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Primary
Postpartum
haemorrhage
Dr. Mohammed Abdalla
Egypt, Domiat General Hospital
Hemorrhage is the
underlying causative
factor in at least 25% of
maternal deaths in
industrialized and
underdeveloped countries
Maternal physiology is well prepared for
hemorrhage:
increase in blood volume .
hypercoagulable state.
the “tourniquet” effect of uterine
contractions.
vital signs may remain near
normal until more than 30% of
blood volume is lost .
tachycardia can be attributed
to pregnancy, stress, pain, and
delivery.
blood supply to the
pelvis
blood supply to the pelvis
internal iliac (hypogastric) a.
ovarian arteries .
Are The main vascular supply to
the pelvis . connected in a
continuous arcade on the lateral
borders of the vagina, uterus, and
blood supply to the pelvis
o/The ovarian arteries :
are direct branches of the aorta
beneath the renal arteries.
They traverse bilaterally and
retroperitoneally to enter the
infundibulopelvic ligaments.
blood supply to the pelvis
h/The hypogastric artery:
retroperitoneally posterior to
the ureter it divides into an
anterior and posterior
divisions.
The hypogastric artery
anterior division
5 visceral branches
Uterine
superior vesical
middle hemorrhoidal
 inferior hemorrhoidal
vaginal
3 parietal branches
Obturator
 inferior gluteal
internal pudendal
The hypogastric artery
posterior division
important collateral to the pelvis.
Iliolumbar
 lateral sacral
superior gluteal
PHYSIOLOGY OF
COAGULATION
PHYSIOLOGY OF COAGULATION
The four components of coagulation
that continuously interrelate are
(1) the vasculature,
(2) platelets,
(3) plasma-clotting proteins,
(4) fibrinolysis.
the vasculature
A disruption in the vessel wall
removes the protective
covering of the endothelial
cells and releases tissue
thromboplastin, which
activates the clotting
mechanism.
platelets
Activation of surface receptors causes
morphologic changes in the platelets
(changing first to a sphere and then to
a spiderlike structure with pseudopods)
and the generation of thromboxane
A2 These lead to platelet aggregation
and eventual formation of a platelet
plug.
plasma-clotting proteins
Activation of the clotting system is
initiated in two ways:
the intrinsic or extrinsic
pathway.
Intrinsic Pathway
requires no extravascular
component for initiation and
begins with Factor XII, which
is activated by contact with
injured epithelium.
Extrinsic Pathway
is activated by the tissue factor
thromboplastin (which subsequently
activates Factor VII) when vascular
disruption occurs. Prothrombin is
converted to thrombin, which catalyzes
the conversion of fibrinogen to fibrin. A
clot is eventually formed at the site of
vascular injury.
fibrinolysis
plasma substrate plasminogen is
activated This substrate is
converted to the active enzyme
plasmin, which lyses fibrin clots
and destroys fibrinogen and
Factors XII and VII.
Etiology of PPH
The causes of postpartum hemorrhage
can be thought of as the four Ts:
tone,
tissue,
trauma,
thrombin
Etiology of PPH
Uterine atony
Multiple gestation,
high parity,
prolonged labor
chorioamnionitis,
augmented labor,
 tocolytic agents
Etiology of PPH
Retained uterine
contents
Products of conception,
blood clots
Etiology of PPH
Placental abnormalities
Congenital
Location
Attachment
Bicornuate Placenta previa Accreta
uterus
Acquired
structural
Leiomyom
a, previous
surgery
Peripartum
Uterine inversion,
uterine rupture,
placental
abruption
Etiology of PPH
Lacerations and trauma
Planned
•Cesarean section,
•episiotomy
Unplanned
•Vaginal/cervical tear,
•surgical trauma
Etiology of PPH
Coagulation disorders
Congenital
Von Willebrand's disease
Acquired
DIC,
dilutional coagulopathy,
heparin
Women in whom these factors have been
identified should be advised to deliver in a
specialist obstetric unit( GRADE B )
odds ratio
for PPH
Risk Factor
•Proven abruptio placentae
13
•Known placenta praevia
12
•Multiple pregnancy
5
•Pre-eclampsia/gestational hypertension
4
The following factors, becoming apparent
during labour and delivery are associated
with an increased risk of PPH. (GRADE B)
Risk factor
•Delivery by emergency Caesarean section
•Delivery by elective Caesarean section
•Retained placenta
•Mediolateral episiotomy
•Operative vaginal delivery
•Prolonged labour (>12 hours)
•Big baby (>4 kg)
odds ratio for
PPH
9
4
5
5
2
2
2
Prophylactic oxytocics should
be offered routinely in the
management of the third
stage of labour as they
reduce the risk of PPH by
about 60%.
