GAUDIUM SPES

I hope I can be the ray of

hope to you, you will be
beacon of light to others
 Bleeding in Pregnancy
 First Half (1-20 wks)  Second half (21-40 wks)
 A. Abortion,  A. Antepartum Hemorrhage,
a.1 Placental abruption,
 B. Ectopic Pregnancy,  a. 2 Previa
 B. Postpartum Hemorrhage,
 C. GTD Gestational b.1 3rd stage bleeding,
trophoblastic disease  b.2 uterine atony,
 b.3 retained placental,
fragments,
 b.4 accreta, increta, percreta,
b.5 inversion,
 b.6 lacerations,
 b.7 puerperal hematoma ,
 b.8 Rupture of the uterus
 ABORTION
 Spontaneous  Induced abortion:
 a. pathology,  History
 b. etiology,  Indications
 c. Fetal factors,  Elective, (voluntary)
 d. Maternal factors,  Consequences of
 e. Paternal factors, elective abotion
 f. Categories of
abortion
 ABORTION
 Definition -Spontaneous or miscarriage w/o
mechanical of medical means to empty the
uterus.
– Pathology – hemorrhage into the decidua basalis
ffed by necrosis of tissues.
– A. early the ovum detaches—uterine contractions---
EXPULSION. Termination- blighted ova,
– B.1 late abortions maceration (skull collapses)
– b.2 compressus (amniotic fluid absorbed),
– b.3 papyraceous, fetus dry & compressed resembles
parchment)
 ABORTION, ETIOLOGY
 Statistics, 80% first 12 weeks & half are
chromosomal anomalies.
 PROFILE :
 ^ with parity & maternal & paternal age,
12% < 20: >40 26% ,
 ^ conception 3 months after term
pregnancy.
 Abortion fetal factors

 FETAL FACTORS- A. abnormal zygotic development,

zygote, embryo, early fetus, placenta. Blighted ova,
noted by Hertig et Sheldon (1943) b. morphological
disorganizations, Poland et al.
 B. Aneuploid abortion – chromosomal abnormalities, 95
% due to maternal gametogenesis errors, 5% paternal
in origin.
 C. Autosomal trisomy,
 D .monosomy X (45 X),
 E.Triplopidy (hydropic molar degeneration, incomplete or
partial,
 F. Tetraplopid abortuses, Euploid < 8 -13 wks
occurrence ^ maternal age 35. ^
 Abortion, maternal factors

 INFECTIONS
 brucella abortus & campylobacter not significant : Listeria
monocytogenes or Chlamydia trachomatis, nor herpes simplex.
Mycoplasma & ureaplasma urealyticum (1983) ??? Toxoplasma
gondii.
 (2002) relation of 2nd trimester spontaneous
abortion w/ bacterial vaginosis.
 CHRONIC debilitating diseases – TB &
Carcinomatosis seldom produces abortion,
 CELIAC SPRUE causes male & female infertility.
 Abortion, endocrine abnormalities

 HYPOTHYROIDISM – iodine deficiency

^abortion, thyroid antibodies ^ BUT
 2000 untreated w/ antithyroid antibodies likely
to have LIVE birth as those w/o antibodies.

 DIABETES MELLITUS - ^ abortion & congenital

malformation w/ insulin dependent diabetes,
related to metabolic control. (2002) ^ insulin
resistance associated w/ recurrent pregnancy
loss.
 Abortion, endocrine abnormalities

 PROGESTERONE DEFICIENCY – Luteal phase defect

associated w/. Abortion. Corpus luteum surgical removed
less than 8-10 wks replacement must be done.
 NUTRITION- no effect just like nausea & vomiting.
 DRUG USE & environmental ^
 a. tobacco controversial as of (2003),
 b. alcohol ^ abortion & congenital anomalies ^
depending on the dose.
 c. caffeine - 5 cups ^ (2004) relation of coffee &
abortion rate.
 RADIATION – dose not known.
 CONTRACEPTION – OC & spermicidals no effect EXCEPT
pregnancy after IUCD failure ^ abortion rate.
 Abortion, environmental toxins

 ENVIRONMENTAL – formaldehyde, arsenic, lead,

benzene, & ethylene oxide ?? (1982).
 (1997) exposure to anesthetic drugs ^ abortion rate.
 IMMUNOLOGICAL (1995) 15 % recurrent loss. TWO
pathophysiological,
 a. autoimmune (immunity against self), antiphospholipid
antibodies are family of antibodies that bind to
negatively charged phospholipids (2003). Therapy 1. low
dose aspirin 2. heparin can ^ live birth (1996)
 b. alloimmune theory( immunity against another person)
 N.b. DO NOT endorse immunotherapy for recurrent
aobrtion.
 Abortion, environmental toxins

 INHERITED THROMBOPHILIA – factor V

Leiden mutation, ^ BUT TX is
controversial.
 LAPOAROTOMY- does not ^ incidence of
abortion, n.b. ovarian tumors <10 wks,
supplementary progesterone needed.
 PHYSICAL TRAUMA – “major abdominal
trauma can precipitate abortion.”
 Abortion, uterine defects

 UTERINE DEFECTS – a. acquired defects large

multiple leiomyomas usually do not cause
ABORTION. If associated location more
important than the size.
 Asherman is a cause can be diagnosed
accurately by hysteroscopy.
 a.Tx. Lyze the adhesions & IUD to prevent
adhesions,
 b. high dose estrogen therapy 90 days following
adhesiolysis. (Abortion decreased following this
treatment. )
 Abortion, developmental defects

