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Abortion & Abnormalities of Early Pregnancy

Dating of Pregnancy
The Gestational Age ( GA ) of a fetus is the age in weeks and days measured from the last
menstrual period (LMP).
Developmental age (DA) is the number of weeks and days since fertilization. Because
fertilization usually occurs about 14 days after the first day of the prior menstrual period,
the GA is 2 weeks more than the DA.

1- ? year old woman her menstrual period has stopped since 7 weeks. She was complaining of
light bleedidng & discomfort. She had +ve pregnancy test at home. The best test for her now
is:
a. B-HCG
b. Human prolactin
C. Progesterone
d. Esteriol
a Prolactine
Abortion is generally defined as delivery or loss of the products of conception before the 20th wk of
pregnancy (which corresponds to a fetal weight of about 500 g [1.1 lb]). Delivery between 20 and
37 wk is considered preterm birth
A viable conceptus can be detected with modern ultrasound as early as 5.5 weeks of gestation.
The ability to visualize the embryo and embryonic heart motion has made evaluation and
management of threatened miscarriage more precise. However, accurate knowledge of gestational
age is necessary for proper interpretation. Ultrasound findings are unreliable at 3 to 4 weeks
gestation, and what appears to be an empty uterus can be misinterpreted as an abnormal intrauterine

or ectopic pregnancy when it is actually a normal early gestation. If there is any doubt of normalcy,
it is best to perform serial -hCG measurements and a follow-up sonogram. From 5 to 6 weeks, the
yolk sac and gestational sac are visible by transvaginal ultrasound, and the embryo with cardiac
activity is seen soon after that. Abnormal gestational sac and yolk sac size, an embryo small for
dates, and slow embryonic heart rates suggest impending pregnancy loss. The presence of an
appropriately sized embryo with a normal cardiac rate is encouraging, even in the setting of uterine
bleeding, and more than two thirds of these will survive. In the absence of signs of miscarriage,
more than 95% of pregnancies continue if a live embryo is demonstrated ultrasonically at 8 weeks
gestation. These embryos have a very low mortality rate during the next few weeks, and the
subsequent pregnancy loss rate is only 1% if a live fetus is seen at 14 to 16 weeks gestation.
this is threatened abortion may be turned to missed abortion or may be stabilised
Missed abortion should be suspected when the uterus fails to enlarge, when fetal heart sounds are
not heard at the appropriate time with Doppler ultrasonography, or when previously present fetal
heart sounds are absent. In a missed abortion, a serum or urine test for the b subunit of human
chorionic gonadotropin (b-hCG) becomes negative earlier than expected or does not double within
72 h; ultrasonography showing no cardiac activity provides the earliest diagnosis. A missed abortion
may lead to the dead fetus syndrome, with disseminated intravascular coagulation, progressive
hypofibrinogenemia, and possible massive bleeding when delivery finally occurs. The syndrome
usually develops only when the loss occurs in the 2nd trimester or later.
2- A 20 year old married lady presented with HX of severe left lower abdominal pain
amenorrhea for 6 weeks. The most appropriate investigation to rule out serious DDx is:
(means ectopic Pregnancy)
a. CBC
b. ESR
C. Pelvic US
d. Abdominal x-ray
e. Vaginal swab for culture & sensitivity
- A 20 y.o. married lady presented with history of left lower abdominal pain & amenorrhea for
6 weeks. The most appropriate investigation to role out serious diagnosis is:
a- CBC.
b- ESR.
c- pelvic US.
d- abdominal XR
e- vaginal swab for culture & sensitivity.
Ectopic pregnancy can be diagnosed as early as 4.5 weeks gestation. Unfortunately, visualizing an
ectopic pregnancy this early is frequently not possible. More importantly, traditional laparoscopic
visualization is now rarely necessary. Routine diagnostic tests are serial measurements of hCG, ultrasonography, serum progesterone levels, and uterine curettage.
Serial -Human Chorionic Gonadotropin Determinations
-hCG determinations used today are based on the enzyme-linked immunosorbent assay
(ELISA), detecting low -hCG concentrations in urine and serum, 20 mIU/mL down to 1
mIU/mL, respectively. The -hCG, produced by trophoblastic cells in normal pregnancy, rises
at least 66% and up to two-fold every 2 days. This generally applies to -hCG values below
10,000 mIU/mL. Eight-five percent of abnormal pregnancies, whether intrauterine or ectopic,
have impaired -hCG production with a prolonged doubling time. -hCG levels that plateau
or fail to rise normally along with a low serum progesterone value should be considered
nonviable. If a viable intrauterine gestation is not visible by transvaginal ultrasonography

when the -hCG is above 2,000 mIU/mL (First International Reference Preparation [IRP])
and no fetal heartbeat can be visualized in the adnexa, uterine curettage can be performed. In
this situation, treatment of a nonviable intrauterine pregnancy is performed or ectopic
pregnancy is diagnosed when the -hCG levels do not fall. These -hCG thresholds are not
universal, and each institution must identify its own values to avoid terminating normal
intrauterine pregnancies.
-hCG determinations are further employed for diagnosis after uterine curettage. If the hCG fails to decline by 15% from a level drawn immediately before surgery, the pregnancy is
presumed ectopic and treatment should be initiated.
Ultrasonography
Although the uterus and adnexa may be evaluated abdominally or vaginally, transvaginal
ultrasonography reliably detects intrauterine gestations when the -hCG levels are between
1,000 and 2,000 mIU/mL (First IRP), as early as 1 week after missed menses. An intrauterine
gestation should almost always be visualized when the -hCG level is greater than 2,000
mIU/mL.

