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Primary Postpartum
haemorrhage
DR. FIROUZABADI
Postpartum Hemorrhage
• EBL > 500 cc
• 10% of deliveries
• If within 24 hrs. pp = 1 pp hemorrhage
• If 24 hrs. - 6 wks. pp = 2 pp hemorrhage
Postpartum Hemorrhage
Incidence
3% of all births
6.4% of cesarean deliveries
3rd most common cause of maternal
mortality
Postpartum Hemorrhage
Definition
 greater than 500cc blood loss (vaginal
delivery) or 1000cc blood loss (cesarean)
 decrease in HCT of 10 or greater
 obstetrical emergency that can follow
vaginal or cesarean delivery with clinical
instability leading to transfusion, shock,
renal failure, acute respiratory distress, and
coagulopathy
Hemorrhage is the
underlying causative
factor in at least 25% of
maternal deaths in
industrialized and
underdeveloped countries
Peripartum Hemorrhage
Causes of maternal death in US (9.1/100,000) •
hemorrhage: 28.7% (*) –
embolism: 19.7% (*) –
PIH: 17.6% (*) –
infection: 13.1% (*) –
anesthesia: 2.5% (*) –
• Hospitalization for delivery and
Availability of blood for
transfusion have reduced the
maternal mortality rate death
from hemorrhage .
• It remains a cause of maternal
mortality.
• Hemorrhage is a reason for
admission of pregnant women to
intensive care units.
• Hemorrhage has been identified as
the single most important cause of
maternal death, accounting for
almost half of all post partum death
in developing countries.
• Incidence of obstetrical hemorrhage can
not be determined precisely
• Defined by a post partum HCT drop of
10 volumes percent or need for
transfusion.
• 3.9% NVD
• 6-8% C/S
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.
• 5% of women delivering vaginally
last more than 1000 ml of blood.
Estimated blood loss is commonly
only about half the actual loss. The
effect of hemorrhage depend to a
degree on the non pregnant blood
volume, magnitude of PIH, degree of
anemia at the time of 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
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.
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
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.
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.
Guideline by 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
•Colloid
•once 3.5 litres infused, GIVE ‘O NEG’ If no
cross-matched blood available OR give
uncross-matched 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
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)
• prostaglandins
• Surgery earlier rather than late
• Hysterctomy early rather than late
If conservative measures fail to control
haemorrhage, initiate surgical
haemostasis SOONER RATHER THAN
LATER
I. laparotomy
II. Bilateral ligation of uterine arteries
III. Bilateral ligation of internal iliac
(hypogastric arteries)
IV. Hysterectomy
Resort to hysterectomy
SOONER RATHER
THAN LATER
(especially in cases of
placenta accreta or
uterine rupture)
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.
Uterine Atony:
Prostaglandins
 myometrial intracellular free Ca++,
enhance action of other oxytocics
Side effects: fever, nausea/vomiting,
diarrhea
15-methyl PG F2 (Carboprost, Hemabate)
may cause bronchospasm, altered VQ,