 DEVELOPMENTAL DEFECTS – probably

secondary to diethlystilbestrol .
Controversy on the treatment but as a last
resort corrective measures may be tried.
 INCOMPETENT CERVIX painless cervical
dilatation in second trimester, w/ prolapse
of membranes & expulsion etc. CERCLAGE
beneficial. DX trans V cervical length &
funneling are being investigated
 Incompetent cervix

 Etiology trauma to the cervix, D&C,

conization, cauterization or amputation, &
? Exposure to diethlystilbestrol.
 CERCLAGE - Between 12-16 wks
– a. simple McDonald (1963)
– b. More complicated Shirodkar after failure
with McDonald.
 Abortion, paternal factors

 PATERNAL – (2003) Carrel et al

chromosomal abnormalities in sperm
associated w/ abortion
Categories of spontaneous abortion
 THREATENED – a. bloody vaginal discharge w/
closed cervix may progress to spotting to
bleeding, overall abortion with ensue HOWEVER
risk is essentially lowered if w/ cardiac activity.
Other risks pre-term delivery, LBW & perinatal
death.
 Differential DX- cervical lesions, polyps.
 TREATMENT- NONE bed rest ? Acetaminophen
might help. Ectopic must be considered. Anti-
immunoglobulin has no EB support (2002) ACOG
 CATEGORIES
 INEVITABLE – a. rupture of membranes,
by leaking of amniotic fluid, b. uterine
contractions, c. if after 48 hours no AF
had not escaped , no bleeding, pain or
fever MAY resume activities BUT NOT
VAGINAL penetration.
 Categories
 Threatened abortion: INEVITABLE ABORTION
a. bloody mucoid a. Rupture of
discharge appears membranes w/
through a CLOSED leaking of amniotic
cervix, fluid,
 b. spotting or actual b. cervix open
bleeding may persist SIGNALS abortion,
may affect 5% of b. uterine
cases. Risk is lower if contractions surely
there are cardiac points to ABORTION
activity.
 Categories
 COMPLETE-  INCOMPLETE –
 a. complete detachment  a.internal cervical os
& expulsion of the remains open to allow
conceptus, passage of blood.
 b. cervix closes.  b. fetus or placenta may
be still in utero,
 c. bleeding depends on
age of gestation,
 d. may proceed to
curettage inspite of
infection provided
antimicrobials are started.
 Missed abortion
 Uterus-
 a. retains the dead fetus for weeks,
 b. cervix close,
 c. may or not have bleeding,
 d. uterus remains stationary fore weeks or even
becomes smaller,
 e. no symptoms EXCEPT amenorrhea.
 Management individualized- Medical or surgical.
Serious complication after prolonged retention is
coagulation defect.
 Abortion , recurrent
 Definition – 3 or more consecutive abortions. (2)
tests in use for investigation,
 a. parental cytogenetic analysis,
 b. Lupus anticoagulant & anticardiolipin
antibodies assays. ACOG Mechanism placental
thrombosis & infarction. May inhibit the release
of prostacyclin , potent vasodilator and inhibit
platelet aggregation.
 PROGNOSIS- with or w/o treatment will have
successful pregnancies
 Abortion, induced
 Definition – medical or surgical
termination of pregnancy before the age
of viability.
 Stats- 20% aged 19 years, majority
younger than 25 years of age.
 60% during first 8 wks AOG
 88% 12 wks AOG.
 Abortion, induced
 Therapeutic abortion – defined as “termination
of pregnancy before the age of viability for the
purpose of saving the life of the mother.”
 Other states extended their laws “ to prevent
serious or permanent bodily injury to the
mother,”
 “ to preserve the life and health of the mother”.
Some states allowed abortion if pregnancy was
to result to grave malformations. (Williams
OBSTETRICS, 22nd edition)
 Induced Abortion
 Therapeutic abortion definition –
“termination of pregnancy before the
period of fetal viability for the purpose of
saving the life of the mother.”
 “To prevent serious or permanent bodily
injury to the mother,”
 “To preserve the life or health of the
woman.”
 Induced abortion
 Roman Catholic Church’s traditional
prohibition of abortion did not receive
the ultimate sanction of universal law
(excommunication) until 1869 (Pilpel and
Norwich 1969)
 Elective Abortion
 Elective or (voluntary abortion) is the
interruption of pregnancy BEFORE
viability at the request of the woman but
not for reasons of impaired maternal
health or fetal distress.
 Executive board of ACOG (2000)
“supports the rights of the woman and
considers this a medical matter between
the woman and her physician.
 Elective Abortion

