or death (see the images below). (See Etiology and
Prognosis.)

A 12-week interstitial gestation, which

eventually resulted in a hysterectomy. Courtesy of Deidra Gundy, MD,
Department of Obstetrics and Gynecology at Medical College of Pennsylvania and
Hahnemann University (MCPHU). A 12-
week interstitial gestation, which eventually resulted in a hysterectomy.
Courtesy of Deidra Gundy, MD, Department of Obstetrics and Gynecology at
Medical College of Pennsylvania and Hahnemann University (MCPHU).

In 1970, the Centers for Disease Control and Prevention (CDC) began to record
statistics regarding ectopic pregnancy, reporting 17,800 cases. By 1992, the
number of ectopic pregnancies had increased to 108,800. Concurrently,
however, the case-fatality rate decreased from 35.5 deaths per 10,000 cases in
1970 to 2.6 per 10,000 cases in 1992. (See Epidemiology.)
The increased incidence of ectopic pregnancy has been partially attributed to
improved ability in making an earlier diagnosis. Ectopic pregnancies that
previously would have resulted in tubal abortion or complete, spontaneous
reabsorption and remained clinically undiagnosed are now detected. (See
Presentation, DDx, and Workup.)
In the 1980s and 1990s, medical therapy for ectopic pregnancy was
implemented; it has now replaced surgical therapy in many cases.[4, 5, 6] As the
ability to diagnose ectopic pregnancy improves, physicians will be able to
intervene sooner, preventing life-threatening sequelae and extensive tubal
damage, as well as, it is hoped, preserving future fertility. (See Treatment and
Medication.)
Implantation sites
The faulty implantation that occurs in ectopic pregnancy occurs because of a
defect in the anatomy or normal function of either the fallopian tube (as can
result from surgical or infectious scarring), the ovary (as can occur in women
undergoing fertility treatments), or the uterus (as in cases of bicornuate uterus
or cesarean delivery scar). Reflecting this, most ectopic pregnancies are located
in the fallopian tube; the most common site is the ampullary portion of the tube,
where over 80% of ectopic pregnancies occur. (See Etiology.)
Nontubal ectopic pregnancies are a rare occurrence, with abdominal pregnancies
accounting for 1.4% of ectopic pregnancies and ovarian and cervical sites
accounting for 0.2% each. Some ectopic pregnancies implant in the cervix (<
1%), in previous cesarean delivery scars, or in a rudimentary uterine horn;
although these may be technically in the uterus, they are not considered normal
intrauterine pregnancies.[7]
 About 80% of ectopic pregnancies are found on the same side as the corpus
luteum (the old, ruptured follicle), when present.[8] In the absence of modern
prenatal care, abdominal pregnancies can present at an advanced stage (>28 wk)
and have the potential for catastrophic rupture and bleeding.[9]
Etiology
An ectopic pregnancy requires the occurrence of 2 events: fertilization of the
ovum and abnormal implantation. Many risk factors affect both events; for
example, a history of major tubal infection decreases fertility and increases
abnormal implantation.
Multiple factors contribute to the relative risk of ectopic pregnancy. In theory,
anything that hampers or delays the migration of the fertilized ovum (blastocyst)
to the endometrial cavity can predispose a woman to ectopic gestation. The
following risk factors have been linked to ectopic pregnancy:
 Tubal damage - Which can be the result of infections such as pelvic
inflammatory disease (PID) or salpingitis (whether documented or not) or can
result from abdominal surgery or tubal ligation or from maternal in utero
diethylstilbestrol (DES) exposure
 History of previous ectopic pregnancy
 Smoking - A risk factor in about one third of ectopic pregnancies; smoking may
contribute to decreased tubal motility by damage to the ciliated cells in the
fallopian tubes
 Altered tubal motility - As mentioned, this can result from smoking, but it can
also occur as the result of hormonal contraception; progesterone-only
contraception and progesterone intrauterine devices (IUDs) have been
associated with an increased risk of ectopic pregnancy
 History of 2 or more years of infertility (whether treated or not)[10] - Women
using assisted reproduction seem to have a doubled risk of ectopic pregnancy
(to 4%), although this is mostly due to the underlying infertility[11]
 History of multiple sexual partners[10]
 Maternal age - Although this is not an independent risk factor[10]
The most logical explanation for the increasing frequency of ectopic pregnancy is
previous pelvic infection; however, most patients presenting with an ectopic
pregnancy have no identifiable risk factor.[12]
A 2009 literature review found 56 reported cases of ectopic pregnancy (by
definition), dating back to 1937, after hysterectomy.[13]
Pelvic inflammatory disease
The most common cause of PID is an antecedent infection caused by Chlamydia
trachomatis. Patients with chlamydial infection have a range of clinical
presentations, from asymptomatic cervicitis to salpingitis and florid PID. More
than 50% of women who have been infected are unaware of the exposure.
Other organisms that cause PID, such as Neisseria gonorrhoeae, also increase the
risk of ectopic pregnancy, and a history of salpingitis increases the risk of ectopic
pregnancy 4-fold. The incidence of tubal damage increases after successive
episodes of PID (ie, 13% after 1 episode, 35% after 2 episodes, 75% after 3
episodes).
Effective vaccination against Chlamydia trachomatis is under investigation. Once
clinically available, it should have a dramatic impact on the frequency of ectopic
pregnancy, as well as on the overall health of the female reproductive system.
History of previous ectopic pregnancy
After 1 ectopic pregnancy, a patient incurs a 7- to 13-fold increase in the
likelihood of another ectopic pregnancy. Overall, a patient with a previous