(GRADE A)
• Women considered at high risk of
thromboembolism may be receiving prophylaxis
in the form of Unfractionated Heparin (UH) or
Low Molecular Weight Heparin (LMWH)
antenatally.
• Women with a lower level of increased risk of
thromboembolism may be receiving aspirin
(75mg daily) antenatally and may begin
intrapartum prophylaxis with the above agents.
In prophylactic dosage, these agents do
not present a haemorrhagic hazard and
should be continued intrapartum.
(ALL GRADE C)
In the event of a woman coming to
delivery while receiving therapeutic
heparin,
the infusion should be stopped.
Heparin activity will fall to safe levels
within an hour. Protamine sulphate
will reverse activity more rapidly, if
required.
•GRADE C
UH and LMWH in prophylactic dosage are
not felt to present a haemorrhagic hazard.
However, in overdosage there can be
bleeding problems and protamine
sulphate is less effective at reversing the
effects of these agents (particularly
LMWH) than of therapeutic heparin
administered by infusion.
Letsky EA. Peripartum prophylaxis of thromboembolism.
In: Greer IA, ed. Thromboembolic disease in obstetrics and
gynaecology. 1997
If women with inherited bleeding
disorders present for preconceptual
counselling, they should be tested
for immunity against hepatitis B
,and immunised if required (as a
safeguard should blood products be
required at delivery). Immunisation
during pregnancy is also safe.
GRADE C
Antenatal assessment
history
The existence of some of the
obstetric risk factors may be
known early in pregnancy from
history and examination.
Antenatal assessment
anemia
Detection of anemia more than
physiologic anemia of pregnancy
is important, because anemia at
delivery increases the likelihood of
a woman requiring blood
transfusion.
Antenatal assessment
Coagulation studies
Coagulation studies may
be required in the
presence of congenital or
acquired coagulation
defects.
Antenatal assessment
Imaging investigations
Imaging investigations are useful
in the detection of placental
abnormalities, with placenta
previa and placenta accreta the
most important identifiable risk
factors for massive hemorrhage.
Antenatal assessment
Imaging investigations
Conventional gray-scale assessment has
a sensitivity of 93%, a specificity of
79%, and a positive predictive value of
78% in the diagnosis of placenta
accreta when previa and previous
cesarean scar are present
Finberg HJ, Williams JW. Placenta accreta: prospective sonographic diagnosis in
patients with placenta previa and prior cesarean section. J Ultrasound Med
1992;11:333-43.
Antenatal assessment
Imaging investigations
Certain characteristics, such as the
”Swiss cheese appearance” with
placenta previa, are associated with
a threefold increase in mean blood
loss during cesarean section
Guy GP, Peisner DB, Timor-Tritsch IE. Ultrasonographic
evaluation of uteroplacental blood flow patterns of abnormally
located and adherent placenta. Am J Obstet Gynecol
Antenatal assessment
Imaging investigations
Color Doppler may increase the specificity
to 96%, which gives a positive predictive
value in high-risk patients of 87% and a
negative predictive value of 95% and
allows better assessment of the depth of
placental myometrial or serosal invasion
Chou MM, Ho ESC, Lee YH. Prenatal diagnosis of placenta
previa accreta by transabdominal color Doppler ultrasound.
Ultrasound Obstet Gynecol 2000;15:28-35.