 Roe vs Wade
 Abortion policy ACOG (2000) affirmed ,
“The intervention of legislative bodies into
medical decision making is inappropriate ,
ill advised and dangerous.”
 Abortion techniques, surgical
 Cervical dilatation, ffed by uterine
evaccuation,
 curettage,
 vacuum aspiration (suction curettage),
Dilatation and evacuation (D & E,
Dilatation and extraction (D & X),
Menstrual aspiration,
 LAPAROTOMY
 a. hysterotomy, b. hysterectomy
 Abortion, Medical techniques
 Intravenous oxytocin, intramanionic
hyperosmotic fluid, 20% saline, 30% urea,
Prostaglandins E2, f2@, E1 & analoques,
a. intramnionic injection,
 b.extra-ovular,
 c.vaginal insertion,
 d.parenteral injection,
 e. oral ingestion
 Consequences
 Maternal mortality – first 2 mons 0.7%/100,000
procedures (Barlett et al 2004). Doubles for each 2 wks
after 8 wks.
 IMPACT on future pregnancies : (Hogue 1986) Studies
must be carefully interpreted:
 a. Fertility is not diminished except infrequently if there
is concomitant infection,
 b. Vacuum aspiration does not ^ 2nd trimester abortion
or preterm delivery,
 c. ectopic pregnancy has not been similarly, except w/
pre-existing chlamydial infection or who develop post-
abortion infection
 d. multiple sharp curetage abortion ^ risk of placenta
previa (Johnson et al 2003)
 Septic Abortion
 (Barrett et al 2002) Serious complications arise
from criminal abortion, even spontaneous
abortions, & legal elective abortion, but severe
hemorrhage sepsis, bacterial shock with lesser
frequency,
 (Vartian Septimus 1991) uterine infection is the
usual outcome
– but parametritis, peritonitis, endocarditis & septicemia
may may occur.
 Resumption of ovulation
 May resume as early as 2 wks postabortal.
 (Lahtennma Ki & Luukkainen (1978)
surges of LH 16-22 days in 15-18 women
studied. Progesterone followed soon
thereafter.
 If contraception is to be practiced one
should use initiated as soon after abortion.
 Test
 Medical induction-  Mechanism- reversing
 Anti-progesterone, the progesterone-
mifepristone induce inhibition of
 Antimetabolite
contraction, (mm) or
methotrexate by stimulating the
myometrium.
 Prostaglandin
misoprostol
 Jousting
 Voluntary abortion  Medical techniques
 Therapeutic abortion  RU 486
 Spontaneous abortion  Vacuum aspiration
 Hemorrhage into the  D&X
decidua basalis,  Extraovular injection
 Request for the  Surgical procedures
procedure not for  Intra-amniotic
reasons of impaired hyperosmotic fluid
maternal health,
 For health reasons
 Jousting
 Inevitable abortion  Threatened
 a. evidence of leaking  a. Bloody mucoid
of fluid, discharge,
 b. fluid between  b.closed cervix,
chorion & amnion,  c. open cervix,
c.internal cervical os  d. cardiac activity
close, good prognosis
 d. cardiac activity
present
 ECTOPIC PREGNANCY
 Risk factors:
 HIGH,
 1.tubal corrective surgery, 21.0
 2.tubal sterilization, 9.3
 3.previous ectopic pregnancy,8.3
 4.in utero DES exposure, 5.6
 5.IUD, 4.2
 6.documented tubal pathology.3.8-2.1
 Risks factors
 Slight risk:
 1. Previous abdominal
 Moderate risk pelvic surgery 0.93-
1. infertility-2.5-2.1 3.8
2. Previous genital  2. smoking, 2.3-2.5
infection, 2.5-3.7  3. douching, 1.1-3.1
3. Multiple partners 2.1  4 intercourse <18 1.6
 Ectopic, other factors
 ASSISTED REPRODUCTION-, GIFT (gamete
intrafallopian transfer ^ (IVF) invitro fertilization
3 % & atypical implantations higher e.g. cornual,
abdominal, cervical, ovarian ,heterotyphic
(uterine & extrauterine).
 FAILED CONTRACEPTION – Lesser because
there are lesser pregnancies but ^ in failed
contraception such as BTL, IUD, & progestin
only pills (Sivin 1991)
 Factors ^ ectopic
 Reports USA, Eastern Europe, Scandinavia & Great
Britain 1979’ -1980’ :
 POSSIBLE reasons:
 a. Prevalence of sexually transmitted tubal infection &
damage (Brunham, Maccato 1992)
 b. earlier diagnosis of ectopic otherwise destined to be
resorbed,
 c. Popularity of contraception & its eventual failure,
 d. BTL,
 e. assisted reproductive techniques,
 f. tubal surgery for reconstruction, e.g. salpingotomy,
tuboplasty.
 Mortality

 Maternal deaths lowered BUT Ectopic ^ &

vacillated secondary to :
 Improved diagnosis & treatment,
 Pathogenesis

 1. Tubal pregnancy,
 2. tubal abortion,
 3. tubal abortion,
– 3.1 Abdominal pregnancy,
– 3.2 broad ligament,
– 3.3 interstitial pregnancy
 Multifetal ectopic

 Heterotypic – tubal + uterine, initially

RARE but advent of assisted reprooduction
technique ^ 1 – 7,000 & as high as 1 –
900 in ovulation induction, (Glassmer et
1990).
 Heterotypic
 POINTS to ponder on:
 1. Post assisted reproductive technique,
 2. Persistent ^ HCG determination post D & C
for induced or spontaneous abortion, 3. Uterine
fundus is bigger than menstrual dates,
 4. More than one corpus luteum,
 5. absence of bleeding/ vagina presence of signs
& symptoms of ectopic pregnancy. 6.
Ultrasonographic evidence (Nugent 1992) N.B.
Twin tubal has been reported.
 Types of ectopic

 Are very uncommon:

