Postpartum Hemorrhage

DR. AJANTA PANDE (SAMANTA)

PPH today
living in the
shadow of
TAJMAHAL

TAJMAHAL-world`s most beautiful tomb,dedicated to the

memory of Queen Mumtaz by her husband Emperor
Sahajahan, who died after her last child birth due to PPH, is a
testimony and a grim reminder of the tragedy of maternal
mortality, that can befall any women in childbirth.

Incidence:

PPH is one of the commonest cause of

maternal mortality & accounts for 1/4th of all
maternal death worldwide.(WHO 2005)
In developing countries it accounts over 1/3rd
of all maternal death.(Khan KS 2006)
14 million cases occur each year with a case
fatality rate of 1%.(WHO 2004)
In 2004 incidence of PPH was 3.2/1000 live
births & in 2005 4.5/1000 live births(Scottish
confidential audit)
In India PPH responsible for 15-20% 0f
maternal death (Mukherjee et al 2002).

Definition

According to American college of Obstetrics

& Gynecology PPH is defined as blood loss
of greater than 500 mL with a vaginal
delivery or greater than 1000 mL with a
cesarean section or a 10% drop in the
hematocrit.
Pitfalls in definition:
Arbitrary, subjective & based on visual
estimation which underestimate actual loss
Change in hematocrit depends upon timing
of test& amount of fluid resuscitation
given& on post partum hemoconcentration.

Ability to tolerate amount of blood loss

without any significant effect on health
depends upon not only antepartum Hb% but
also on amount of pregnancy hypervolumia
Eg- preeclampsia, eclampsia.
Conclusion : reliance on classification
solely based on the amount of blood loss,
without considering clinical signs &
symptoms may lead to inconsistency with
management.
So we need a clinical & prognostic
classification.

Proposed classification. adapted from

Benedetti,2002

Hemorrhage
class

Estimated blood
loss
(ml)

<500

500-1000

Blood volume
loss
(%)
<10
15

1200-1500

20-25

1800-2100

30-35

>2400

>40

Clinical signs &

symptoms

none
minimal
urine output
pulse rate
respiratory rate
Postural
hypotension
Narrow pulse pr

management

none
Observation+/-RP
Tx
Replacement
therapy with
oxytocics

Hypotension
Tachycardia
Tachypnea
Cold clammy

Urgent active
management

Profound shock

Critical active Mx

Types of PPH

Immediate/primary PPH- occurs within

24 hrs of delivery)

Third stage hemorrhage

2. PPH after 3rd stage
1.

Late/secondary PPH- occurs after 24

hrs & within 6 wks/upto 12
wks(ACOG practice bulletin,2007)

Causes & Predisposing factors of

primary PPH
1. Tone
Uterine atony
2. Tissue
Retained placental tissue
3. Trauma
Large episiotomy
Lacerations of perineum,vagina,cervix
Ruptured uterus
4. Thrombine

Pathophysiology
Blood vessels(spiral arteries) supplying
placental bed pass through an interlacing
network of muscle fibres of myometrium.
Myometrial contraction is main driving force
for placental separation & constriction of blood
vessels.
This hemostasic mechanism is known as
physiological sutures or living ligatures
So bleeding occures from placental beds due to
Uterine atony(myometrium fails to contract)
Retained products(that interferes contraction)

BIO-PHYSICS FOR CONTROLLING

HAEORRHAGE
YOUNG LAPELACE RELATIONSHIP

F= 2T/r
F= The compressive force acting on the uterine
vessels.
T= The wall tension (generated by uterine
contraction)
r = The radius of the uterus
It is apparent that the force compressing the
vessels can not be high if r is large
[Schellenberg JC .Geneva University Hospital]
So PPH occurs with atonic overdistended
uterus

Uterine atony

1.
2.
3.
4.
5.
6.
7.
8.
9.

It is responsible for upto 80% of primary PPH.

Predisposing factorsGrand Multipara
Over distended uterus(large fetus , twins ,
hydroamnios)
Malnutrition
APH
Anesthesia (general anesthesia)
Malformed uterus
Tumor(fibroid uterus)
Abnormal uterine contraction(Precipitate/prolonged
labor)
Induced/augmented labor

Coagulation defects
Congenital :Von Willebrand`s disease
Acquired

DIC(placental abruption, IUFD, sepsis)

Dilusional coagulopathy(fluid
resuscitation/massive BT)
Hypoxia & acidosis
Severe PET/Eclampsia

Secondary PPH
1.
2.
3.
4.
5.
6.