ectopic pregnancy has a 50-80% chance of having a subsequent intrauterine
gestation and a 10-25% chance of a future tubal pregnancy.
History of tubal surgery and conception after tubal ligation
Previous tubal surgery has been demonstrated to increase the risk of developing
ectopic pregnancy. The increase depends on the degree of damage and the extent
of anatomic alteration. Surgeries carrying higher risk of subsequent ectopic
pregnancy include salpingostomy, neosalpingostomy, fimbrioplasty, tubal
reanastomosis, and lysis of peritubal or periovarian adhesions.
Conception after previous tubal ligation also increases a women's risk of having
an ectopic pregnancy; 35-50% of patients who conceive after a tubal ligation are
reported to experience an ectopic pregnancy. Failure after bipolar tubal cautery
is more likely to result in ectopic pregnancy than is occlusion using suture, rings,
or clips. This failure is attributed to fistula formation that allows sperm passage.
In one study, 33% of pregnancies occurring after tubal ligation were ectopic;
those who underwent electrocautery and women younger than 35 years were at
higher risk.[14]
Ectopic pregnancies following tubal sterilizations usually occur 2 or more years
after sterilization rather than immediately after. In the first year, only about 6%
of sterilization failures result in ectopic pregnancy.
Smoking
Cigarette smoking has been shown to be a risk factor for ectopic pregnancy
development. Studies have demonstrated an elevated risk ranging from 1.6 to
3.5 times that of nonsmokers. A dose-response effect has also been suggested.
Based on laboratory studies in humans and animals, researchers have postulated
several mechanisms by which cigarette smoking might play a role in ectopic
pregnancies. These mechanisms include one or more of the following: delayed
ovulation, altered tubal and uterine motility, and altered immunity. To date,
however, no study has supported a specific mechanism by which cigarette
smoking affects the occurrence of ectopic pregnancy.
Use of oral contraceptives or an intrauterine device
All contraceptive methods lead to an overall lower risk of pregnancy and
therefore to an overall lower risk of ectopic pregnancy. However, among cases of
contraceptive failure, women at increased risk of ectopic pregnancy compared
with pregnant controls included those using progestin-only oral contraceptives,
progestin-only implants, or IUDs and those with a history of tubal ligation.[15]
The presence of an inert, copper-containing or progesterone IUD traditionally
has been thought to be a risk factor for ectopic pregnancy. Data from the
Contraceptive CHOICE Project demonstrated a relative risk of 3.16 for ectopic
pregnancy in women not using any form of contraception as compared with
women using the progesterone IUD.[16] Nevertheless, if a woman ultimately
conceives with an IUD in place, it is more likely to be an ectopic
pregnancy.[17] The incidence of ectopic pregnancy in IUD users is 1 in 1000 over a
5-year period.[16]
Emergency contraception (levonorgestrel, or Plan B) does not appear to lead to a
higher-than-expected rate of ectopic pregnancy.[18]
Use of fertility drugs or assisted reproductive technology
Ovulation induction with clomiphene citrate or injectable gonadotropin therapy
has been linked to a 4-fold increase in the risk of ectopic pregnancy in a case-
control study. This finding suggests that multiple eggs and high hormone levels
may be significant factors.
One study demonstrated that infertility patients with luteal phase defects have a
statistically higher ectopic pregnancy rate than do patients whose infertility is
caused by anovulation. In addition, the risk of ectopic pregnancy and heterotopic
pregnancy (ie, pregnancies occurring simultaneously in different body sites)
dramatically increases when a patient has used assisted reproductive
techniques—such as such as in vitro fertilization (IVF) or gamete intrafallopian
transfer (GIFT)—to conceive.[19]
In a study of 3000 clinical pregnancies achieved through in vitro fertilization, the
ectopic pregnancy rate was 4.5%, which is more than double the background
incidence. Furthermore, studies have demonstrated that up to 1% of pregnancies
achieved through IVF or GIFT can result in a heterotopic gestation, compared
with an incidence of 1 in 30,000 pregnancies for spontaneous conceptions.[20]
Increasing age
The highest rate of ectopic pregnancy occurs in women aged 35-44 years. A 3- to
4-fold increase in the risk of developing an ectopic pregnancy exists compared
with women aged 15-24 years. One proposed explanation suggests that aging
may result in a progressive loss of myoelectrical activity in the fallopian tube;
myoelectrical activity is responsible for tubal motility.
Salpingitis isthmica nodosum
Salpingitis isthmica nodosum is defined as the microscopic presence of tubal
epithelium in the myosalpinx or beneath the tubal serosa. These pockets of
epithelium protrude through the tube, similar to small diverticula. Studies of
serial histopathologic sections of the fallopian tube have revealed that
approximately 50% of patients treated with salpingectomy for ectopic
pregnancy have evidence of salpingitis isthmica nodosum. The etiology of
salpingitis isthmica nodosum is unclear, but proposed mechanisms include
 postinflammatory and congenital changes, as well as acquired tubal changes,
such as those observed with endometriosis.[21]
DES exposure
Before 1971, several million women were exposed in utero to DES, which was
given to their mothers to prevent pregnancy complications. In utero exposure of
women to DES is associated with a high lifetime risk of a broad spectrum of
adverse health outcomes, including infertility, spontaneous abortion, and ectopic
pregnancy.[22]
Other
Other risk factors associated with increased incidence of ectopic pregnancy