3- A women came to Antenatal Care ANC at 8th week of gestation. Diagnosed as case of
cervical incompetence, which of the following is the appropriate management?
a) Insert a suture in the same week.
b) insert suture at 14-16 wks gestation
c) Confirm the Dx by inserting Hegars Dilator.
d) Admit the patient throught the Pregnancy time in the hospital for observation.
e) Give Beta-mimetic agent (Ritodrine)

Cervical Incompetence Incompetent cervix, also called premature cervical dilation, is an


important cause of second-trimester pregnancy loss.
It is characterized by gradual, painless dilation of the cervix with bulging and rupture of the
membranes and subsequent expulsion of a fetus too immature to survive.
Pregnancy loss from this cervical abnormality usually occurs in the second trimester and is thought
to be an entirely different and distinct entity from a first-trimester miscarriage or premature labor in
the third trimester.
It results from different factors, presents a distinctive clinical picture, and requires different
management. Moreover, miscarriage and premature labor are common, but mid-trimester premature
cervical dilation is relatively rare. Unlike the rest of the uterus, the cervix is fundamentally a
connective tissue structure. The cause of cervical incompetence is obscure, and various etiologic
factors have been proposed. Previous surgery or trauma to the cervix, such as D&C, amputation,
conization, cauterization, loop electrosurgical excision procedure (LEEP), or traumatic delivery,
seem to be factors in some cases. In other instances, congenital cervical structural defects, uterine
anomalies, or abnormal cervical development associated with in utero diethylstilbestrol exposure
appear to play a role. Little agreement can be found regarding the diagnosis of cervical
incompetence, except that it is one of exclusion that requires careful evaluation to rule out other
potential causes of mid-trimester pregnancy loss. Other causes of very early delivery include
abruptio placentae, chorioamnionitis, and uterine anomalies, but they usually present different
clinical pictures.
Whether or not the condition can be diagnosed
during the nonpregnant state by methods designed to calibrate the diameter of the endocervical
canal or
during early pregnancy by sonographic findings is questionable.
The absolute diagnosis of cervical incompetence can be made only by seeing the fetal membranes
bulging through the partially dilated cervix of a patient in the second trimester of pregnancy who is
not in labor.
More typically, a presumptive diagnosis is made from the characteristic history of apparently silent
dilation of the cervix followed by rupture of the membranes and a relatively painless, rapid labor
with delivery of an immature infant. Also, the fetus is typically alive at the time of presentation to
the hospital; delivery of a dead, macerated fetus makes the diagnosis of cervical competence
questionable. Upon inspection in the nonpregnant state, the cervix may be shortened with a patulous
os or may be deformed with lacerations that sometimes extend to the vaginal fornix. Although bed
rest, various intravaginal devices, and pharmacologic agents have been used with some success, the
generally accepted treatment for incompetent cervix is surgical. Various methods have been
described, but the McDonald or Shirodkar procedures ( Fig. 4.5) are most commonly employed
prophylactically. These are techniques performed vaginally, usually under regional anesthesia,
designed to reinforce the cervix close to the level of the internal os. If there is insufficient cervical
tissue to allow placement of a cerclage vaginally, an abdominal approach is sometimes used. The
reinforcement suture is usually placed toward the end of the first trimester after ultrasound
documentation of a live fetus, after the risk of miscarriage has passed, and before the cervix starts to
dilate.

FIG. 4.5. Incompetent cervix can be treated by three procedures. A: In the McDonald cerclage
procedure, a multiple-bite suture using large, monofilament nylon is placed around the cervix and
tied securely to reduce the diameter of the cervical canal to a few millimeters. B: In the Shirodkar
procedure, Merseline tape encircling the cervix is passed under the mucosa and anchored to the
cervix anteriorly and posteriorly with interrupted sutures. C: With transabdominal cervicoisthmic
cerclage, a Merseline band is placed in an avascular space medial to the uterine vessels at the level
of the cervicouterine junction.
Placement of the cerclage in the second trimester after cervical change has occurred is sometimes
necessary but appears less effective. The procedure should not be used if the diagnosis is in doubt, if
membranes are ruptured, or if vaginal bleeding and cramping are part of the clinical picture. There
is no evidence that postoperative antibiotics, progesterone, or tocolytic agents are useful adjuvants.
If membranes rupture or labor ensues at any time, removal of the cerclage should be strongly
considered to prevent chorioamnionitis, sepsis, cervical laceration, and rupture of the uterus.
Otherwise, the suture is removed when fetal maturity is achieved, usually after 37 weeks gestation,
which is often followed by the onset of labor and a relatively rapid delivery. If the patient desires
further pregnancies, some physicians leave the cerclage in place and deliver by cesarean section.
Often, the history is not typical, and it is difficult to determine whether or not premature cervical
dilation will occur in a subsequent pregnancy. These patients are usually followed with frequent
vaginal examinations and serial sonograms to diagnose potential cervical changes. Transvaginal
ultrasound can be used to accurately assess cervical length and may be useful in deciding for or
against cerclage in women with an unclear history. The effectiveness of cerclage has often been
questioned, even in women with a classic clinical picture. Nevertheless, when patients are carefully
selected, this type of management is 80% to 90% successful in preventing delivery of an immature
fetus. There is little difference in the fetal survival rates between the McDonald and Shirodkar
techniques. The procedure has also been used prophylactically for patients with previous preterm
deliveries with less convincing evidence for cervical incompetence. Results from prospective
randomized studies have led to conflicting conclusions.
4- Recurrent abortion:
a) Genetic abnormality
b) Uterine abnormality
c) Thyroid dysfunction
d) DM
e) Increased prolactin
Habitual abortion: The risk of recurrent abortion after three consecutive losses in early pregnancy is
about 35%. Women who have habitual abortions are more likely to have 2nd-trimester and early
3rd-trimester stillbirths and preterm labor. Balanced chromosomal translocations in the parents,
uterine and cervical anomalies, infections, connective tissue diseases, and hormonal abnormalities
should be ruled out before pregnancy is reattempted.
RECURRENT MISCARRIAGE
Recurrent miscarriage (RM), traditionally defined as three or more consecutive first-trimester
spontaneous losses,
affects up to 1% of couples. Primary recurrent miscarriage is diagnosed in women who have never
had a successful pregnancy, and secondary recurrent miscarriage in those whose repetitive losses
follow a live birth.