shunt, hypoxemia, HTN
250 mg IM or intramyometrially q 15-30 min, up
to max 2 mg.
 contraindications: asthma, hypoxemia
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
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.
The Use of Blood and
Blood Components
• Various blood components
and how they function
• The indications and
contraindications for use
Red Blood Cells - RBC
Description:
 Whole blood is collected into an anticoagulant
then centrifuged to separate the red cells from
the plasma.
 The plasma is then expressed from the whole
blood bag and the remaining red blood cells
(RBC) are filtered.
 The filtering process removes all but 5 x 106
white blood cells (WBCs).
 85% of the original RBC volume will remain
after filtration.
Red Blood Cells - RBC
Function:
Increase the oxygen carrying capacity of
the blood by increasing the circulating
red blood cell mass.
Carry oxygen and nourishment to the
tissues and take away carbon dioxide.
Red Blood Cells - RBC
Indications:
Component of choice for virtually all patients
with a deficit of oxygen carrying capacity, e.g.,
blood loss or anemia.
The majority of the WBC are removed thereby
decreasing the risk of cytomegalovirus (CMV)
infection in immunocompromised patients. This
is because the CMV virus is carried in the
WBC.
Use of RBC reduces the risk of the patient
forming antibodies against WBC (HLA)
Red Blood Cells – RBC
Contraindications:
RBC should not be used:
when anemia can be corrected with
specific medications, e.g., iron, B12, folic
acid, erythropoietin, etc
for volume replacement
Platelets – PC
Descriptions:
Platelets are prepared from a random unit of whole
blood collected in CP2D anticoagulant solution and
filtered to remove leukocytes. PC contain less than
8.3 x 106 leukocytes.
Platelets are suspended in a small amount of the
original plasma. A unit contains at least 55 x 109
platelets suspended in 50-55 mL of plasma.
Trace amounts of red blood cells can be present in
some units.
These will appear pink to salmon colored.
Platelets - PC
Function:
• The primary role of platelets is to prevent
bleeding of injured blood vessel walls by
forming an aggregate at the site of injury.
• Platelets also participate in blood coagulation,
inflammation and wound healing.
• The transfusion of platelets to a patient with
thrombocytopenia or bleeding should produce
a rise in the platelet count and control
Platelets - PC
Indications:
• For treatment of patients with bleeding due to
severely decreased production or abnormal function
of platelets.
• Treatment of bleeding patients with platelet
consumption or dilutional thrombocytopenia (in most
instances of dilutional thrombocytopenia, bleeding
stops without transfusion).
• Useful if given prophylacticaly to patients with
rapidly falling or low platelet counts, less than 10 x
109/L (10,000/uL), secondary to cancer or
Platelets – PC
Contraindications:
• Platelets should not be used if bleeding is
unrelated to decreased numbers or abnormal
platelet function.
• Should not be used in patients with
consumption of endogenous and exogenous
platelets, such as in Thrombotic
Thrombocytopenia Purpura (TTP) or
Idiopathic Thrombocytopenia Purpura
Platelet Incubator
Stored with constant
agitation
Fresh Frozen Plasma - FFP
Description:
►Fresh frozen plasma is separated from
whole blood and frozen within 8 hours of
collection. It can be obtained from a
whole blood donation (approx. 250 mL)
or by apheresis (approx. 500 mL).
►Fresh frozen plasma contains a normal
concentration of fibrinogen and the labile
coagulation factors VIII and V.
Fresh Frozen Plasma – FFP
Function:
Fresh frozen plasma contains the clotting
factors that are necessary for hemostasis.
Plasma also has volume expansion and
oncotic properties.
Fresh Frozen Plasma – FFP
Indications:
• The majority of clinical situations for which
FFP is currently used do not require FFP.
• FFP is indicated for massive transfusion
(replacement of the patient’s blood volume
in < 24 hours) with a demonstrated
deficiency of Factor VIII and V, otherwise
frozen plasma is adequate.
• Fresh frozen plasma is also indicated in
Fresh Frozen Plasma – FFP
Contraindications:
• Fresh frozen plasma should not be used
when a coagulopathy can be corrected more
effectively with specific therapy, such as
vitamin K, cryoprecipitate, or Factor VIII
concentrates.
• Fresh frozen plasma has the same infectious
disease risk as whole blood.
• Fresh frozen plasma should not be used
when the blood volume can be replaced with
Frozen Plasma – FP
Frozen plasma is prepared from whole
blood, collected in CP2D anticoagulation
solution.
The plasma is separated after cold
centrifugation and processed to the
frozen state within 24 hours of collection.
Frozen Plasma – FP
Frozen plasma contains stable coagulation
factors such as Factor IX and fibrinogen in
concentrations similar to FFP, but reduced
amounts of Factor V
 and VIII.
On average, each unit of frozen plasma
contains an average of 250 mL (>100 mL)
of anticoagulated plasma.
The indications and side effects are the
same as for FFP, except that FP should not
be used to treat coagulation factor
Fresh Frozen Plasma (FFP)
Unit of FFP
(Approx. 250 mL)
Apheresis FFP
(Approx. 500 mL)
Cryoprecipitate (Cryo)
Description:
• Cryoprecipitate is prepared by thawing
fresh frozen plasma at a temperature
between 1°C and 6°C. After centrifugation,
the supernatant plasma is removed and the
insoluble cryoprecipitate is refrozen.
• On average, each unit of cryoprecipitate
contains 80 IU or more Factor VIII
(FVIII:C) and at least 150 mg of
Cryoprecipitate (Cryo)
Function:
Cryoprecipitate provides a source of
coagulation factors. Factor VIII, Factor
XIII and von Willebrand Factor.
Fibrinogen and fibronectin are present.
Cryoprecipitate (Cryo)
Indications:
Currently the main indication for this
component is as a source of fibrinogen
or Factor XIII.
It may be used as a source of Factor
VIII only when inactivated
fractionation products or recombinant
Factor VIII are not available.
Cryoprecipitate (Cryo)
Contraindications:
• Cryoprecipitate should not be used unless results
of laboratory studies indicate a specific
hemostatic defect for which this product is
indicated.
• Specific factor concentrates are preferred, when
available, because of their reduced risk of
transmissible diseases (because of viral
inactivation during manufacturing).
• Cryoprecipitate can be used to make fibrin glue.
Alternatively, virally inactivated commercial
Cryoprecipitate (Cryo)
Cryoprecipitate
Pooling Cryoprecipitate
Blood & its Usage
Components
Cells
Plasma
molecules &
ions
water
Function
Medium of transport
Oxygen
Carbon dioxide
Other gases
Ions
Carbohydrates, proteins,
fats
Immune response
Humoral
Cells
Erythrocyres
White cells