 1.tubo-uterine, implantation interstitial
 2. tubo-abdominal, fimbriated portion
 3. tubo-ovarian – adherent partly tubal &
ovarian.
 Clinical features, ectopic
 REMINDER –In contemporary practice,
symptoms & signs of ectopic are often
subtle or even absent.
Classical – normal menstruation
are now spotting.
 Rupture – severe abdominal pains, sharp,
stabbing or tearing in character. Exquisite pains
on wiggling, bulging cul-de-sac, diaphragmatic
irritation.
 Signs & symptoms, ectopic

 Pain – pelvic & abdominal pains (95%)

amenorrhea some degree of spotting (60-
80%), might mistake for a normal
menses, profuse bleeding is rarely
ECTOPIC,
 GIT (80%),
 dizziness light headedness (58%).
 W/ rupture pains anywhere.
 Signs & Symptoms, ectopic
 Uterine changes –
 may be displaced by the ectopic mass,
25% enlarges because of hormonal
effects,
 decidua is variable, , uterine decidua w/
trophoblast suggest ectopic but not
absolutely, 5-10%
 decidual casts are passed out.
 Pelvic mass
 Pelvic mass may range from 5-15 cm in 20% of
cases, posterior or lateral soft & elastic, might
firm with infiltration, overzealous exams might
cause RUPTURE of the mass.
 Blood pressure & pulse, <rupture normal, 25
women w/ ectopic noted heart rate >100 beats
& systolic pressure >100 (Birkhahn et al (2003).
(StabileGrudzinskas) 1- 50 presented in state of
shock.
 Culdocentensis nothing new.
 Laboratory, ectopic
 Hemogram depleted volume replaced w/
hemodilution within 24 hours. Might not show so much
changes, stressing monitoring more valuable than the
initial reading. Leucocytosis up to 30,000/ul.
 Chorionic gonadotrophin assays – cannot be
diagnosed by a (+) pregnancy test. ELISA sensitive to 10
-20 ml/u/ml & (+) 99%.
 Serum progesterone – single test can denote viability,
25ng/ml excludes ectopic, values below 5-25ng signifies
dead fetus or ECTOPIC but not conclusive.
 Role of ultrasound
 Indispensable to CONFIRM the clinical DX of
ectopic, size & location. A. abdominal UTZ 5-6
wks or 28 days post ovulation , gestational sac
within the uterine cavity, ectopic rarely co-exists,
 however in its absence BUT
 1.w/ a positive pregnancy test
 2. fluid in the cul de sac,
 3. an abnormal pelvic mass ECTOPIC is almost
certain (Romero et 1988). There are some false
(+ ), corpus luteum cysts & matted bowels can
simulate tubal pregnancies.
 UTZ
 VAGINAL – earlier & more specific dx of
tubal, has been the imaging of choice as
early as (1) wk after missed menses.
Serum B-hCG > 1000 u/ml gestational
sac is seen in half the cases.
 (Dart Et al 2002) fluid seen in the cul de
sac & its amount^ likelihood of tubal
pregnancy in 50%.
 DX, ectopic
 MULTI-MODALITY DIAGNOSIS – 80% diagnosed
decreasing maternal mortality appreciably. ACC
to (Barnhart,1994, 1999,Kaplan 1996 et al found
the following (5) key components,
 1. vaginal sonography,
 2. Serum b hCG both initial level & rise & fall,
3.serum progesterone,
 4. uterine curettage,
 5. laproscopy & less frequently laparotomy.
 Controversies
 Trade offs- Strategies that maximize all may
result in the interruption of a normal pregnancy
1 for every 100 women.
 Those who will be more conservative or do not
employ curettage result in unnecessary medical
or surgical therapy for tubal (Barnhart 2002).
N.B. These strategies only apply to
hemodynamically STABLE patients, those w/
presumed RUPTURE prompt SURGERY.
 Fine tuning
 Discriminatory serum b hCG – above levels
& (-) vaginal UTZ uterine cavity may mean
TUBAL.
 If below b hCG be done serially (+) repeat
vaginal UTZ.
 PROGESTERONE - <5ng/ml -25 ng/ml ^
25 unlikely to be tubal.
 N.B. progesterone may be higher in
assisted reproductive techniques.
 Surgical diagnosis

 Laparoscopy- more cost effective as

compared to laparotomy and post op care
shorter.
 Laparotomy done if hemodynamically
unstable.
 Treatment & Prognosis
 Anti D immunoglogulin – w/ an ectopic who are not
sensitized should be given.
 SURGICAL MTX. 1. earlier dX & TX < rupture higher
subsequent pregnancy rate.
 a. laparoscopy preferred, if tubal salvage done referred
to as conservative. Salpingectomy is RADICAL,
 b. salpingostomy less than 2 cm & located in the distal
3rd of the tube,
 c. salpingotomy same except it is still to b sutured,
 d. salpingectomy,
 e. segmental resection & anastomosis
 Persistent ectopic
 1. small pregnancies less than 2 cm,
 2. early therapy < 42 menstrual day,
 3. b hCG >3,ooo,lu/ml,
 4. implantation medial to the
salpingostomy site,
 5. in the case that b hCG ^^^ additional
medical or surgical tx needed.
 Medical treatment
 Systemic – Methotrexate acts as a folic acid antigonist &
is highly effective against proliferating trophoblast.
Tanaka used it (1982). Medical contraindication is
ACTIVE intra-abdominal bleeding, if size is 4 cm >
ACOG contraindications
 a. breast feeding,
 b. immunodeficiency,
 c. alcoholism,
 d. liver or renal disease,
 e. blood dyscrasias,
 f. active pulmonary TB & peptic ulcer.
 Medical Treatment
 Direct injection,
 oral methotrexate,
 expectant mtx.
 1.decreasing b hCG,
 2. tubal pregnancies only,
 3. no bleeding or rupture by UTZ,
 4. ectopic mass not bigger than 3.5 cm.
 Abdominal pregnancy
 PARKLAND Hospital ectopic is quite common abdominal
1-25,000. Risk factors re the same as in ectopic
pregnancy.
 Signs & symptoms of ectopic can be used
retrospectively. Pregnancy does not “feel right”. Cervix
usually displaced can dilate but effacement is unusual.
Uterus may be palpated in the lower part of the
pregnancy mass.
 LAB- 1. transient anemia after the rupture,
 2. unexplained ^ in alpha feto-protein,
 3. UTZ –may miss the Dx, oligohydramnios not specific.
 Management of abdominal
pregnancy