include anatomic abnormalities of the uterus such as a T-shaped or bicornuate
uterus, fibroids or other uterine tumors, previous abdominal surgery, failure
with progestin-only contraception, and ruptured appendix.
The physical examination of patients with ectopic pregnancy is highly variable
and often unhelpful. Patients frequently present with benign examination
findings, and adnexal masses are rarely found. Patients in hemorrhagic shock
from ruptured ectopic may not be tachycardic.[49]
Some physical findings that have been found to be predictive (although not
diagnostic) for ectopic pregnancy include the following:
 Presence of peritoneal signs
 Cervical motion tenderness
 Unilateral or bilateral abdominal or pelvic tenderness - Usually much worse on
the affected side
Abdominal rigidity, involuntary guarding, and severe tenderness, as well as
evidence of hypovolemic shock, such as orthostatic blood pressure changes and
tachycardia, should alert the clinician to a surgical emergency; this may occur in
up to 20% of cases. However, midline abdominal tenderness or a uterine size of
greater than 8 weeks on pelvic examination decreases the risk of ectopic
pregnancy.[50]
On pelvic examination, the uterus may be slightly enlarged and soft, and uterine
or cervical motion tenderness may suggest peritoneal inflammation. An adnexal
mass may be palpated but is usually difficult to differentiate from the ipsilateral
ovary.
The presence of uterine contents in the vagina, which can be caused by shedding
of endometrial lining stimulated by an ectopic pregnancy, may lead to a
misdiagnosis of an incomplete or complete abortion and therefore a delayed or
missed diagnosis of ectopic pregnancy.
http://emedicine.medscape.com/article/2041923-clinical#showall
MOLA HIDATIDOSA
 Gestational trophoblastic disease encompasses several disease processes that
originate in the placenta. These include complete and partial moles, placental
site trophoblastic tumors, choriocarcinomas, and invasive moles.
Almost all women with malignant gestational trophoblastic disease can be cured
with preservation of reproductive function. The following discussion is limited to
hydatidiform moles (complete and partial).
Pathophysiology
A complete mole contains no fetal tissue. Ninety percent are 46,XX, and 10% are
46,XY.[1, 2] Complete moles can be divided into 2 types:
 Androgenetic complete mole
oHomozygous
 These account for 80% of complete moles.
 Two identical paternal chromosome complements, derived from duplication
of the paternal haploid chromosomes.
 Always female; 46,YY has never been observed.
o Heterozygous
 These account for 20% of complete moles.
 May be male or female.
 All chromosomes are of parental origin, most likely due to dispermy.
 Biparental complete mole: Maternal and paternal genes are present but failure
of maternal imprinting causes only the paternal genome to be expressed.[3]
o The biparental complete mole is rare.
o A recurrent form of biparental mole, which is familial and appears to be
inherited as an autosomal recessive trait, has been described. Al-Hussaini
describes a series of 5 women with as many as 9 consecutive molar
pregnancies.[4, 5]
o Mutations in NLRP7 at 19q13.4 have been identified as causative in recurrent
molar pregnancies.[6, 7, 8]
With a partial mole, fetal tissue is often present. Fetal erythrocytes and vessels in
the villi are a common finding. The chromosomal complement is 69,XXX or
69,XXY.[9] This results from fertilization of a haploid ovum and duplication of the
paternal haploid chromosomes or from dispermy. Tetraploidy may also be
encountered. As in a complete mole, hyperplastic trophoblastic tissue and
swelling of the chorionic villi occur.
 Complete mole: The typical clinical presentation of complete molar pregnancies
has changed with the advent of high-resolution ultrasonography. Most moles are
now diagnosed in the first trimester before the onset of the classic signs and
symptoms.[21, 22]
 Vaginal bleeding: The most common classic symptom of a complete mole is
vaginal bleeding. Molar tissue separates from the decidua, causing bleeding.
The uterus may become distended by large amounts of blood, and dark fluid
may leak into the vagina. This symptom occurs in 50% of cases.
 Hyperemesis: Patients may also report severe nausea and vomiting. This is due
to extremely high levels of human chorionic gonadotropin (hCG).
 Hyperthyroidism: Signs and symptoms of hyperthyroidism can be present due
to stimulation of the thyroid gland by the high levels of circulating hCG or by a
 thyroid stimulating substance (ie, thyrotropin) produced by the
trophoblasts.[23]
 Partial mole: Patients with partial mole do not have the same clinical features as
those with complete mole. These patients usually present with signs and
symptoms consistent with an incomplete or missed abortion.
 Vaginal bleeding
 Absence of fetal heart tones
Physical
 Complete mole (See images below.)
 Size inconsistent with gestational age: A uterine enlargement greater than
expected for gestational age is a classic sign of a complete mole. Unexpected
enlargement is caused by excessive trophoblastic growth and retained blood.
However, patients present with size-appropriate enlargement or smaller-than-
expected enlargement at a similar frequency.
 Preeclampsia: Pelvic ultrasonography has resulted in the early diagnosis of
most cases of hydatidiform mole and preeclampsia is seen in less than 2% of
cases.[22]
 Theca lutein cysts: These are ovarian cysts greater than 6 cm in diameter and
accompanying ovarian enlargement. These cysts are not usually palpated on
bimanual examination but are identified by ultrasonography. Patients may
report pressure or pelvic pain. Because of the increased ovarian size, torsion is
a risk. These cysts develop in response to high levels of beta-hCG. They
spontaneously regress after the mole is evacuated, but it may take up to 12

