Postpartum Haemorrhage

King Khalid University Hospital
Department of Obstetrics & Gynecology

Course 482
Postpartum Haemorrhage
Definition
– Any blood loss than has potential to
produce or produces hemodynamic
instability
Incidence
– About 5% of all deliveries
Definition
 >500ml after completion of the third
stage, 5% women loose >1000ml at
vag delivery
 >1000ml after C/S
 >1400ml for elective Cesarean-hyst
 >3000-3500ml for emergent
Cesarean-hyst
 woman with normal pregnancy-
induced hypervolemia increases
blood-volume by 30-60% = 1-2L
 therfore, tolerates similar amount of
blood loss at delivery
 hemorrhage after 24hrs = late PPH
Hemostasis at placental site
 At term, 600ml/min of blood flows through
intervillous space
 Most important factor for control of
bleeding from placenta site = contraction
and retraction of myometrium to
compress the vessels severed with
placental separation
 Incomplete separation will prevent
appropriate contraction
Etiology of Postpartum Haemorrhage
Tone Uterine atony 95%
Tissue Retained tissue/clots
Trauma laceration, rupture,
inversion
Thrombin coagulopathy
Predisposing factors- Intrapartum
 Operative delivery
 Prolonged or rapid labour
 Induction or agumentation
 Choriomnionitis
 Shoulder dystocia
 Internal podalic version
 coagulopathy
Predisposing Factors- Antepartum
 Previous PPH or manual removal
 Abruption/previa
 Fetal demise
 Gestational hypertension
 Over distended uterus
 Bleeding disorder
Postpartum causes
 Lacerations or episiotomy
 Retained placental/ placental
abnormalities
 Uterine rupture / inversion
 Coagulopathy
Prevention
 Be prepared
 Active management of third stage
– Prophylactic oxytocin
– 10 U IM
– 5 U IV bolus
– 10-20 U/L N/S IV @ 100-150 ml/hr
– Early cord clamping and cutting
– Gentle cord traction with surapubic
countertraction
Remember!
 Blood loss is often underestimated
 Ongoing trickling can lead to
significant blood loss
 Blood loss is generally well tolerated
to a point
Management-
 talk to and assess patient
 Get HELP!
 Large bore IV access
 Crystalloid-lots!
 CBC/cross-match and type
 Foley catheter
Diagnosis ?
 Assess in the fundus

 Inspect the lower genital tract
 Explore the uterus
– Retained placental fragments
– Uterine rupture
– Uterine inversion
 Assess coagulation
Management- Assess the fundus
 Simultaneous with ABC’s
 Atony is the leading case of PPH
 Bimanual massage
 Rules out uterine inversion
 May feel lower tract injury
 Evacuate clot from vagina and/ or cervix
 May consider manual exploration at this
time
Management- Bimanual Massage
Management- Manual Exploration
 Manual exploration will:
– Rule out the uterine inversion
– Palpate cervical injury
– Remove retained placenta or clot from
uterus
– Rule out uterine rupture or dehiscence
Replacement of Inverted Uterus
Management- Oxytocin
 5 units IV bolus
 20 units per L N/S IV wide open
 10 units intramyometrial given
transabdominally
Management- Additional Uterotonics
 Ergometrine (caution in hypertension)
– .25 mg IM 0r .125 mg IV
– Maximum dose 1.25 mg
 Hemabate (asthma is a relative
contraindication)
– 15 methyl-prostaglandin F2 alfa
– O.25mg IM or intramyometrial
– Maximum dose 2 mg (Q 15 min- total 8 doses)
 Cytotec (misoprostol) PG E1
– 800-1000 mcg pr
Management- Bleeding with Firm Uterus
 Explore the lower genital tract
 Requirements
• Appropriate analgesia
• Good exposure and lighting
 Appropriate surgical repair
• May temporize with packing
Management – ABC’s
ENSURE THAT YOU ARE ALWAYS
AHEAD WITH YOUR
RESUSCITATION!!!!
 Consider need for Foley catheter,