There is no specific classification for women who have multiple miscarriages interspersed with
normal pregnancies. It is generally agreed that a workup for possible causes of RM is indicated in
most patients after two or three consecutive miscarriages.
The management of couples with RM is controversial.
This clinical entity has received much attention in the lay and medical literature during the past
decade. A definite cause is established in no more than 50% of couples, and several alleged causes
of RM are controversial.
Despite publicity to the contrary, there is little evidence that
poor nutrition,
infections,
unrecognized diabetes,
toxic agents, or
psychological trauma are significant etiologic factors.
Some alleged experts and Internet sites inappropriately emphasize unproven hypotheses and results
from poorly designed clinical studies. Seeking a solution, some patients and physicians may explore
less well-accepted etiologies and empirical or alternative treatments.
Moreover, new diagnostic tests for RM are continually being proposed to replace those that have
been disproved and discarded. For example, antithyroid antibodies, elevated follicular-phase
luteinizing hormone levels, circulating maternal embryotoxic factor, and abnormal lymphocyte
subset ratios (elevated CD56 + levels) have been touted within the last decade. It is beyond the
scope of this chapter to critically analyze each new treatment or assay, but the mechanism of
pregnancy loss and potential relationship to each of these remains largely theoretical. Until effective
treatments are identified and proven by properly designed studies, these screening tests have little
use in the routine evaluation of patients with RM.
Typically, investigation of anatomic, hormonal, genetic, and infectious factors has been
recommended. Even these may be criticized because the derivation of their diagnostic use and
treatments advocated are empirical and have come under scrutiny because they were never
submitted to properly designed study. Importantly, evidence has mounted that the average women
with RM has a fairly good prognosis for a successful next pregnancy without any specific treatment.
Known and Suspected Causes of Recurrent Miscarriage:
Structural Uterine Defects Hysterosalpingography, magnetic resonance imaging, hysteroscopy,
sonohysteroscopy, and laparoscopy can be used to diagnose septate uterus, other mllerian
anomalies, uterine defects associated with diethylstilbestrol exposure, submucous myomas, and
intrauterine synechiae.
Endocrine Problems
The luteal phase defect (LPD) has long been thought to be a cause of spontaneous abortion, but
the evidence linking LPD to recurrent abortion is subject to criticism. It is traditionally thought that
women with LPD have short menstrual cycles, postovulatory intervals less than 14 days, and
secondary infertility. LPD was initially thought to be due to failure of the corpus luteum to make
enough progesterone to establish a mature endometrial lining suitable for placentation. This theory
has evolved to implicate poor follicular-phase oocyte development, which results in disordered
estrogen secretion, inadequate ovarian steroidogenesis, and subsequent maldevelopment of
endometrial receptors. In turn, these effects could result from excess luteinizing hormone or