 Life-threatening & clinical management

depends on the AOG. AWAIT fetal
viability- dangerous because of bleeding.
Because of the risk termination is the
usual treatment. Management of placenta
etc refer to p 266-268, 22nd edition
Williams Obstetrics
 Obstetrical Hemorrhage
 ANTEPARTUM –
a. Placental Abruption,
b. Placenta previa.

c. HYPOVOLEMIC SHOCK
 Obstetrical Hemorrhage
 POSTpartum bleeding:
 Third-stage bleeding,
 Uterine atony, Consumption coagulopathy
 Retained placental Placental abruption,
fragments, IUFD & delayed delivery,
 Accreta, percreta,increta, Amnionic fluid embolism,
 Inversion, Septicemia,
 Gen Tract lacerations, Abortion.
 Hematoma,
 Rupture of the uterus.
 Classifications
 Abnormal placentation, Other factors
 Placenta previa Obesity
 Placental abruption, Native AM
 Accreta, percreta, increta, Prev PPH
 Ectopic,
 & Hydatidiform mole.
Trauma, intrapartum & delivery
 Episiotomy, difficult  Small maternal blood
vaginal delivery, Low- volume,
mid- forceps, CS or/&  small women,
hysterectomy, hypervolemia not yet
UTERINE RUPTURE, attained,
prev.scarred uterus,  constricted
high parity, hypervolemia,
hyperstimulation,
obstructed labor,  Pre-eclampsia,
severe,
 IU manipulation,
 Eclampsia.
 mid-forceps rotation.
 Uterine atony
 OVERDISTENDED
UTERUS,
 large fetus,
 multiple fetuses,
 hydramnions,
 distension w/ blood
clots.
 ANESTHESIA,
halogenated agents
conduction/hypotension.
EXHASUTED MYOMETRIUM
RAPID LABOR,
PROLONGED LABOR
oxytocin or prostaglandin,
chorioamnionitis,
PREVIOUS UTERINE
AAATONY
Coagulation defects
 Abruptio placenta,
– IUFD,delayed delivery,
– amnionic fluid embolism,
saline-induced abortion, sepsis
syndrome,
– severe intravascular hemolysis,
– massive transfusions,
– severe PET,
– congenital coagulopathies,
anticoagulant treatment.
 Antepartum bleeding
 Def- premature separation of a normally
implanted placenta, (Latin “rendering
asunder” denotes a sudden accident.)
 a. concealed, carries a worst maternal &
fetal prognosis, not only because of
consumptive coagulopathy
 & also bleeding not visible, b. external
 Differentiate from a painless, causeless
bleeding “placenta previa”.
Abruptio, perinatal morbidity & mortality
 ^ mortality rate is because of the association of
abruption to PRE TERM delivery & even to term
neonates.
 SURVIVORS have neurological sequelae.
 Etiological factors,
 a. ^ w/ maternal age,
 b. great parity,
 c. race: African-american,
 d. most common association is HYPERTENSION, pet,
50% chronic HPN & the rest is gestation in nature.
 ( Ananth 1999 a 3X w/ CHVD, 4X Pet severe.)
 Abruption
 Incidence of abruption lowered if treated a. w/
mag sulfate,
 b.^ of abruption w/ preterm premature ruptured
membranes.
 c. cigarette smoking,
 d. cocaine abuse, 8 still births resulted,
 e. thrombophilias, factor V Leiden or
prothrombin gene mutation,
 f. trauma not much of an association,
 & g. leiomyomas especially behind placental
implantation,
 Pathology, abruption
 Hemorrhage into the basalis, decidual spiral
artery consequently results into
 a. concealed or retained blood behind the
placenta,
 a.1 placenta completely detached but
membranes are still attached,
 a.2 blood gains entry into the amnionic sac,
 a.3 fetal head so closely adherent that the
blood cannot pass through.
 Abruption, signs & symptoms
 Sign or symptom %
 Bleeding/vagina 78 (-) UTZ do not
 Uterine tenderness 66 exclude
 Fetal distress 60 ABRUPTION
 Pre-term labor 22
 Frequency contractions 17
 Hypertonus 17
 Dead fetus 15
 Diagnosis of abruption
 Very diverse – external may be associated w/ no
shock at all, vice versa. Presenting symptoms
was epistaxis she had IUFD, etc.
 SHOCK- Intensity of shock is seldom out of
proportion to the maternal blood loss. IUFD and
it amounted to half of the blood volume of the
mother. Hypotension is not a usual finding even
in cases of concealed hemorhage. Oliguria
secondary to inadequate renal perfusion is
responsive to treatment of hypovolemia.
 Differential diagnosis