Retained bits of placenta

Placental polyp
Subinvolution of placental site
Endometritis
Infected sloughing from cervicovaginal
wound
Puerperal inversion of uterus

management of PPH
postpartum Hemorrhage (PPH)

Predict

Prepare

Handle

Prevention of PPH
Patients at
risk

1. - Prepare for PPH

2. - Timing of Delivery
3. - proper labor management
4. -exploration of cervicovaginal canal
5. -intense monitoring upto 1hr
6. - Increased postpartum/postoperative surveillance

Prevention of PPH
1.- Prepare for PPH
Personnel

-Nursing
-Anesthesia
- Surgical
assistance

Drugs/Equipment

-Oxytocin

-Crystalloids

-Carbetocin

-Blood/Bl.products

-Methergine

-Surg. Instruments

-Prostaglandins

-Hemostatic ballons
( Cook, S-B, Foley)

Prevention of PPH
2.- Timing of Delivery

Elective C/S
after completion of 37 weeks
Avoids uterine rupture
Avoids significant hemorrhage

- Placenta previa
- Previous classical cs
- Previous
myomectomy
- Fibroid uterus

Proper labor management

Management of proloned labor
Slow delivery of baby
Active management of 3rd stage

Administration of uterotonics (oxytocin

10U/Ergometrine 0.2mg IM)
2. Placental delivery by controlled cord
traction
3. Uterine massage after placental delivery
1.

Diagnosis & Management

PPH BOWL AND BAG

Soakage characteristics of 1010cm pads

It is used for rough

estimation of blood loss
in rural India where
facilities are not
available

Blood drained into an fixed

container for measurement

BRASSS-V DRAPE
low cost
Having calibrated receptacle at
the bottom
Developed by NICHD funded
global network
Name was coined by adding 1st
letters of the seven collaborators

Easy to miss
Physicians underestimate blood loss by
50%. Estimate blood loss accurately.
Slow steady bleeding can be fatal. Evaluate
all bleeding, including slow bleeds.
Abdominal or pelvic bleeding can be
hidden. If mother develops hypotension,
tachycardia or painrule out intraabdominal blood loss.

Stages of shock:clinical assessment of bl loss

classification

Class I

Class II

Class III

Class IV

Blood loss (% )

10-15

15-30

30-40

>40

Consciousness

alert

Respiratory rate

Complexion

Extremities

Anxious, restless Agitated,confused

Milded

unconscious

raised

raised

pale

pale

grey

cool

cool

cold

Capillary refill

slow

slow

Minimal/absent

Pulse rate

elevated

Fast but thready

SBP

N/slighted

hypotension

Urine output

reduced

reduced

oligoanuric

HAEMOSTASIS algorithm
H- ask for help
A- assess (vitals, blood loss) & resuscitate
E1. Establish etiology(tone,tissue,trauma,thrombine)
2. Ecbolics (syntometrine,ergometrine)
3. Ensure availability of blood
M - massage the uterus
O oxytocin infusion & prostaglandin

S shift to operating theatre

Bimanual compression
Pneumatic anti-shock garment
T- Tissue & trauma to be excluded
A-apply compression sutures
S-systematic pelvic devascularisation
I -interventional radiology
S-subtotal/total hysterectomy

The golden hour of resuscitation

Golden hour is the time by which
resuscitation must be initiated to ensure
better survival.
Rule of 30-if SBP falls by 30mmHg,HR
rises by 30beats/min,RR to
30breaths/min, Hct drop by 30%,urine
output <30ml/hr she is likely to have lost at
least 30% of her bl vol&is in moderate
shock leading to severe shock.
Shock index-SBP/HR.normal value-0.50.7.with significant hge -0.9-1.1.better
indicator for early acute bl loss.

Emergency resuscitation sh be initiated if

blood loss >1/3rd of total blood volume/
>1000ml/a change in hemodynamic status.
Two large bore I.V infusion system should
be established.
An indwelling bladder catheter should be
inserted.
Crystalloids are typically used,3ml/ml of
blood loss(three times the blood loss).
Colloids are equally effective but
expensive.(SAFE study,Finfer,2002).

Intravenous fluids:

CRYSTALLOIDS

SALINE

Cheap, easily available

Disadvantage:
hyperchloremic acidosis,
some procoagulant effect.

HARTMANNS
SOLUTION

No risk of anaphylaxis, minimal effect

on base defficit, easily available.

Mildly hypotonic

5% DEXTROSE

No place in acute expansion of

intravascular volume

Hypotonic, rapid distribution to

intacellular & extracellular space

HYPERTONIC
SALINE

Rapid expansion of intravascular space,

beneficial effect on endothelial edema

Insufficient data.

COLLOIDS
GELATINS

Largely remains in
intravascular space
for 2-4 hrs

Risks of anaphylaxis,
no clear survival over
crystalloids

4% HUMAN
ALBUMIN

More physiological
than gelatin,remains
intravascular for 12
hrs

Expensive, no clear
advantage over
crystalloids

HYDROXY
ETHYL
STERCH

Remains in
Risk of coagulopathy,
intravascular space for renal injury
12-24 hrs

Establishment of etiology
T-tone-thorough assesment of uterine size&
tone
Uterine atony
T-tissue-manual exploration of uterine cavity
anaesthesia
Retained products
T-trauma-exanaesthesia 4 extended tear in
cervix,vagina
lacerations
T-thrombine-defect in coagulation

Uterine atony

Uterine massage-manual(over fundus) /

bimanual

Oxytocin-slow i.v bolus(10U)

/infusion(40U in 500ml NS@125ml/hr)
S/E- hypotension, volume overload(prolong
use), ischaemic changes in echo.