hyperandrogenic states. Some investigators claim that LPD accounts for over one fourth of cases of
RM, but studies of this disorder have not included concurrently tested controls. Also, there is little
agreement on the criteria necessary to make the diagnosis. Endometrial biopsy or luteal-phase
serum progesterone levels are the most widely accepted diagnostic tests. Both are timed for the late
luteal phase of the cycle. The endometrial biopsy is histologically dated, and a lag greater than 2 to
3 days is considered suspect. However, this should be confirmed by repeat biopsy, because delayed
endometrial histology can occur sporadically in women with no reproductive problems. To further
confuse the issue, normal women have endometrial histology suggestive of LPD in up to 50% of
single menstrual cycles and 25% of sequential cycles. Though the association between LPD and
RM remains speculative, many clinicians have treated women with RM with progesterone in their
next pregnancy. One commonly advocated treatment is a 25-mg progesterone suppository inserted
into the vagina twice a day (morning and night) beginning after ovulation and continuing until
menses begin or through the first 8 to 10 weeks of pregnancy. Comparable doses of oral micronized
progesterone have also been used. No properly designed studies have evaluated the role of
progesterone treatment in women with RM with LPD. Older studies and meta-analyses are difficult
to interpret because of marked differences in inclusion criteria and how LPD was diagnosed, the use
of various progesterone compounds, and the small number of women studied. In a more recent
randomized trial, a subgroup of women with polycystic ovary syndrome (PCOS) and three or more
miscarriages were randomized to treatment with either progesterone or placebo pessaries. There was
no difference in the pregnancy outcomes. Clomiphene and other ovulatory agents have been tried to
improve follicular development and corpus luteum function, but the results have been variable.
Human chorionic gonadotropin has been used in an attempt to stimulate the corpus luteum support
of pregnancy in women with RM. One placebo-controlled, multicentered trial found no significant
difference in the successful pregnancy rates (83% vs. 79%). In summary, the relationship between
the LPD and recurrent pregnancy loss remains a subject of controversy. It has not been shown
conclusively that progesterone treatment or corpus luteum support influences pregnancy outcome in
women with recurrent pregnancy loss.
PCOS has been found in one third or more of women with RM. However, the diagnosis of PCOS in
women with RM does not predict a worse pregnancy outcome than in women with RM without
PCOS. There is no known effective therapy for women with PCOS and RM.
Genetic Abnormalities Parental chromosomal anomalies are found in approximately 3% to 5%
of couples with RM. Cytogenetic examination of both partners is helpful to predict recurrence and
forms the basis for genetic counseling. Most abnormalities are balanced translocations, with twothirds being reciprocal translocations and one-third robertsonian translocations. Couples with
balanced translocations have spontaneous loss rates ranging from 50% for reciprocal translocations
to 25% for robertsonian translocations. All couples with a parental chromosomal abnormality
deserve counseling about genetic amniocentesis or chorionic villus sampling in any future
pregnancy to exclude a serious fetal chromosomal abnormality. Parental chromosomal
abnormalities do not usually preclude further attempts at pregnancy, because most couples
eventually have normal offspring. For the rare homologous robertsonian translocation that prevents
successful pregnancy, therapeutic possibilities include artificial donor insemination, in vitro
fertilization with donor oocytes, and adoption. Chromosomal analysis of the products of conception
is also clinically useful, particularly in the evaluation of the reason for failure of a treatment
regimen. Molecular mutations that may be shown in the future to cause recurrent miscarriages
include lethal, single-point mutations, possibly linked to MHC genes; mutations in genes that code
for products critical for normal development; mutations in homeobox genes that control
transcriptional regulation; mutations that lead to severe metabolic errors and embryonic death; and
disorders of protooncogenes and oncogenes. One group has shown that certain polymorphisms of
the HLA-G gene are associated with significantly higher rates of miscarriage among couples
presenting with RM. Also, marked skewing of the normal 50:50 distribution of X chromosome

inactivation in the mother, a condition termed highly skewed X-chromosome inactivation, may be
associated with otherwise unexplained RM. Before testing is recommended, confirmation of these
molecular genetic associations in different populations is required. For now, commercially available
tests for these conditions are not widely available, and there are no proven treatment options.
Autoimmune Disorders
Antiphospholipid Syndrome Antiphospholipid syndrome (APS) has been recognized as a proven
cause of pregnancy loss for over a decade. Approximately 5% to 15% of women with RM have
lupus anticoagulant (LA), anticardiolipin (aCL), or both. These acquired antiphospholipid
autoantibodies are induced by as yet unknown stimuli in the setting of aberrant immunoregulation.
Low levels of immune globulin G or immune globulin M aCL are of questionable significance.
Though women with APS may present with RM in the first trimester, fetal death in the second or
early third trimesters may be more specific for the condition. Patients with high levels of aCL or a
history of prior fetal death are at greatest risk of another fetal loss. The cause of fetal death appears
to be a decidual vasculopathy that results in decidual infarction and insufficient blood flow to the
placenta. Intervillous thrombosis has also been described. However, these lesions are nonspecific,
and the degree of pathology is not always sufficient to explain the fetal death. The mechanisms by
which aCL may cause decidual vasculopathy and fetal death are unknown. A number of
pathophysiologic mechanisms have been proposed, including an imbalance of local prostacyclin
and thromboxane production, enhanced platelet aggregation, decreased activation of protein C,
increased tissue factor, and decreased trophoblast annexin V production or availability. Most
recently, the complement system has been invoked as having a major role in antiphospholipid
syndrome-related pregnancy loss. Maternally administered heparin is widely considered the
treatment of choice for APS pregnancies, both to improve embryo-fetal outcome and protect the
mother from thrombotic events ( Table 4.2). Treatment is usually initiated in the early first trimester
after ultrasonographic demonstration of a live embryo. The dose of heparin required for safe and
effective treatment, however, is debated. Some experts use relatively low doses of heparin (e.g.,
5000 U of standard heparin b.i.d.), particularly when treating women with recurrent preembryonic
or embryonic losses. However, higher doses of heparin are recommended for patients with APS
with prior thrombosis, and some experts urge full anticoagulation. The optimal dose of heparin is
controversial for women whose APS is diagnosed because of prior fetal loss or neonatal death after
delivery before 34 weeks gestation due to severe preeclampsia or placental insufficiency, but who
do not have a history of thromboembolism. These women are at risk for thromboembolic disease,
and it is our opinion that these cases should receive sufficient thromboprophylaxis. Low molecularweight heparins (LMWHs) are widely used in Europe for the treatment of APS pregnancy, and there
is little reason to suspect that the appropriate use of LMWHs differs from that of standard heparin
with regard to efficacy. In most case series and trials, daily low-dose aspirin is included in the
treatment regimen. One important caveat deserves mentiona small, placebo-controlled trial found
that otherwise healthy women with RM and low titers of antiphospholipid antibodies do not require
treatment.