weeks for complete regression. Theca

lutein cysts. Complete mole.

 Complete mole with an area of clot near
cervix consistent with bleeding.
 Partial mole
 Uterine enlargement and preeclampsia is reported in only 5% of patients.[24]
 Theca lutein cysts, hyperemesis, and hyperthyroidism are extremely rare.
 Twinning (See image below.)
 Twinning with a complete mole and a fetus with a normal placenta has been
reported (see image below). Cases of healthy infants in these circumstances
have been reported.[25, 9]
 Women with coexistent molar and normal gestations are at higher risk for
developing persistent disease and metastasis[26] . Termination of pregnancy is a
recommended option.
 The pregnancy may be continued as long as the maternal status is stable,
without hemorrhage, thyrotoxicosis, or severe hypertension. The patient
should be informed of the risk of severe maternal morbidity from these
complications.[27]
 Prenatal genetic diagnosis by chorionic villus sampling or amniocentesis is
recommended to evaluate the karyotype of the fetus.

Twin gestation. Complete mole and

normal twin.
Causes
A diet deficient in animal fat and carotene may be a risk factor

14. Bagaimana tatalaksana?

Semuanya saja.
Mola = kuret
Ket =
 Pemeriksaan, penegakan diagnosis, faktor resiko.gejala tanda dan
komplikasi masing2 kelainan pada perdarahan pervagina pada trimester
1.