Ergot alkaloids-0.2mg methyl ergonovine IM

C/I: Hypertension, S/E:Hypertension,M.Ischaemia

Prostaglandins Carboprost /15methylPGF2:80-90% effective in

refractory atony.0.25mg IM/intramyometrial,
repeated every 15-90 min, max 8 times(2mg),
C/I:Asthma,
S/I:Diarrhoea,vomiting,fever,headache,flushing.
Dinoprostone /PGE2:P/v gel(get washed out)/P/R
suppositories(20mg).stored in 4C.

Misoprostol/PGE1:tab 400-600g orally /800g

rectally have been tried.
In a randomised trial(Derman et al,2006)600g
oral miso compared wth placebo-shows PPH
reduced from12 to 6% & severe hge from
1.2-.2% in misoprostol group
However Recent cochrane review(Mousa&
Alfirevic,2007) concluded no benefit of
misoprostol in comparison to standard therapy
with oxytocin&ergometrine.(cochrane database
sys review 2007)

S/E- pyrexia, shivering. have a clear dose effect

relationship.
WHO pilot trial,2000

Misoprostol 600g

Misoprost Oxytocin 10IU

ol 400g

Shivering

56/199(28%)

38/198(19
%)

Pyrexia>38C

15/199(7.5%)

4/195(2%) 6/199(3%)

25/200(12.5%)

Rectal misoprostol was shown to be well tolerated.

If efficacy of rectal miso is confirmed in larger
studies in controlling PPH then low rate of s/e will
be an important advantage.

Blood replacement in PPH

Indication: continuing bleeding, loss of
>30% bl vol, hemodynamic instability,hct
<30 vol%
Compatible whole bl is ideal for Ac.hge
Platelet transfusion is considered in a
bleeding patient wth PL<50,000/L
1lt of FFP sh be transfused wth every 6U of
bl to prevent dilutional coagulopathy/when
fibrinogen level<100mg/dl.

Recombinant activated factor vii/

novoseven: FDA approved 4 tx of bleeding
in Hemophilia.Now it has been using for
severe life threatening obstetrical hge
without Hemophilia, bt these are off label
use.

Blood products commonly transfused

product

Volume/unit

Contents/unit

Effects

Whole blood

500ml

RBCs, plasma,
fibrinogen

Volume restoration
Hct 3-4 vol%

Packed RBCs

250ml

RBCs only

Hct 3-4 vol%

Fresh frozen plasma 250ml

Colloids &
fibrinogen & all
clotting Factors

Volume restoration
Clotting factors
supplementation

Cryoprecipitate

15ml

Fibrinogen, FcVIII,
XIII, VWF,
fibronectin

Restore fibrinogen

Platelets

50ml

Platelets only

Platelet
supplementation

Coagulopathies :
Coagulopathies are rare.
Suspect if oozing from puncture sites noted.
Work up with platelets, PT, PTT, fibrinogen
level, fibrin split products, and possibly
antithrombin III.

Treatment of secondary PPH

sonographic evaluation

if retained product
Gentle suction & curettage

if cavity empty& patient

stable
oxytocin/ergometrine

Unnecessary curettage avoided, it may worsen PPH

Proper antimicrobial coverage given if endometritis
suspected
If bleeding continues for prolonged period without
definite cause-HCG estimation to rule out chorioCa

Combating PPH in India: moving forward

EOC project by FOGSI- 5 EOC training centers in
rural India to train non specialist medical officers to
provide high quality EOC services where skilled
obstetricians are not available.
Labor management workshops are being held
across the country.
The AOFOG PPH initiative prog: focuses on active
management of 3rd stage in areas with skilled birth
attendants to prevent PPH.

Conclusion
Most of the deaths & disabilities attributed to
childbirth are avoidable, because the medical
solutions are well known. Indeed 99% of maternal
deaths occur in developing countries that have an
inadequate transport system, limited access to
skilled care givers & poor emergency obstetric
service.(Abou Zahr C. 1998)
So ,we need an Intelligent anticipation, skilled
supervision, prompt detection and effective
institution of therapy to prevent disastrous
consequences of PPH.

women are not dying because of a

disease we cannot treat. They are
dying because societies have yet to
make decision that their lives are
worth saving
Mamoud Fathalla,
Precident of FOGSI.1997

Special thanks to

DR S PATI
DR S BHATTACHARYA
DR A HALDER
DR P MISTRI
DR A MITRA