TABLE 4.2. Subcutaneous heparin regimens used in the treatment of antiphospholipid syndrome
during pregnancy
Intravenous immune globulin has also been used during pregnancy, usually in conjunction with
heparin and low-dose aspirin, especially in women with particularly poor past histories or recurrent
pregnancy loss during heparin treatment. However, a randomized, controlled, pilot study of

intravenous immune globulin treatment during pregnancy in unselected APS cases proved negative.
Anticoagulant coverage of the postpartum period in women with APS and prior thrombosis is
critical. We prefer switching the patient to warfarin thromboprophylaxis as soon as she is clinically
stable from delivery. In most cases, an international normalized ratio of 3.0 is desirable, and
postpartum coverage should extend for 6 to 8 weeks after delivery. Because of their risk for
thrombosis, the same strategy is recommended in women without prior thrombosis but in whom
APS is diagnosed because of prior fetal loss or neonatal death after delivery at or before 34 weeks
gestation for severe preeclampsia or placental insufficiency. Both heparin and warfarin are safe for
nursing mothers. The need for postpartum anticoagulation in women with primary APS diagnosed
solely on the basis of recurrent preembryonic and embryonic losses is unclear.
Other Autoimmune Disorders Autoantibodies to thyroid antigens are associated with a modest
increased rate of pregnancy loss if identified in early pregnancy or immediately before pregnancy.
Some investigators have found a significant proportion of women with RM to have antithyroid
antibodies; others have not. Even if antithyroid antibodies are associated with RM, no treatment
options have proven beneficial. Approximately 15% of women with RM have detectable antinuclear
antibodies (ANA). Subsequent pregnancy outcomes among women with a positive ANA test result
are similar to those among women with a negative ANA test result. A randomized treatment trial of
women with recurrent pregnancy loss and a positive autoantibody result, including ANA, found no
benefit to treatment with prednisone and low-dose aspirin and treatment with placebo. Thus,
currently available data do not support testing women with recurrent pregnancy loss for ANA.
Thrombophilic Disorders The relationship between inherited thrombophilic disorders and recurrent
miscarriage has been the subject of intense study within the last several years. The most common
inherited thrombophilic disorders are factor V Leiden and prothrombin G20210A mutation, found in
approximately 8% and 3%, respectively, of Caucasian women in the United States. These mutations
are associated with approximately 25% of isolated thrombotic events and approximately 50% of
familial thrombosis. Other less common thrombophilias include deficiencies of the anticoagulants
protein C, protein S, and antithrombin III. Hyperhomocysteinemia, most commonly due to the
C677T polymorphism of the methylenetetrahydrofolate reductase (MTHFR) gene, is also associated
with venous thrombosis. Data regarding the association of these thrombophilic abnormalities and
RM do not allow clear and consistent conclusions. The rather obvious fact that most women with
common thrombophilic mutations, such as factor V Leiden, the prothrombin G20210A mutation, or
the MTHFR C677T mutation, do not have RM further confounds the picture. One prospective study
of next pregnancies in women with RM found a significantly lower successful pregnancy rate
among those with the factor V Leiden mutation compared to those without (37.5% vs. 69.3%).
Various studies are more consistent in finding an association between thrombophilias and secondor third-trimester fetal loss. The odds ratio for stillbirth is significantly higher in women with
combined thrombophilic defects. Some women with RM have evidence of ongoing, perhaps
chronic, thrombin generation or the formation of thrombosis-related microparticles. These studies
underscore the potential importance of prothrombotic states to pregnancy loss, but more research is
required to bring the current findings into the clinical realm. Despite the recent interest in this field,
no treatment trials have been performed. Thus, which therapy, if any, is effective in promoting
successful pregnancy among women with recurrent pregnancy loss and thrombophilia is uncertain.
Cervical Incompetence Incompetent cervix, also called premature cervical dilation, is an important
cause of second-trimester pregnancy loss. It is characterized by gradual, painless dilation of the
cervix with bulging and rupture of the membranes and subsequent expulsion of a fetus too
immature to survive. Pregnancy loss from this cervical abnormality usually occurs in the second
trimester and is thought to be an entirely different and distinct entity from a first-trimester
miscarriage or premature labor in the third trimester. It results from different factors, presents a
distinctive clinical picture, and requires different management. Moreover, miscarriage and
premature labor are common, but mid-trimester premature cervical dilation is relatively rare.

Recommendations for Recurrent Miscarriage


The scheme for a reasonable and cost-effective evaluation of women with RM shown in Table 4.3 is
based on current guidelines published by the American College of Obstetricians and Gynecologists
and the Royal College of Obstetricians and Gynaecologists. A sympathetic attitude by the physician
is crucialestablishment of trust and rapport and a sincere appreciation of the distress and grief
experienced by these couples permit tactful and thorough discussions with patient and partner. It is
reasonable to institute an evaluation after two consecutive miscarriages in anxious women or if the
patient has few reproductive years remaining or has had an infertility problem. Couples interested in
an investigational protocol are perhaps best referred to legitimate research centers.