KET

Methotrexate is an antimetabolite chemotherapeutic agent that binds to the

enzyme dihydrofolate reductase, which is involved in the synthesis of purine
nucleotides. This interferes with deoxyribonucleic acid (DNA) synthesis and
disrupts cell multiplication.
Methotrexate has long been known to be effective in the treatment of leukemias,
lymphomas, and carcinomas of the head, neck, breast, ovary, and bladder. It has
also been used as an immunosuppressive agent in the prevention of graft versus
host disease and in the treatment of severe psoriasis and rheumatoid arthritis.
The effectiveness of methotrexate on trophoblastic tissue has been well
established and is derived from experience gained in using this agent in the
treatment of hydatiform moles and choriocarcinomas. As used in the treatment
of ectopic pregnancy, methotrexate is administered in a single or in multiple
intramuscular (IM) injections.
Treatment with methotrexate is an especially attractive option when the
pregnancy is located on the cervix or ovary or in the interstitial or the cornual
portion of the tube. Surgical treatment in these cases is often associated with
increased risk of hemorrhage, often resulting in hysterectomy or oophorectomy.
In a study by Verma et al, only 1 of 64 cervical, cornual, or cesarean delivery scar
pregnancies treated with systemic methotrexate alone or combined with
intracardiac injection required surgery.[59]
Successful medical treatment using methotrexate has been reported in the
literature with good subsequent reproductive outcomes. By avoiding surgery,
the risk of tubal injury is reduced.[60]
Indications
Medical therapy for ectopic pregnancy involving methotrexate may be indicated
in certain patients. To determine acceptable candidates for methotrexate
therapy, first establish the diagnosis by one of the following criteria:
 Abnormal doubling rate of the beta–human chorionic gonadotropin (β-HCG)
level and ultrasonographic identification of a gestational sac outside of the
uterus
 Abnormal doubling rate of the β-HCG level, an empty uterus, and menstrual
aspiration with no chorionic villi
A number of other factors must also be considered once the diagnosis is
established, as follows:
 The patient must be hemodynamically stable, with no signs or symptoms of
active bleeding or hemoperitoneum (must be met by every patient)
 The patient must be reliable, compliant, and able to return for follow-up care
(must be met by every patient)
 The size of the gestation should not exceed 4cm at its greatest dimension (or
exceed 3.5 cm with cardiac activity) on ultrasonographic measurement -
Exceeding this size is a relative, but not absolute, contraindication to medical
therapy
 Absence of fetal cardiac activity on ultrasonographic findings - The presence of
fetal cardiac activity is a relative contraindication
 No evidence of tubal rupture - Evidence of tubal rupture is an absolute
contraindication
 β-HCG level less than 5000 mIU/mL - Higher levels are a relative
contraindication
Contraindications
A β-HCG level of greater than 5,000 IU/L, fetal cardiac activity, and free fluid in
the cul-de-sac on ultrasonographic images (presumably representing tubal
rupture) are contraindications to medical therapy with methotrexate.
Although patients with β-HCG levels above 5,000 IU/L and fetal cardiac activity
have been treated successfully with methotrexate, these patients require much
greater surveillance and carry a higher risk of subsequent operative
intervention. There is an inverse association between β-HCG levels and
successful medical management of an ectopic pregnancy. A systematic review by
Menon et al confirmed that there is a substantial increase in failure of medical
management of ectopic pregnancy with single-dose methotrexate when the
initial β-HCG is above 5,000 IU/L.[61]
Other contraindications to the use of methotrexate include the following :
 Documented hypersensitivity to methotrexate
 Breastfeeding
 Immunodeficiency
 Alcoholism
 Alcoholic liver disease
 Any other type of liver disease
 Blood dyscrasias
 Leukopenia
 Thrombocytopenia
 Anemia
 Active pulmonary disease
 Peptic ulcer disease
 Renal, hepatic, or hematologic dysfunction
Adverse effects and mandatory patient counseling
Adverse effects associated with the use of methotrexate can be divided into
adverse drug effects and treatment effects. Adverse drug effects include the
following:
 Nausea
 Vomiting
 Stomatitis
 Diarrhea
 Gastric distress
 Dizziness
Transient elevation in liver enzymes is also known to occur. Serious reactions
such as bone marrow suppression, dermatitis, pleuritis, pneumonitis, and
reversible alopecia can occur with higher doses but are rare with doses used in
the treatment of ectopic pregnancy.
Treatment effects of methotrexate include an increase in abdominal pain
(occurring in up to two thirds of patients), an increase in β-HCG levels during the
first 1-3 days of treatment, and vaginal bleeding or spotting.
The medical treatment of ectopic pregnancy requires compulsive compliance.
The physician must emphasize the importance of patient follow-up and have
patient information on hand, including the patient's home address, telephone