 Painful & painless bleeding per vagina had

been the hall mark of diagnosis. Painless
bleeding may be accompanied by labor
suggestive of abruption. Or there might
already be abruption but no PAINS AT
ALL.
 Abruption
 Consumption coagulopathy- overt
hypofibrinogenemia < 150mg/dl-
important feature is activation of
plasminogen to plasmin lyzes fibrin
microemboli maintaining the patency of
microcirculation, fibrinogen – fibrin
degradation products re found in the
maternal serum. N. B. post-transfusions
may result in thrombocytopoenia.
 Abruption
 RENAL FAILURE may be observed in
severe cases, reversible tubular necrosis
accounts for 75% of renal cases failure, if
accompanied by PET renal vasospasm is
likely intensified. Without or w/o
preeclampsia proteinuria is common w/
severe forms of abruption.
 COUVELAIRE uterus do not interfere with
uterine contractions.
 Fetal distress, in Abruption
 Placental abruption

Maternal bleeding Fetal bleeding Uterine

hypertonus
Placental
separation Fetal distress
Del. Infant transfusion
Prompt delivery
Prompt delivery
Transfusion + Prompt
delivery
 Tocolysis
 Hurd et al 1983:  Sholl (1987)
Abruption Coombs(1992) use of
unrecognized for a tocolysis IMPROVED
dangerous long time. outcome in a highly
 CONCLUSION- selected group of pre-
continue trials & term w/ abruption.
study TILL then we  Towers (1999), mag
consider TOCOLYSIS sulfate, terbutaline,
a contraindication for pereinatal mortality
ABRUPTION. 5% no different
untreated
 CESAREAN SECTION
 Kayani et al 2003 relationship between
rapidity & neonatal outcome in 33
patients, it was concluded from the
rapidity depends the better fetal outcome.
 VAGINAL – Placental separation severe,
fetus dead, unless bleeding is so BRISK &
other contraindications to vaginal.
 Other factors
 Labor –hypertonus may be difficult to
palpate for labor.
 Amniotomy –
 a. no longer for the reason of minimizing
spreading of thromboplastin materials
therefore minimizing efects of coagulation
defects
 b. hasten labor is still acceptable provided
the fetus is mature.
 Other factors
 OXYTOCIN – if there are no rhythmic
contractions then oxytocin has a role.
There is no evidence that shows oxytocin
to be a factor in disseminating
thromboplastin into the circulation to
enhance consumption coagulopathy (Clark
colleagues 1995) Pritchard & Brekken
1967)
 Timing of delivery
 Fetus is previable or dead – no need to
establish when to DELIVER. Determine
factors are the adequate blood & fluid
replacement RATHER than the interval to
delivery,(University of Virginia &
Parkland)(Brame et al 1968, Pritchard &
Brekken 1967). Intelligent expectancy w/
transfusion did not produce more
complications compared to the delivery
earlier.
 Placenta Previa
 Def.- placenta located over or very near the internal os.
 Four degrees:
 a. Total,
 b. Partial,
 c. Marginal,
 d. Low-lying, placental edge does not reach the internal
os but in close proximity.
 Vasa Previa –fetal membranes cross the fetal
membranes & present at the cervical os. Uncommon
cause of bleeding BUT associated w/ high rate of fetal
death.
 Placenta Previa

 The degree of previa depends on the cervical

dilatation during examination,
 e.g. 1. a low-lying at 2 cm. becomes a partialis
at 8 cm because of the dilatation,
 2. a totalis may become a partialis at 4 cm.
dilatation.
 This also implies a certain amount of bleeding
because of the separation an inevitable
consequence of the lower segment formation.
 Placenta Previa

 A question to ponder on a, painless
bleeding from focal separation of the
placenta in the lower uterine segment but
away from partially dilated cervical os be
a previa or an abruption??? (Answer)
 P.Previa
 Perinatal morbidity & mortality – Pre-term
delivery is a major cause of perinatal death.
Ananth (2003b)^neonatal death even w/ term
pregnancy, fetal growth restriction (Crane et al
found no ^ incidence after controlling w/
gestational age & limited prenatal care. (?)
congenital anomalies also ^, ?? Maternal age.
Ananthet al 20001a, previa, growth restriction,&
pre-term delivery. The only common
denominator was PRE-TERM delivery.
 P.Previa

 Etiology –
 1. advancing age (Age 19 1- 1,500 : Age 35 1 per 100,
 2. multiparity 2.2% & in multifetal 40%,
 3. Prior cesarean section ^ 3X & in the number of prev.
CS 2X is 1.9%: CS 3X or more 4.1% ^ Cesarean
hysterectomy, 4. smoking –carbon monoxide hypoxemia
causes compensatory placental hypertrophy.
 DEFECTIVE VASCULARIZATION – possible result of
inflammatory or atrophic changes is implicated in the
development of PREVIA
 P.Previa, clinical findings