5- A 25 year old G3P1 present to the emergency room complaining of lower abdominal
crampy pain 6 wk from her last normal period .She has had significant vaginal bleeding but
no passage of tissue.
-the pts most likely diagnosis is:
a- Incomplete abortion.
b- Complete abortion.
c-Missed abortion.
d- Threatened abortion.
e- Ectopic pregnancy.
-the most important step in this pts evaluation should be:
a- Sonography.
b- Physical exam.
c-CBC.
d- Quantitative B-hCG.
May be after sonography
e- Detailed menstrual history.
Diagnosis
Most patients present with bleeding from the vagina . Other findings include :
1. cramping, abdominal pain, and decreased symptoms of pregnancy.
2. The physical examination should include vital signs to rule out shock and febrile illness.
3. A pelvic examination can be performed to look for sources of bleeding other than uterine
and for changes in the cervix suggestive of an inevitable abortion.
4. The laboratory tests ordered include a quantitative level of -hCG, complete blood count,
blood type, and antibody screen.
5. An ultrasound can assess fetal viability and placentation.
Because patients with ectopic pregnancy also present with vaginal bleeding, it needs to be ruled
out of the differential diagnosis. An ultrasound showing fetal cardiac activity or serial -hCG levels
doubling every 48 hours in early pregnancy are consistent with a viable IUR
- Transvaginal ultrasonography would most likely reveal:
a- Fetal heart motion.
b- An intact gestational sac.
c- A discrete yolk sac.

d- A thickened endometrium with no gestational sac.


e- Fetal heart motion in the adnexae.
A viable conceptus can be detected with modern ultrasound as early as 5.5 weeks of gestation.
The ability to visualize the embryo and embryonic heart motion has made evaluation and
management of threatened miscarriage more precise.
However, accurate knowledge of gestational age is necessary for proper interpretation.
Ultrasound findings are unreliable at 3 to 4 weeks gestation, and what appears to be an empty
uterus can be misinterpreted as an abnormal intrauterine or ectopic pregnancy when it is actually a
normal early gestation.
If there is any doubt of normalcy, it is best to perform serial -hCG measurements and a followup sonogram.
From 5 to 6 weeks, the yolk sac and gestational sac are visible by transvaginal ultrasound, and
the embryo with cardiac activity is seen soon after that. Abnormal gestational sac and yolk sac size,
an embryo small for dates, and slow embryonic heart rates suggest impending pregnancy loss. The
presence of an appropriately sized embryo with a normal cardiac rate is encouraging, even in the
setting of uterine bleeding, and more than two thirds of these will survive.

Laboratory Studies

Qualitative urine pregnancy test, to confirm pregnancy


Complete blood count with differential
Blood type and Rh factor
o Blood type must be documented for every pregnant patient with vaginal bleeding.
o If Rh-negative, administer RhoGAM to prevent hemolytic disease of the newborn in
this pregnancy and subsequent pregnancies.
Hemoglobin and hematocrit: These studies establish baseline and detect hemorrhagic
anemia.
Quantitative human chorionic gonadotropin-beta
o The discriminatory level of beta-hCG is approximately 1500 mIU/mL above which
there should be sonographic evidence of early intrauterine pregnancy, if present.
o Beta-hCG level rises at rate of doubling approximately every 48 hours for 85% of
intrauterine pregnancies. The remaining 15% may rise with a different slope or be
plateaued.
o A higher likelihood of ectopic pregnancy or subsequent miscarriage exists if hCG
blood level is lower than predicted by estimated gestational age (GA) based on the
last menstrual period (LMP).
o The possibility of molar pregnancy exists if beta-hCG is very high and out of
proportion to predicted gestational age. This pregnancy occurs with or without
evidence of early normal trophoblast growth and function, as indicated by adequately
rising beta-hCG levels.
Factor XIII and fibrinogen, if indicated per history

Imaging Studies
Ultrasonography is used widely and is the imaging study of choice. Advantages of ultrasonography
include bedside use, availability, low cost, and noninvasiveness. Disadvantages include operator
dependency. Ultrasonography aids identification of retained products of conception, fetal demise,

incomplete miscarriage, ectopic pregnancy, or empty uterus; therefore, it provides a clinically


relevant classification of early pregnancy loss. Following spontaneous first-trimester complete
miscarriage, endovaginal ultrasonography has been found to be 81% sensitive and 94% specific in
detection of retained products of conception.6 Ultrasonography is the most accurate diagnostic
modality in the confirmation of a viable pregnancy during the first trimester.6
Indications for ultrasonography in the ED include abdominal or pelvic pain, vaginal bleeding,
persistently open cervical os, adnexal mass or fullness, cervical motion tenderness, discrepancy
between uterine size and last menstrual period (LMP), and discrepancy between expected and
measured beta-hCG levels.
A high-resolution vaginal ultrasound probe can detect pregnancy at 3-4 weeks' gestation and
fetal heart activity at 5 and a half weeks. The presence of fetal cardiac activity in women with
bleeding in early pregnancy has been noted to have a sensitivity of 97% and a specificity of 98% for
fetal survival to the 20th week of pregnancy.6
Fetal studies are limited in the first trimester due to small fetal size. Ultrasonography usually
provides information in 3 major areas: location of pregnancy, pregnancy size, and absence or
presence of fetal cardiac activity.
An apparently empty uterus revealed by ultrasonography in a pregnant woman (ie, positive betahCG findings, LMP within last 20 wk) suggests a very early pregnancy (ie, <3 wk GA), a
completed miscarriage, or an ectopic pregnancy. (See Bedside Ultrasonography, First-Trimester
Pregnancy.)

Sonographic signs suggestive of a nonviable pregnancy include the following:


o Irregular gestational sac (ie, gestational sac >25-mm mean sac diameter [MSD] on
transabdominal sonogram; >16-mm MSD on endovaginal sonogram without a
detectable embryo)
o Nonliving embryo (embryo without a heartbeat)
o Presence of abnormal hyperechoic material within the uterine cavity, as depicted in
the sonogram below
o

This endovaginal longitudinal view demonstrates fluid within the uterus


(Ut). Echogenic debris also is present within the endometrial cavity. This
image shows a large pseudogestational sac of an ectopic pregnancy.