Granulocyes

neutophiles

Eosinophiles

Basophiles

Lymphocyes

Monocytes
Molecules & ions
Ions
Na+, Cl-, K+, HCO2-, etc
Molecules
Proteins – enzymes, precursors,
active agents, immunoglobulins,
carriers
Proteoglycans
Body Water
Intracellular 55%
Interstitial Fluid 20%
Plasma 7.5%
Connective Tissue 7.5%
Bone Water 7.5%
Transcellular Fluid 2.5%
Blood products
• Whole blood
• Blood components
•
•
•
•
•
Red cells
Platelets
Granulocytes
Whole plasma (FFP, reconstituted)
Cryoprecipitate
• Plasma fractions
•
•
•
•
Clotting factor concentrates
Immunoglobulin preparations
Saline albumin solution
Salt-poor albumin
Volume replacement
Haemorrhage or burns
Replacement with RBC mass at
early stage necessary in massive
haemorrhage
Initiate with rapid transfusion of
plasma expanders, electrolyte
solutions & get blood type & match
in 30 minutes
Unmatched Grp O Rh- blood rarely
Massive Blood Transfusion
• pH & K+ increase impair myocardial
function
• Citrate lowers ionised Ca++
• Significant hypothermia
• Platelet & WBC aggregates precipitate
ARDS
Prevention
1 unit of fresh blood for every 5 – 10 units
of stored blood
IV 10% calcium gluconate 10 mls with
every litre of transfused citrated blood
Warming blood
Microaggregate blood filters
Fresh Blood
•
•
•
•
DIVC
Massive haemorrhage
Major liver trauma
Bleeding associated
with liver disease
Clotting factors
Clotting disorders
Haemophilia
Liver disease
Complications of Blood
Transfusion
•
•
•
•
Febrile reactions
Bacterial contamination
Immune reactions
Physical complications
–Circulatory overload
–Air embolism
–Pulmonary embolism
–Thrombophlebitis
Complications of Blood
Transfusion
• Metabolic complications
– Hyperkalaemia
– Citrate toxicity & hypocalcaemia
– Release of vasoactive peptides
– Release of plasticizers from PVC-phthalates
• Haemorrhagic reactions
– After massive transfusion of stored blood
– Disseminated intravascular coagulation
Complications of Blood
Transfusion
• Transmission of disease
– Hepatitis, CMV. EBV
– AIDS (Factor VIII)
– Syphilis
– Brucellosis
– Toxoplasmosis
– Malaria
– Trypanosomiasis
Autologous transfusion
• Uses pt own blood
• Remove 500 ml & store
• 2 weeks later, may be transfused in
op
or 1000 mls taken to increase the
stored amount
• Multiplier effect