 Painless bleeding, 2nd semester or

thereafter, w/o any warning & or pain in a
very normal pre-natal care, fortunately
initial is minimal ceases spontaneously
then recurs. If implantation not over the
os N.B. there might be NO BLEEDING at
all till labor mimicking abruptio.
 P.Previa

 Accreta, increta, & percreta – area of

poorly developed lower uterine segment.
7% (Frederiksen 1999).
 COAGULATION DEFECT- Rare even
w/complete separation from implantation
site. Not so much because thromboplastin
usually EXISTS through the cervix.
 P.Previa
 DIAGNOSIS – a. History of Bleeding of any
nature last 20 wks is either Previa or abruptio,
 b. sonography,
– b.1 abdominal locate the placenta “with considerable
accuracy. Pitfalls should be minimized.
– b.2 trans vaginal more accuracy but danger of
provoking bleeding. Authors affirmed the superiority
of TVUZ inspite of dangers. Transperineal better than
transabdominal.
– c. previa can only be established firmly “passing the
finger through the cervical os & touching t he
placenta.” Never done unless in double set-up.
– MRI will very unlikely replace ultrasound in PREVIA
 P.Previa

 Migration – Placentae that lie close to os

BUT not over it , during the 2nd trimester
or even early 3rd are unlikely to PERSIST
by term. May in cases of previous CS
 P.Previa, management

 1. Pre-term no indication for delivery,

 2. fetus reasonably term,
 3. those in labor, (double set-up)
 4. Profuse hemorrhage though the fetus
immature mandates delivery.
 Delivery, P.Previa
 CS “is practically necessary in all patients”.
Transverse is usually the incision of choice
UNLESS the placenta is anterior fetal bleeding
may be dangerous.
 WARD (2003) avoids hitting the placenta by
looking for the cleavage where the neonate can
be delivered. N.B. When the lower uterine
segment shows bleeding even in the absence of
histological finding of accreta. The present
management for accreta is hysterectomy since
conservatism had produced 25%maternal
mortality.
 Prognosis
 Morality rate went down with blood
transfusion & Cesarean were done.
Prematurity still poses the highest morality
in the presence of previa.
 Butler et al (2001) previa patients had
maternal serum alpha-fetoprotein at least
2.0 multiples of the median (MOM) ^ risk
in prematurity & previa.
 POSTPARTUM hemorrhage

 Def. blood loss of >500 ml of blood after

completion of third stage of labor. It is
reported that almost ½ of women lose
500 ml or more during delivery. Pritchard
et al noticed in 5% of cases loss of 1Liter.
 EBL was also noted to be half of the actual
loss.
 PPH, placental site
 Implantation site –
 a.uterine atony, a.1 halogenated hydrocarbons,
a.2 poorly perfused myometrium – hypotension,
a.2.1 hemmorhage, conduction anesthesia,
 b. overdistension of the uterus,
 c. prolonged labor, precipitate labor, d.
augmentation, e. high parity, f. history of uterien
atony, g. chorioamnionitis, h. retained placental
tissues,
 avulsed cotyledons, succenturiate,accreta,
percreta & increta,
 Immediate causes
 Trauma to genital  COAGULATION
tract, DEFECTS – intensifies
 a. large episiotomy all.
including extensions,
 b. lacerations of
perineum, vagina, or
cervix, ruptured
uterus
 Highlights, PPH

 Pregnancy induced hypervolemia ^ 30-

60% (1,500 – 2,000 ml) average (1965
Pritchard).
 Hematocrit lower than I obtained on
admission blood loss can be estimated as
sum of calculated pregnancy induced
hypervolemia + 500 cc.
 Calculation maternal total blood
volume (TBV)
 Non-maternal TBV :
 [Ht (inches) X 50] + Wt (lbs) X 25] divide
by 2 =TBVcc
 PREGNANT tbv – Add 50% to non-
pregnant TBV BUT remember the
pregnancy induced hypervolemia
 Sheehan Syndrome
 RARE but the classical case is
characterized by
 a. failure to lactate,
 b. amenorrhea,
 c. breast atrophy,
 d. loss of pubic & axillary hair,
 e. hypothyroidism,
 f. and adrenal cortical insufficiency.
 Sheehan Syndrome
 Reported that pituitary necrosis associated
with obstetrical blood loss may cause
hypopituitarism. (Vaphiades 2003) these
events are very RARE.