This endovaginal longitudinal view demonstrates fluid within the uterus (Ut).
Echogenic debris also is present within the endometrial cavity. This image
shows a large pseudogestational sac of an ectopic pregnancy.

Consider the sonographic diagnosis of early pregnancy failure in relationship to


developmental stage.
o Subclinical or preclinical loss: This occurs within the first 2 weeks after conception.
Sonographic evidence of pregnancy does not exist at this stage.
o Loss at 5-6 weeks: Loss at this stage is based upon gestational sac characteristics.
Abnormal gestational sac size is the most reliable indicator of abnormal outcome.
Gestational sacs should be 5-mm mean sac diameter (MSD) by the fifth gestational
week. An abnormally large gestational sac, as determined by high-frequency
endovaginal sonography (HFEVS), is observed when the MSD is more than 8 mm
without a demonstrable yolk sac or is more than 16 mm without a demonstrable
embryo.
o Loss at 7-8 weeks: Sonographic evidence is based upon demonstration of an
abnormal embryo or gestational sac.
o Loss at 9-12 weeks: Sonographic diagnosis of embryonic demise is usually made on
demonstration of an abnormal fetus. Sonographic evidence of a fetus lacking cardiac
activity is the most specific indicator of embryonic demise. This is depicted in the
sonogram below.
o

This endovaginal ultrasonogram reveals an irregular gestational sac with an


amorphic fetal pole. No fetal cardiac activity was noted. This image represents a
missed miscarriage or fetal demise.

Caution is advised in the diagnosis of embryonic demise. Determination of whether the


viewed structure is the embryo is critical, as no other morphologically recognizable
structures, other than a heartbeat, exist at this stage of development. The embryo must be
scanned thoroughly for evidence of a heartbeat.
o Most recommendations call for 2 independent examiners to view the embryo, either
concurrent with the ED visit or at follow-up.
o Most sonographers recommend repeating the scan within 3-7 days to determine if
normal development is occurring.
o On follow-up, a falling beta-human chorionic gonadotropin (hCG) level, as well as
abnormal fetal development, confirms embryonic demise.
Sonography can identify presence of a subchorionic hematoma or hemorrhage (ie, bleeding
between the endometrium and the gestational sac).
o A subchorionic hemorrhage is the most commonly identified source of first-trimester
bleeding, appearing on sonography as a crescent-shaped hypoechoic area next to the
gestational sac.
o Subchorionic hemorrhage encompasses a spectrum of sonographic findings.
Subchorionic fluid can be classified in relation to gestational sac size and length of
gestation. Subchorionic bleeding is present when pulsation of the subchorionic fluid
is noted.
o Size of the subchorionic hemorrhage should be taken into consideration, as greater
size relates to an increased risk of spontaneous miscarriage. A large subchorionic
hematoma (ie, surrounding greater than 50% of the gestational sac) is a poor
prognostic indicator for the pregnancy outcome. A subchorionic hemorrhage is
depicted below.
o

This endovaginal ultrasonographic image demonstrates a subchorionic


hemorrhage (SH) less than half the gestational sac size.
[ CLOSE WINDOW ]

This endovaginal ultrasonographic image demonstrates a subchorionic


hemorrhage (SH) less than half the gestational sac size.
Subchorionic bleeding can be demonstrated using color Doppler imaging.
Endovaginal ultrasonography should be applied whenever possible to limit image
distortion due to patient habitus or an overdistended bladder.
An incomplete miscarriage may demonstrate a variety of sonographic findings as follows:
o The gestational sac may be misshaped or collapsed, or it may be intact, containing a
nonliving embryo. In addition, an irregular complex mass within the endometrial or
endocervical canal may be present. Sonogram of an incomplete miscarriage is shown
below.
o
o

This image shows an endovaginal longitudinal view of a low-lying


gestational sac (GS) within the uterus (Ut), representing an incomplete
miscarriage.
[ CLOSE WINDOW ]

This image shows an endovaginal longitudinal view of a low-lying gestational


sac (GS) within the uterus (Ut), representing an incomplete miscarriage.
Echogenic material or debris within the endometrial canal may represent retained
products of conception or clotted blood.
o First-trimester molar pregnancies may simulate an incomplete miscarriage, with
echogenic material within the endometrial cavity that has no characteristic vesicles
or cysts.
o Intrauterine fluid collections may represent pseudogestational sacs found in ectopic
pregnancies.
o Studies suggest no statistically significant relationship between the initial presence of
a gestational sac or endometrial thickness and the success rate of expectant
management.
A complete miscarriage may demonstrate the following sonographic findings:
o An empty uterus noted on endovaginal sonogram suggests a complete miscarriage;
however, sonographic diagnosis includes ectopic pregnancy and early intrauterine
pregnancy.
o Careful scanning for adnexal masses and/or free fluid is advised.
o

No single ultrasonographic measurement of the different anatomical features in the first trimester
has demonstrated a high predictive value for determining early pregnancy outcome. Recent research
suggests the finding of blood flow in the intervillous space in cases of first-trimester miscarriage
using color Doppler ultrasonography as useful in the prediction of successful expectant
management. Miscarriages with intervillous space blood flow were 4 times more likely to complete
with expectant management.