Antenatal assessment
Imaging investigations
Further imaging by MRI is
recommended to assess bladder
involvement in percreta and
assess high-risk cases
Thorp Jr. JM, Councell RB, Sandridge DA, et al. Antepartum
diagnosis of placenta previa percreta by magnetic resonance
imaging. Obstet Gynecol 1992;80:506-8.
Guidelines
by the Scottish Executive
Committee of the RCOG
COMMUNICATE.
RESUSCITATE.
 MONITOR / INVESTIGATE.
STOP THE BLEEDING.
COMMUNICATE
call 6
•
•
•
•
•
•
Call experienced midwife
Call obstetric registrar & alert consultant
Call anaesthetic registrar , alert consultant
Alert haematologist
Alert Blood Transfusion Service
Call porters for delivery of specimens / blood
RESUSCITATE
•
•
•
•
IV access with 14 G cannula X 2
Head down tilt
Oxygen by mask, 8 litres / min
Transfuse
•Crystalloid (eg Hartmann’s)
•Colloid (eg Gelofusine)
•once 3.5 litres infused, GIVE ‘O NEG’ If no crossmatched blood available OR give uncrossmatched own-group blood, as available
•Give up to 1 liter Fresh Frozen Plasma and 10 units
cryoprecipitate if clinically indicated
MONITOR / INVESTIGATE
•
•
•
•
•
•
•
•
Cross-match 6 units
Full blood count
Clotting screen
Continuous pulse / BP /
ECG / Oximeter
Foley catheter: urine output
CVP monitoring
Discuss transfer to ITU
STOP THE BLEEDING
• Exclude causes of bleeding other than uterine atony
• Ensure bladder empty
• Uterine compression
• IV syntocinon 10 units
• IV ergometrine 500 mg
• Syntocinon infusion (30 units in 500 ml)
• IM Carboprost (500 mg)
• Surgery earlier rather than late
• Hysterctomy early rather than late
(GRADE B)
If conservative measures fail to control
haemorrhage, initiate surgical
haemostasis SOONER RATHER THAN
LATER I. At laparotomy, direct
intramyometrial injection of
Carboprost (Haemabate) 0.5mg
II. Bilateral ligation of uterine arteries
III. Bilateral ligation of internal iliac
(hypogastric arteries)
IV. Hysterectomy
(GRADE C)
Resort to hysterectomy
SOONER RATHER
THAN LATER
(especially in cases of
placenta accreta or
uterine rupture)
(GRADE C)
Whole blood frequently is used for
rapid correction of volume loss
because of its ready availability,
but component therapy is ideal. A
general practice has been to
transfuse 1 unit of fresh-frozen
plasma for every 3 to 4 units of
red cells given to patients who are
bleeding profusely
Genital tract lacerations
Genital trauma always
must be eliminated
first if the uterus is
firm.
Management of uterine atony
• Explore the uterine cavity.
• Inspect vagina and cervix for lacerations.
• If the cavity is empty, Massage and give
methylergonovine 0.2 mg, the dose can be
repeated every 2 to 4 hours.
• Rectal 800mcg. Misoprostol is beneficial.
Management of uterine atony
During the administration of uterotonic agents,
bimanual compression may control
hemorrhage. The physician places his or her
fist in the vagina and presses on the anterior
surface of the uterus while an abdominal
hand placed above the fundus presses on
the posterior wall. This while the Blood for
transfusion made available.
Retained placenta
Retained placental fragments are a leading cause
of early and delayed postpartum hemorrhage.
Treatment is manual removal, General
anesthesia with any volatile agent (1.5–2
minimum alveolar concentration (MAC)) may be
necessary for uterine relaxation
On rare occasions, a retained placenta is an
undiagnosed placenta accreta, and massive
bleeding may occur during attempted manual
removal.
Placenta accreta
• Placenta accreta is defined as an abnormal
implantation of the placenta in the uterine
wall, of which there are three types:
(1) accreta vera, in which the placenta adheres to
the myometrium without invasion into the muscle.
(2) increta, in which it invades into the myometrium.