 ACUTE may have persistent hypotension,

tachycardia, hypoglycemia, & failure of
lactation.
 Third Stage bleeding

 DUNCAN mechanism of detachment –

sudden escape of blood .
 SCHULTZE mechanism – bleeding may be
concealed behind the placenta.
 N.B. Delivery of the placenta by traction ,
ESPECIALLY if the uterus is atonic may
lead to INVERSION.
 DX
 Uterine atony,
 a. e.g. big uterus, secondary to large fetus,
multiple pregnancies, or hydramnios may lead
to BLEEDING.
 b. Overactivity of the uterus or barely active,
 c. initiated or augmented labor,
 d. Gravida 7 ^,
 e. previous PPH,
 f. mismanagement of the third stage of labor
premature or hastening the stage of labor.
 MTX
 1. Ergot – may be administered intramuscular in slow
fashion, rapid infusion of oxytocin may not be as
effective. Ergot has the tendency to cause dangerous
Hypertension.
 2. Prostaglandin- 15 METHYL derivative of
prostaglandin F2 @ Carboprost tromethamine (.25
mgms) Im repeated up to maximum of (8) doses. S.E.
diarrhea, hypertension, vomiting, fever, flushing &
tachycardia. May develop arterial desaturation
developing 15 minutes may due to pulmonary artery &
vascular constriction,
 & 3. Misoprostol not so effective for PPH.
 Bleeding unresponsive to MTX
 1. C OMPRESSION of the uterus bimanually,
 2. O BTAIN help,
 3. A DD a second big bore for crystalloids
infusion,
 4. B EGIN blood transfusion,
 5. E XPLORE the uterine cavity for retention,
 6. I NSPECT the vagina, cervix for sources of
bleeding,
 7. I NSERT a Foley bag catheter,
 8.W ATCH for hypovolemic shock.
 Other measures
 1. Internal iliac artery ligation,
 2. Uterine compression sutures, B Lynch,
 3. Uterine packing, not very popular because of
concealed hemorrhage, Foley 24 F catheter,
 4, hysterectomy,
 5. post hysterectomy an umbrella introduced & left
tightly packing the pelvis w/ a tail protruding through the
vagina,
 6. Recombinant activated factor VII (Vitamin K ) BUT
thrombotic complications have been reported,
 6. ANGIOGRAPHIC embolization may be tried.

 7. LASTLY PRAY
 Puerperal hematomas
 Associated risk factors,
 a. nulliparity,
 b. episiotomies,
 c. forceps deliveries,
 d. injury to the blood vessel w/o laceration & the
event is delayed.
 Classification, a. vulvar,
 b.vulvovaginal,
 c. paravaginal,
d. retroperitoneal.
Classification of uterine rupture
 Endometrial  Coincidental
surgery, a. CS or uterine rupture,
hysterotomy, b.  a. abortion w/
Previously repaired instrumentation,
 c. Myomectomy  b. sharp or blunt
(myometrium) trauma,
 d. Deep cornual  c. silent rupture in
resection, previous
 e. metroplasty pregnancy.
 CONGENITAL ANOMALY
 Uterine rupture
 Ante partum  INTRA-PARTUM
 1. persistent, intense,  a. internal version,
spontaneous  b. difficult forceps
contractions, delivery,
 2. stimulated labor,  c. breech extraction,
 3. intra-amnionic  d. fetal anomaly,
instillation,  e. vigorous uterine
 4. perforation by an pressure,
internal uterine pressure  f. difficult manual removal
catheter, of placenta.
5. external version,
6. blunt instrument, &
7. uterine overdistension.
 Acquired uterine rupture

 1. Placenta increta, percreta,

 2. Gestational trophoblastic neoplasia,
 3. Adenomyosis,
 4. sacculation or trapped retroverted
uterus.
 Consumptive Coagulopathy

 1901 De Lee reported “temporary

hemophilia” in placental abruption and
IUFD (long dead macerated fetus).
 Consumptive Coagulopathy
 1. Pregnancy hypercoagulopathy –
 a.^ in coagulation factors, (fibrinogen), VII,
VIII, IX & X.
 b.^ Plasminogen levels, yet plasmin activity
lowered,
 2. Pathological activation of coagulation, ^
activation of platelet, clotting, & fibrinolytic
mechanism. (Gerbasi et al ) ^fibrinopeptide A ,
B thromboglobulin, platelet factor 4 &
fibrinogen fibrin degradation products.
 Consumptive coagulopathy
 Pathological states
 a. extrinsic pathway – from tissue destruction,
 b. intrinsic pathway – collagen & other tissue
components, when there is loss of endothelial
integrity, page 843 22nd edition Williams
OBSTETRICS.
 N.B. Is always seen as an identifiable,
underlying pathological process which treatment
is to REVERSE the defibrination.
Consumptive coagulopathy, clinical
& laboratory
 a. Persistent oozings from venipuncture sites, b.
nicks from shavings the perineum or the
abdomen, trauma from catheter insertion etc,
 b. Laboratory, b.1 hypofibrinogenemia, to
promote coagulation the level should be at least
150 mg/dl, b.2 fibrin- fibrin degradation
products, monoclonal antibodies are used to
detect d-dimers w/ clinical consumption the
levels must.^
 Laboratory
 B.3 thrombocytopoenia- serious if petechiae
abundant, if clotted blood fails to retract in (1)
hour’s time or if platelets are absent in a smear,
e.g. qualitative dysfunction w/severe pre-
eclampsia or eclampsia,
 b.4 prothrombin & partial thromboplastin time,
might not be a consequence of consumption,
HEPARIN is mentioned to be condemned
at the moment.
 Consumptive coagulopathy

 Epsilon amino-caproic acid – control

fibrinolysis by inhibiting the conversion of
plasminogen to plasmin, inhibits the
proteolytic action of plasmin on fibrinogen.
Consumptive Coagulopathy
 Placental abruption most common cause
of consumption coagulopathy:
 FETAL death & delayed delivery –
coagulation defects rarely developes
before less than one month after fetal
death. But 25% develop the malady.
Fibrinogen levels goes down to 100mg/dl
critically, FFDP ^
 Amnionic Fluid embolism

 Clinical findings in AFE

1. Hypotension,
2. fetal distress,
3. pulmonary edema ARDS
4. Cardiopulmonary arrest,
5. cyanosis,
6. coagulopathy,
7. dyspnea,
8. Seizure