CVP, arterial line, etc.
 Consider need for more expert help
Management- Evolution
 Panic
 Panic
 Hysterectomy
 Pitocin
 Prostaglandins
 Happiness
MANAGEMENT OF PPH
Management- Continued Uterine Bleeding
 Consider coagulopathy
 Correct coagulopathy
– FFP, cryoprecipitate, platelets
 If coagulation is normal
– Consider embolization
– Prepare for O.R.
Surgical Approaches
 Uterine vessel ligation
 Internal iliac vessel ligation
 Hysterectomy
Conclusions
 Be prepared
 Practice prevention
 Assess the loss
 Assess the maternal status
 Resuscitate vigorously and appropriately
 Diagnose the cause
 Treat the cause
Summary: Remember 4 Ts
 Tone
 Tissue
 Trauma
 Thrombin
Summary: remember 4 Ts
 “TONE”  Palpate fundus.
 Rule out Uterine  Massage uterus.
Atony  Oxytocin
 Methergine
 Hemabate
 “Tissue”
 Inspect placenta for
missing cotyledons.
 R/O retained
placenta
 Explore uterus.
 Treat abnormal
implantation.
 “TRAUMA”
 Obtain good
exposure.
 R/O cervical or
vaginal lacerations.
 Inspect cervix and
vagina.
 Worry about slow
bleeders.
 Treat hematomas.
 “THROMBIN”  Check labs if

suspicious.
CONSUMPTIVE
COAGULOPATHY (DIC)
 A complication of an identifiable,
underlying pathological process
against which treatment must be
directed to the cause
Pregnancy Hypercoagulability
  coagulation factors I (fibrinogen),
VII, IX, X
  plasminogen;  plasmin activity
  fibrinopeptide A, b-
thromboglobulin, platelet factor 4,
fibrinogen
Pathological Activation of
Coagulation mechanisms
 Extrinsic pathway activation by
thromboplastin from tissue destruction
 Intrinsic pathway activation by collagen
and other tissue components
 Direct activation of factor X by proteases
 Induction of procoagulant activity in
lymphocytes, neutrophils or platelets by
stimulation with bacterial toxins
Significance of Consumptive
Coagulopathy
 Bleeding
 Circulatory obstructionorgan
hypoperfusion and ischemic tissue
damage
 Renal failure, ARDS
 Microangiopathic hemolysis
Causes
 Abruptio placentae (most common
cause in obstetrics)
 Sever Hemorrhage (Postpartum hge)
 Fetal Death and Delayed Delivery
>2wks
 Amniotic Fluid Embolus
 Septicemia
Treatment
 Identify and treat source of
coagulopathy
 Correct coagulopathy
– FFP, cryoprecipitate, platelets
Fetal Death and Delayed Delivery
 Spontaneous labour usually in 2 weeks

post fetal death
 Maternal coagulation problems < 1 month
post fetal death
 If retained longer, 25% develop
coagulopathy
 Consumptive coagulopathy mediated by
thromboplastin from dead fetus
 tx: correct coagulation defects and
delivery
Amniotic Fluid Embolus
 Complex condition characterized by
abrupt onset of hypotension,
hypoxia and consumptive
coagulopathy
 1 in 8000 to 1 in 30 000 pregnancies
 “anaphylactoid syndrome of
pregnancy”
 Pathophysiology: brief pulmonary
and systemic
hypertensiontransient, profound
oxygen desaturation (neurological
injury in survivors)  secondary
phase: lung injury and coagulopathy
 Diagnosis is clinical
 Management: supportive
Prognosis:
 60% maternal mortality; profound
neurological impairment is the rule in
survivors
 fetal: outcome poor; related to arrest-to-
delivery time interval; 70% neonatal
survival; with half of survivors having
neurological impairment
Septicemia
 Due to septic abortion, antepartum
pyelonephritis, puerperal infection
 Endotoxin activates extrinsic clotting
mechanism through TNF (tumor
necrosis factor)
 Treat cause
Abortion
Coagulation defects from:

 Sepsis (Clostridium perfringens
highest at Parkland) during
instrumental termination of
pregnancy
 Thromboplastin released from
placenta, fetus, decidua or all three
(prolonged retention of dead fetus)

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King Khalid University Hospital

Department of Obstetrics & Gynecology

 Assess in the fundus

 Consider need for Foley catheter,

 “THROMBIN”  Check labs if

 Spontaneous labour usually in 2 weeks

Coagulation defects from:

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