(3) percreta, in which it invades the full thickness of
the uterine wall and possibly other pelvic structures,
most frequently the bladder.
Placenta accreta
In a patient with a previous cesarean
section and a placenta previa:
Previous one has 14% risk of placenta accreta.
Previous two has 24% risk of placenta accreta.
Previous three has 44% risk of placenta accreta.
UTERINE RUPTURE
Rupture of the uterus is
described as complete or
incomplete and should be
differentiated from dehiscence
of a cesarean section scar.
UTERINE RUPTURE
The reported incidence
for all pregnancies is 0.05%,
After one previous lower segment cesarean section 0.8%
After two previous lower segment cesarean section is 5%
all pregnancies following myomectomy may be
complicated by uterine rupture.
UTERINE RUPTURE
Complete rupture describes a
full-thickness defect of the
uterine wall and serosa
resulting in direct
communication between the
uterine cavity and the
peritoneal cavity.
UTERINE RUPTURE
Incomplete rupture describes
a defect of the uterine wall
that is contained by the
visceral peritoneum or broad
ligament. In patients with
prior cesarean section,
UTERINE RUPTURE
dehiscence describes partial
separation of the scar with
minimal bleeding, with the
peritoneum and fetal
membranes remaining
intact.
Management of Rupture
Uterus
The identification or suspicion of uterine
rupture must be followed by an immediate
and simultaneous response from the
obstetric team.
Surgery should not be delayed owing to
hypovolemic shock because it may not be easily
reversible until the hemorrhage is controlled.
Management of Rupture
Uterus
Upon entering the abdomen, aortic
compression can be applied to decrease
bleeding.
 Oxytocin should be administered to effect
uterine contraction to assist in vessel
constriction and to decrease bleeding.
Hemostasis can then be achieved by
ligation of the hypogastric artery, uterine
artery, or ovarian arteries.
Management of Rupture
Uterus
 At this point, a decision must be made to perform
hysterectomy or to repair the rupture site. In most
cases, hysterectomy should be performed.
 In selected cases, repair of the rupture can be
attempted. When rupture occurs in the body of the
uterus,
 bladder rupture must be ruled out by clearly
mobilizing and inspecting the bladder to ensure
that it is intact. This avoids injury on repair of the
defect as well.
Management of Rupture
Uterus
 A lower segment lateral rupture can cause
transection of the uterine vessels. The vessels
can retract toward the pelvic side wall, and the
site of bleeding must be isolated before placing
clamps to avoid injury to the ureter and iliac
vessels.
 Typically, longitudinal tears, especially those in a
lateral position, should be treated by
hysterectomy, whereas low transverse tears may
be repaired.
Uterine Artery Ligation
Uterine artery ligation involves
taking large purchases through
the uterine wall to ligate the
artery at the cervical isthmus
above the bladder flap .
Hypogastric Artery Ligation
The hypogastric artery is exposed by
ligating and cutting the round ligament
and incising the pelvic sidewall
peritoneum cephalad, parallel to the
infundibulopelvic ligament The ureter
should be visualized and left attached to
the medial peritoneal reflection to prevent
compromising its blood supply.
Hypogastric Artery Ligation
The
. common, internal, and external
iliac arteries must be identified
clearly. The hypogastric vein, which
lies deep and lateral to the artery,
may be injured as instruments are
passed beneath the artery, resulting
in massive, potentially fatal bleeding.
Hypogastric Artery Ligation
The hypogastric artery should be completely
visualized. A blunt-tipped, right-angle clamp
is gently placed around the hypogastric
artery, 2.5 to 3.0 cm distal to the bifurcation
of the common iliac artery. Passing the tips
of the clamp from lateral to medial under the
artery is crucial in preventing injuries to the
underlying hypogastric vein .
Hypogastric Artery Ligation
the artery is double-ligated with a
nonabsorbable suture, with 1-0 silk,
but not divided .The ligation is then
performed on the contralateral side
in the same manner.
Dr. Mohammed Abdalla
Egypt , Domiat G. Hospital