Procedures

Transabdominal ultrasonography of the pelvis provides an overall view of the pelvic


structures. A full bladder is required as a sonographic window.
Endovaginal ultrasonography gives a detailed view of the endometrium of the uterus,
ovaries, adnexa, and cul-de-sac. An empty bladder is required for optimal imaging.

Ultrasonography
o US probably is the most important tool in diagnosing an extrauterine pregnancy.
More frequently, it is used to confirm an intrauterine pregnancy. Visualization of an
intrauterine sac, with or without fetal cardiac activity, often is adequate to exclude
ectopic pregnancy. The exception to this is in the case of heterotropic pregnancies,
which occur from 1 in 4000 to 1 in 30,000 spontaneous pregnancies. Screening the
adnexa by US is mandatory despite visualization of an intrauterine pregnancy in
patients undergoing ovarian stimulation and assisted reproduction because they have
a 10-fold increased risk of heterotropic pregnancy.
o Transvaginal US, with its greater resolution, can be used to visualize an intrauterine
pregnancy by 24 days postovulation, or 38 days after last menstrual period, which is
about 1 week earlier than transabdominal US. The gestational sac, which is a
sonographic term and not an anatomic term, is the first structure that is recognizable
on transvaginal US. It has a thick echogenic rim surrounding a sonolucent center
corresponding to the trophoblastic decidual reaction surrounding the chorionic sac.
Structures that represent a developing embryo cannot be recognized until a later
time.

A pseudosac is a collection of fluid within the endometrial cavity created by bleeding


from the decidualized endometrium often associated with an extrauterine pregnancy
and should not be mistaken for a normal early intrauterine pregnancy. The true
gestational sac is located eccentrically within the uterus beneath the endometrial
surface, whereas the pseudosac fills the endometrial cavity.
o The yolk sac is the first visible structure within the gestational sac, and it resembles a
distinct circular structure with a bright echogenic rim and a sonolucent center. It can
first be recognized 3 weeks postconception, about 5 weeks after last menstrual
period. The embryo is recognized first as a thickening along the edge of the yolk sac,
and embryonic cardiac motion can be observed 3.5-4 weeks postconception, about
5.5-6 weeks after the last menstrual period.
o In the absence of reliable menstrual and ovulatory history, a discriminatory zone of
bhCG levels validates the US findings. The discriminatory zone is the level of bhCG,
using the Third International Standard for quantitative bhCG, at which all
intrauterine pregnancies should be visible on US. With abdominal US, that level is
6000-6500 mIU/mL, but high-resolution transvaginal US has reduced this level to
1500-1800 mIU/mL. If transvaginal US does not reveal an intrauterine pregnancy
when the discriminatory bhCG levels are reached, the pregnancy generally can be
considered extrauterine.
o An exception to this is multiple gestations. Kadar et al reported that patients with
normal multiple gestates were found to have levels of bhCG above the
discriminatory zone before any US evidence of the gestation was apparent.1 They
showed multiple gestations with bhCG levels of up to 2300 mIU/mL before
transvaginal US recognition. Therefore, if a multiple gestation is suspected, as in
pregnancies resulting from assisted reproduction, the bhCG discriminatory zone
must be used cautiously. Remember that a discriminatory zone is operator and
institution dependent, and the clinician must be aware of the zone used by that
institution prior to interpreting results.
o The effectiveness of using US with discriminatory zone of bhCG levels has been
well established in the literature.

In one large study of more than 1200 patients by Barnhart et al, 78.8% of
patients were diagnosed definitively at the initial visit using an algorithm that
included the use of US along with serum bhCG levels above the
discriminatory zone.4 According to this study, if the patient's serum bhCG
level was above the established discriminatory zone at initial presentation and
an intrauterine sac was not identified, an operative approach involving
curettage and possible operative laparoscopy was used to diagnose ectopic
pregnancy.

If the patient's serum bhCG levels were below the discriminatory zone, serial
bhCG titers were performed every 2 days. Once a patient's levels reached the
discriminatory zone, US was performed. If, however, the patient's bhCG
levels failed to rise appropriately (ie, at least 66% in 2 d), operative
intervention was undertaken with dilatation and curettage or laparoscopy to
exclude the diagnosis of ectopic pregnancy. With this protocol, Barnhart et al
reported 100% sensitivity and a specificity of 99.9%.4
o The value of US is highlighted further in its ability to demonstrate free fluid in the
cul-de-sac. While free fluid could represent hemoperitoneum, it is not specific for
ruptured ectopic pregnancy. Free fluid on US can represent physiological peritoneal
fluid or blood from retrograde menstruation and unruptured ectopic pregnancies.
Furthermore, US can be used to detect the presence of other pathological conditions
that may display the signs and symptoms of ectopic pregnancy.
Doppler US
o

Color-flow Doppler US has been demonstrated to improve the diagnostic sensitivity


and specificity of transvaginal US, especially in cases where a gestational sac is
questionable or absent. A study of 304 patients at high risk for ectopic pregnancy
found that the use of color-flow Doppler US, compared with transvaginal US alone,
increases the diagnostic sensitivity from 71-87% for ectopic pregnancy, from 2459% for failed intrauterine pregnancy, and from 90-99% for viable intrauterine
pregnancy.
The addition of color-flow Doppler US may expedite earlier diagnosis and eliminate
delays caused by using levels of bhCG for diagnosis. Furthermore, color-flow
Doppler US can potentially be used to identify involuting ectopic pregnancies that
may be candidates for expectant management.

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