numbers at home and work, and the means to reach a contact person in case
attempts to reach the patient directly are unsuccessful. Proper documentation of
attempts to reach the patient, including records of telephone calls and certified
mail are important medical-legal considerations.
Before injection of methotrexate, the patient must be counseled extensively on
the risks, benefits, and adverse effects of the treatment and on the possibility of
failure of medical therapy, which would result in tubal rupture and necessitate
surgery. Patients should be aware of the signs and symptoms associated with
tubal rupture, and they should be advised to contact their physician with
significantly worsening abdominal pain or tenderness, heavy vaginal bleeding,
dizziness, tachycardia, palpitations, or syncope.
Most patients experience at least 1 episode of increased abdominal pain, which
usually occurs 2-3 days after the injection. Increased abdominal pain is believed
to be caused by the separation of the pregnancy from the implanted site. It can
be differentiated from tubal rupture in that it is milder, of limited duration
(lasting 24-48 h), and is not associated with signs of acute abdomen or
hemodynamic instability.
Advise patients to avoid alcoholic beverages, vitamins containing folic acid,
nonsteroidal anti-inflammatory drugs (NSAIDs), and sexual intercourse, until
advised otherwise. A signed written consent demonstrating the patient's
comprehension of the course of treatment must be obtained. Provide an
information pamphlet to all patients receiving methotrexate; the pamphlet
should include a list of adverse effects, a schedule of follow-up visits, and a
method of contacting the physician or the hospital in case of emergency.
Methotrexate Treatment Protocols
A number of accepted protocols with injected methotrexate exist for the
treatment of ectopic pregnancy.
Multiple-dose regimen
Initial experience used multiple doses of methotrexate with leucovorin to
minimize adverse effects. Leucovorin is folinic acid that is the end product of the
reaction catalyzed by dihydrofolate reductase, the same enzyme inhibited by
 methotrexate. Normal dividing cells preferentially absorb leucovorin; hence, it
decreases the action of methotrexate, thereby decreasing methotrexate’s adverse
systemic effects.
This regimen involves administration of methotrexate as 1 mg/kg IM on days 0,
2, 4, and 6, followed by 4 doses of leucovorin as 0.1 mg/kg on days 1, 3, 5, and 7.
Because of a higher incidence of adverse effects and the increased need for
patient motivation and compliance, the multiple dosage regimen has fallen out of
favor in the United States.
Single-dose regimen
The more popular regimen today is the single-dose injection, which involves
injection of methotrexate as 50 mg/m2 IM in a single injection or as a divided
dose injected into each buttock. Studies comparing the multiple methotrexate
dosage regimen with the single dosage regimen have demonstrated that the 2
methods have similar efficacy. With smaller dosing and fewer injections, fewer
adverse effects are anticipated, and the use of leucovorin can be abandoned.
The protocol for single-dose methotrexate is detailed below. Using this protocol,
Stovall et al achieved a 96% success rate with a single injection of
methotrexate.[6]
Day 0
Obtain β-HCG level, ultrasonography, and +/- dilatation and curettage.
Day 1
Obtain levels of the following:
 β-HCG
 Liver function - Eg, aspartate aminotransferase (AST or serum glutamic-
oxaloacetic transaminase [SGOT]), alanine aminotransferase (ALT or serum
glutamic-pyruvic transaminase [SGPT])
 Blood urea nitrogen (BUN)
 Creatinine
Evidence of hepatic or renal compromise is a contraindication to methotrexate
therapy. Blood type, Rh status, and antibody screening are also performed, and
all Rh-negative patients are given Rh immunoglobulin.
Methotrexate (50 mg/m2) is administered by IM injection. Advise patients not to
take vitamins with folic acid until complete resolution of the ectopic pregnancy.
They should also refrain from alcohol consumption and intercourse for the same
period.
Day 4
The patient returns for measurement of her β-HCG level. The level may be higher
than the pretreatment level. The day-4 hCG level is the baseline level against
which subsequent levels are measured.
Day 7
Draw β-HCG and AST levels and perform a complete blood count (CBC). If the β-
HCG level has dropped 15% or more since day 4, obtain weekly β-HCG levels
until they have reached the negative level for the lab. If the weekly levels plateau
or increase, a second course of methotrexate may be administered.
If the β-HCG level has not dropped at least 15% from the day-4 level, administer
a second IM dose of methotrexate (50 mg/m2) on day 7, and observe the patient
similarly. If no drop has occurred by day 14, surgical therapy is indicated.
If the patient develops increasing abdominal pain after methotrexate therapy,
repeat a transvaginal ultrasonographic scan to evaluate for possible rupture.
Treatment monitoring protocols
The best predictor of success of medical therapy is the initial β-HCG level. Based
on efficacy studies done by Lipscomb et al, success exceeded 90% for single-dose
