Abortions - Technion moodle

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Pregnancy Wastage

Human reproduction is an inefficient
enterprise

Incidence of abortions:
15-20% of clinical pregnancies
50-75% of conceptions
Of all pregnant women, how many will
experience an abortion?
incidental abortion: 25%
 recurrent abortion: 0.5-1.0%

Risk increases: age, parity, smoking
Risk decreases: gestational age
“Abortions act as a screening device
for abnormal pregnancies”
Clinical types of abortions
Spontaneous
Threatened
Incomplete
Missed
Induced
Septic
Inevitable
Complete
Blighted Ovum
Intrauterine fetal death (IUFD)
< 20 weeks - spontaneous abortion 
(missed abortion)
> 20 weeks - antepartum fetal death 
Management:
confirm death
evacuate (D&E, PG, Pitocin)
Recurrent (Habitual) Abortions
The estimated risk: ?
difficulties in the scientific evaluation of therapies.
Number of previous
abortions
1
% of abortions
2
26
3
32
4
26
24
Recurrent Abortion Etiology (1)
There are 5 major diagnostic categories:
 genetic
 endocrine
 anatomic
 infectious
 immunologic
(A random abortion has, similarly, numerous
possible etiologic causes)
Recurrent Abortion - etiology (2)
Genetic factors:
 Translocation - structural rearrangement in
one of the parents - passed to the embryo
 Parental balanced translocation:
1.9 per 1000 in general population
3% in recurrent abortion cases
27% with history of both early abortion &
malformed fetus
 Management: donor oocyte or sperm

Incidence of chromosomal aberrations in
sporadic abortions:
50-60%
mostly trisomies (16, 22, 21, 18, 13)
monosomy x,
triploidy, tetraploidy
Recurrent Abortion - etiology (3)
Endocrine Factors
 Corpus luteum dysfunction
luteal progesterone inadequacy
tests: serum progesterone
“out of phase” endometrial biopsy
causes: Hypothalamic-Pituitary dysfunction
(hyperprolactinemia, nutrition, chronic dis)
Management: Progesterone, HCG, clomiphene

(Diabetes M.; Thyroid disorder)
Recurrent Abortion - etiology (4)
Anatomic factors
 Congenital: Uterine anomalies
DES
cervical incompetence
 Acquired: Intrauterine adhesions
submucous fibroids
cervical incompetence
 Investigation: history, hysteroscopy, HSG
Management: surgical or “expectant Rx”
Recurrent Abortion - etiology (5)
Infectious causes:
 mostly associated with single abortions
In recurrent abortion:
 Mycoplasma hominis, U. Urealyticum ?
 Tuberculosis ?
 Bacterial Vaginosis
Management:
 Doxycycline, Erythromycin ?
Recurrent Abortion - etiology (6)
Immunologic factors
 Role is undefined and controversial
 Blocking antibodies are absent or low in
sera of women with recurrent abortions.
Explained by parental sharing of
antigens.
Management: (controversial)
Immunization of mother with paternal
or mixed lymphocytes; IG infusion
Recurrent Abortion - etiology (7)


More recent findings:
Antiphospholipid syndrome (autoimmune)
anticardiolipin antibodies
lupus anticoagulants
Activated protein C resistance (genetic)
Clinical features: thrombosis, preg. wastage,
complications of pregnancy.
Management: Prednisone, Aspirin (mini doze),
Heparin, Clexane
Recurrent Abortion - etiology (8)
Toxic and environmental factors
 anesthetic gases ?
 alcohol
 smoking
 environmental pollutants
Recurrent Abortion - etiology (9)
Chronic Disease
 any chronic disease
 maternal congenital cardiac disease
 hypothyroidism (rare cause)
 diabetes mellitus (advanced dis.)
 Systemic Lupus Erythematosus
anatomy
(6-12%)
endocrine
(15-20%)
unexplained
50-60%
repeated abortions
infections
(5%)
others:
APCR
cardiolipin
genetic
(5%)
Preconceptual evaluation of couples
with recurrent abortions


remember the main etiologies: genetic, endocrine,
anatomic, immnologic, infectious
Diagnostic studies
karyotype of parents
hysterosalpingography, hysteroscopy
APC resistance
anticardiolipin atb, activated PTT,
luteal phase endometrial biopsy?
platelet assessment (for thrombocytosis)
HLA typing, Mixed lymphcyte reaction ?
Thyroid function, Endometrial cultures ?
Early pregnancy management
following recurrent abortions





treatments are as yet poorly validated
as many as 50 - 75% of pregnancies are successful
even after 3 previous failures
Treatment:
general management guidelines (bed rest, coitus)?
general (HCG, progesterone)
specific (surgery, cerclage, progesterone, steroids,
minidoze aspirin, clexane, antibiotics)
Differential Diagnosis of suspected
early pregnany & vaginal bleeding
early viable & non viable pregnancy
 ectopic pregnancy
 other causes of enlarged uterus
Diagnostic aids:
 clinical assessment
 sonography
 laparoscopy (culdocentesis)