methotrexate when β-HCG levels were less than 5000 mIU/mL but dropped to
about 80% when levels were 5-10,000 mIU/mL. Success was less than 70% with
an initial β-HCG level of greater than 15,000 mIU/mL.[5]
Before initiating therapy, draw blood to determine baseline laboratory values for
renal, hepatic, and bone marrow function, as well as a baseline β-HCG level.
Determine blood type, Rh factor, and the presence of antibodies. Patients who
are Rh negative should receive Rh immunoglobulin.
Obtain repeat β-HCG levels 4 days and 7 days after the methotrexate injection.
An initial increase in β-HCG levels often occurs by the third day and is not a cause
for alarm. A decline in β-HCG levels of at least 15% from days 4 to 7 postinjection
indicates a successful medical response. Other effective monitoring protocols
have also been reported.[62] The patient's β-HCG levels should be measured
weekly, until they become undetectable.
Failure of medical treatment is defined when β-HCG levels increase, plateau, or
fail to decrease adequately by 15% from days 4 to 7 postinjection. At this time,
surgical intervention may be warranted. A repeat single dose of methotrexate
can also be a viable option after reevaluation of the patients' indications and
contraindications (including repeat ultrasonography) for medical therapy.
Investigational Medical Treatments
The use of oral methotrexate is under investigation; although preliminary
reports show promising results, efficacy remains to be established. Direct local
injection (salpingocentesis) of methotrexate into the ectopic pregnancy under
laparoscopic or ultrasonographic guidance has also been reported in the
literature; however, these studies have yielded inconsistent results, and the
advantage of this technique over IM injection remains to be established.
Although methotrexate has remained the most effective and popular drug used
in medical therapy for an ectopic pregnancy, other protocols have been used,
such as potassium chloride, hyperosmolar glucose, mifepristone (RU 486), and
prostaglandins, and these agents have been administered orally, systemically,
and locally into the ectopic pregnancy directly. These therapies remain
experimental at present because the efficacy of such treatments, as well as their
advantage over standard methotrexate protocol, has not been established.
Salpingostomy and Salpingectomy
Within the last 2 decades, a more conservative surgical approach to unruptured
ectopic pregnancy using minimally invasive surgery has been advocated to
preserve tubal function. The conservative approaches include linear
salpingostomy and milking the pregnancy out of the distal ampulla. The more
radical approach includes resecting the segment of the fallopian tube that
contains the gestation, with or without reanastomosis.
Laparoscopy has become the recommended approach in most cases. Laparotomy
is usually reserved for patients who are hemodynamically unstable or for
patients with cornual ectopic pregnancies; it also is a preferred method for
surgeons inexperienced in laparoscopy and in patients in whom a laparoscopic
approach is difficult (eg, secondary to the presence of multiple dense adhesions,
obesity, or massive hemoperitoneum).
Multiple studies have demonstrated that laparoscopic treatment of ectopic
pregnancy results in fewer postoperative adhesions than laparotomy.
Furthermore, laparoscopy is associated with significantly less blood loss and a
reduced need for analgesia. Finally, laparoscopy reduces cost, hospitalization
time, and convalescence period.
Linear salpingostomy along the antimesenteric border to remove the products of
conception is the procedure of choice for unruptured ectopic pregnancies in the
ampullary portion of the tube. Ectopic pregnancies in the ampulla are usually
located between the lumen and the serosa and, thus, are ideal candidates for
linear salpingostomy. Several studies have demonstrated no benefit of primary
closure (salpingotomy) over healing by secondary intention (salpingostomy).
Total salpingectomy is the procedure of choice in a patient who has completed
childbearing and no longer desires fertility, in a patient with a history of an
ectopic pregnancy in the same tube, or in a patient with severely damaged tubes.
In cases involving uncontrolled bleeding and hemodynamic instability,
conservative treatment methods are avoided in favor of radical surgery.
Linear salpingostomy
In linear salpingostomy, the involved tube is identified and freed from
surrounding structures. To minimize bleeding, a dilute solution containing 20 U
of vasopressin in 20 mL of isotonic sodium chloride solution may be injected into
the mesosalpinx just below the ectopic pregnancy. Make sure that the needle is
not in a blood vessel by aspirating before injecting, because intravascular
injection of vasopressin may precipitate acute arterial hypertension and
bradycardia.
Next, using a microelectrode, scissors, harmonic scalpel, or laser, a 1- to 2-cm
linear incision is made along the antimesenteric side of the tube along the
thinnest segment of the gestation. (See the image below.)
 Linear incision being made at the antimesenteric
side of the ampullary portion of the fallopian tube.

At this time, the pregnancy usually protrudes out of the incision and may slip out
of the tube. Occasionally, it must be teased out using forceps or aqua-dissection,
which uses pressurized irrigation to help dislodge the pregnancy. (See the
images below.)

Laparoscopic picture of an ampullary

ectopic pregnancy protruding out after a linear salpingostomy was performed.

Schematic of a tubal gestation being

teased out after linear salpingostomy.

Coagulation of oozing areas may be necessary and can be accomplished using

microbipolar forceps. Some ampullary pregnancies can be teased out and
 expressed through the fimbrial end (milking of the tube) by using digital
expression, suction, or aqua-dissection. However, this approach carries with it a
higher rate of bleeding, persistent trophoblastic tissue, tubal damage, and
recurrent ectopic pregnancy (33%).
Segmental tubal resection and total salpingectomy
In some cases, resection of the tubal segment containing the gestation or a total
salpingectomy is preferred over salpingostomy. This is true for isthmic
pregnancies, in which the endosalpinx is usually damaged. These patients do
poorly with linear salpingostomy, with a high rate of recurrent ectopic
pregnancy occurring.
Segmental tubal resection is performed by grasping the tube at the proximal and
distal borders of the segment of the tube containing the gestation and
coagulating thoroughly from the antimesenteric border to the mesosalpinx. This
portion of the tube is then excised. The underlying mesosalpinx is also
coagulated and excised, with particular attention to minimize the damage to the
surrounding vasculature.
Delayed microsurgical reanastomosis can be performed to reestablish tubal
patency if enough healthy fallopian tube is present. Take care to minimize the
thermal injury to the tube during excision, so that an adequate portion of healthy
tube remains for the reanastomosis.
Total salpingectomy can be achieved by progressively coagulating and cutting
the mesosalpinx, starting from the fimbriated end and advancing toward the
proximal isthmic portion of the tube. At this point, the tube is separated from the
uterus by coagulating and excising with scissors or laser.
Preoperative details
The optimal surgical management for a patient with an ectopic pregnancy
depends on several factors, including the following:
 Patient's age, history, and desire for future fertility
 History of previous ectopic pregnancy or pelvic inflammatory disease (PID)
 Condition of the ipsilateral tube - Ie, ruptured or unruptured
 Condition of the contralateral tube - Eg, adhesions, tubal occlusion
 Location of the pregnancy - Ie, interstitium, ampulla, isthmus
 Size of the pregnancy
 Presence of confounding complications
In a patient who has completed childbearing and no longer desires fertility, in a
patient with a history of an ectopic pregnancy in the same tube, or in a patient
with severely damaged tubes, total salpingectomy is the procedure of choice. The
presence of uncontrolled bleeding and hemodynamic instability warrants radical
surgery over conservative methods. The preferred approach based on the
location of the pregnancy varies, as previously discussed. In all instances,
regardless of desired fertility, fully inform the patient of the possibility of a
laparotomy with bilateral salpingectomy.
Intraoperative details
Throughout the procedure, take care to minimize blood loss and reduce the
potential for retained trophoblastic tissue, which can reimplant and persist.
Remove large gestations in an endoscopic bag, and perform copious irrigation
and suctioning to remove any remaining fragments. Inspect the peritoneal cavity
and remove any detected residual trophoblastic tissue.
Note the condition of the contralateral tube, the presence of adhesions, or other
pathologic processes because this helps in the postoperative counseling of the
patient with regard to future fertility potential.
Postoperative details
Proper pain control and hemodynamic stability are important postoperative
considerations. Most often, patients treated with laparoscopy are discharged on
the same day of surgery; however, overnight admission may be necessary for
some patients in order to monitor postoperative bleeding and achieve adequate
pain control. Patients treated by laparotomy are usually hospitalized for a few
days.
Monitoring
After surgical excision of an ectopic gestation, weekly monitoring of quantitative
beta–human chorionic gonadotropin (β-HCG) levels is necessary until the level is
zero to ensure that treatment is complete. This is especially true following
treatment with conservative surgery, ie, salpingostomy, which carries a 5-15%
rate of persistent trophoblastic tissue. The average time for β-HCG to clear the
system is 2-3 weeks, but up to 6 weeks can be required.
After tubal-sparing surgical removal of an ectopic pregnancy, a fall in β-HCG
levels of less than 20% every 72 hours represents incomplete treatment.
Although most of these cases are caused by incomplete removal of trophoblastic
tissue, some actually may represent multiple ectopic pregnancies in which only 1
gestation is initially recognized and treated.
The incidence of persistent trophoblastic tissue is greater with higher initial β-
HCG levels and is relatively rare with titers of less than 3000 IU/L. The risk of
persistent trophoblastic tissue is very significant when a hematosalpinx is
greater than 6cm in diameter, a β-HCG titer is more than 20,000 IU/L, and a
hemoperitoneum is greater than 2 L.
While resolution without any further intervention is the general rule, the
persistence of trophoblastic tissue has been associated with tubal rupture and
hemorrhage even in the presence of declining β-HCG levels. Further medical
treatment with methotrexate or surgery in symptomatic patients may be
necessary if β-HCG levels do not decline or persist. Some authors have suggested
administration of a prophylactic dose of methotrexate after conservative surgery
to reduce the risk of persistent ectopic pregnancy.
http://emedicine.medscape.com/article/2041923-differential
 Mola Hidatidosa

Medical Care
 Stabilize the patient.
 Transfuse for anemia.
 Correct any coagulopathy.
 Treat hypertension.
 Watch for and be prepared to treat thyroid storm, a rare complication.
Surgical Care
 Evacuation of the uterus by dilation and curettage is always necessary.
 Prostaglandin or oxytocin induction is not recommended because of the
increased risk of bleeding and malignant sequelae.
 Intravenous oxytocin should be started after dilation of the cervix at the
initiation of suctioning and continued postoperatively to reduce the likelihood of
hemorrhage. Consideration of using other uterotonic formulations (eg,
Methergine, Hemabate) is also warranted.
 Respiratory distress can occur at the time of surgery. This may be due to
trophoblastic embolization, high-output congestive heart failure caused by
anemia, or iatrogenic fluid overload. Distress should be aggressively treated with
assisted ventilation and monitoring, as required.[33]
Consultations
A gynecologic oncologist should be consulted if the patient is believed to be at
risk for or has developed malignant disease (ie, gestational trophoblastic
neoplasia).
Diet
No special diet is required.
Activity
 Patients may resume activity as tolerated.
 Pelvic rest is recommended for 2-4 weeks after evacuation of the uterus, and the
patient is instructed not to become pregnant for 6 months. Effective
contraception is recommended during this period.[34]
 Monitor serial beta-hCG levels to identify the rare patient who develops
malignant disease. If a pregnancy does occur, the elevation in beta-hCG would be
confused with development of malignant disease.
http://emedicine.medscape.com/article/254657-treatment#showall