Abortion - Aim of Treatment
Uterine evacuation
 avoidance of infection
 prevention of Rh sensitization

Evacuation of the uterus - technical aspects






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“menstrual regulation”
suction curettage
sharp curettage
cervical dilatation: hegar, laminaria, balloon
anesthesia: general, paracervical, sedation
mid trimester abortions:
route: intraamniotic or extraamniotic
agent: prostaglandins (hypertonic solutions)
antiprogesterone: RU486
Complications of uterine evacuation



Early
bleeding, coagulation disorders (IUFD)
cervical laceration, perforation
Delayed
retained products, infection, bleeding
Late
chronic infection
infertility, ectopic pregnancy
Rh sensitization
psychological sequelae
ECTOPIC PREGNANCY
Pregnancy that develops after implantation of
the blastocyst anywhere other than the
endometrium lining the uterine cavity
Heterotopic preg.: combined intrauterine and
extrauterine preg.
ECTOPIC PREGNANCY –
Incidence
?
in USA – 1992 – 20/1000 reported preg.
higher rate in older women
& multigravid women
increasing due to:
increased salpingitis
improved diagnostic techniques
ECTOPIC PREGNANCY –
mortality




Major cause of maternal death
most common cause in first half of preg.
34 deaths in 1989, USA
4 deaths per 10,000 women with ectopic
(USA, 1989)
Cause: blood loss –
88%
infection 3%
anesthesia complications – 2%
ECTOPIC PREGNANCY –
etiology


Infection: major cause of 1st episode; due to
morphologic changes
in 40% (1st episode) cause unknown:
physiologic: delay of passage of embryo to uterine
cavity more than 7 days – when implantation occurs
ovulation from contralateral ovary – uncommon
hormonal imbalance (ovulation induction, prog.releasing IUD)  impaired tubal transport
ECTOPIC PREGNANCY –
tubal pathology
Salpingitis (6 fold increased risk of TP)
  agglutination of the plicae (folds) of the
endosalpinx  sperm passes, but larger
morula does not.
 Adhesions between tubal serosa and bowel
or peritoneum  altered tubal motility
 Prior ectopic preg.
 Prior tubal surgery
ECTOPIC PREGNANCY –
contraception failure
Sterilization failure – 1/3 of pregnancies
 P only pill – 5%
 Levonorgestrel (Mirena) releasing IUD
 Copper IUD

ECTOPIC PREGNANCY –
pathology
Tubal – 98 %, mostly in the ampullary portion
Abdominal – 1.4%, mostly secondary
Ovarian/cervical - < than 1%
ECTOPIC PREGNANCY –
pathology (cont.)



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The morula does not grow mainly in the tubal
lumen.
The trophoblast invades the muscularis of the
oviduct and grows mainly between the lumen of
the tube and its peritoneal covering
Hemorrhage is mainly extraluminal
Rupture: the serosa is streched by bleeding,
producing necrosis secondary to an inadequate
blood supply
ECTOPIC PREGNANCY –
pathology, cont.



Slow growth of trophblastic tissue 
slow rise of BHCG
Endometrium: secetory – 40%
proliferative – 20%
decidual – 20%
arias stella (endometrial glands
hypertrophied, hyperchromatism, pleomorphism,
increased mitotic activity) – 20%
Decidual cast: all the decidua passing through the
cervix (DD – abortion)
ECTOPIC PREGNANCY –
symptoms
Abdominal pain – nearly universal
 Amenorrhea
 Vaginal bleeding
 Dizziness, fainting


Often, atypical presentation
ECTOPIC PREGNANCY –
signs
Adnexal tenderness
 Abdominal tenderness
 Adnexal mass
 Uterine enlargement
 Orthostatic changes
 Fever - uncommon

ECTOPIC PREGNANCY –
diagnosis
Serial testing
Beta HCG
normal preg. – doubling every 2-3 days
ectopic preg. - slow rise
falling levels
 Progesterone (less than 5 ng/ml)

ECTOPIC PREGNANCY –
diagnosis (cont.)
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
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Ultrasound
normal preg. – at BHCG 1500-2000 mIU/ml
a gestational sac in seen
ectopic preg. – no IU sac
presence of adnexal mass or
gestational sac in oviduct
D&C
Culdocentesis
Laparoscopy
ECTOPIC PREGNANCY –
management
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
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Surgery: mostly laparoscopically
salpingectomy, salpingostomy
segmental resection
Persistent EP: 5% following salpingostomy
Medical Therapy – methotrexate
success: low BHCG - < 5,000 - above 90%
> 15,000 – 68%
Expectant management
Remember the Rh factor
ECTOPIC PREGNANCY –
subsequent conception
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
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Following ectopic – 60%-70% conceive  1/3
ectopic
Higher conception rates (above 80%) following
unruptured EP, conservative treatment, no infection
Repeat EP – following 1 EP – 20 % (8% to 27%)
following 2 EP – nearly half
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