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Postpartum HaemorrhagePostpartum HaemorrhageDr. G. Al-ShaikhDr. G. Al-Shaikh
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DefinitionDefinition
– Any blood loss than has potential to produce or produces hemodynamic instability
– About 5% of all deliveries
IncidenceIncidence
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DefinitionDefinition
>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
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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
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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
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Etiology of Postpartum HaemorrhageEtiology of Postpartum Haemorrhage
Tone Uterine atony 95%
Tissue Retained tissue/clots
Trauma laceration, rupture, inversion
Thrombin coagulopathy
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Predisposing factors- IntrapartumPredisposing factors- Intrapartum
Operative deliveryProlonged or rapid labourInduction or agumentationChoriomnionitisShoulder dystociaInternal podalic versioncoagulopathy
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Predisposing Factors- AntepartumPredisposing Factors- Antepartum
Previous PPH or manual removalAbruption/previaFetal demiseGestational hypertensionOver distended uterus Bleeding disorder
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Postpartum causesPostpartum causes
Lacerations or episiotomyRetained placental/ placental
abnormalitiesUterine rupture / inversionCoagulopathy
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PreventionPrevention
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
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Remember!Remember!
Blood loss is often underestimated Ongoing trickling can lead to
significant blood loss Blood loss is generally well tolerated
to a point
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Management-Management-
talk to and assess patient Get HELP! Large bore IV access Crystalloid-lots! CBC/cross-match and type Foley catheter
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Diagnosis ?Diagnosis ?
Assess in the fundus Inspect the lower genital tract Explore the uterus– Retained placental fragments– Uterine rupture– Uterine inversion
Assess coagulation
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Management- Assess the fundusManagement- 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
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Management- Bimanual Massage Management- Bimanual Massage
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Management- Manual ExplorationManagement- 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
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Replacement of Inverted Uterus Replacement of Inverted Uterus
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Management- OxytocinManagement- Oxytocin
5 units IV bolus 20 units per L N/S IV wide open10 units intramyometrial given
transabdominally
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Replacement of Inverted UterusReplacement of Inverted Uterus
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Replacement of Inverted Uterus
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Management- Additional Management- Additional UterotonicsUterotonics 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
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Management- Bleeding with Firm Management- Bleeding with Firm Uterus Uterus Explore the lower genital tract Requirements
• Appropriate analgesia • Good exposure and lighting
Appropriate surgical repair• May temporize with packing
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Management – ABC’sManagement – 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
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Management- Evolution Management- Evolution
Panic Panic Hysterectomy
PitocinProstaglandinsHappiness
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MANAGEMENT OF PPHMANAGEMENT OF PPH
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Management- Continued Uterine Management- Continued Uterine Bleeding Bleeding Consider coagulopathy Correct coagulopathy– FFP, cryoprecipitate, platelets
If coagulation is normal– Consider embolization– Prepare for O.R.
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Surgical Aproches
Uterine vessel ligationInternal iliac vessel ligationHysterectomy
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Conclusions Conclusions
Be prepared Practice prevention Assess the loss Assess the maternal status Resuscitate vigorously and appropriately Diagnose the cause Treat the cause
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Summary: Remember 4 TsSummary: Remember 4 TsToneTissueTraumaThrombin
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Summary: remember 4 TsSummary: remember 4 Ts “TONE” Rule out Uterine
Atony
Palpate fundus. Massage uterus. Oxytocin Methergine Hemabate
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Summary: remember 4 TsSummary: remember 4 Ts “Tissue” R/O retained
placenta
Inspect placenta for missing cotyledons.
Explore uterus. Treat abnormal
implantation.
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Summary: remember 4 TsSummary: remember 4 Ts “TRAUMA” R/O cervical or
vaginal lacerations.
Obtain good exposure.
Inspect cervix and vagina.
Worry about slow bleeders.
Treat hematomas.
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Summary: remember 4 TsSummary: remember 4 Ts “THROMBIN” Check labs if
suspicious.
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CONSUPMTIVE COAGULOPATHY (DIC)A complication of an identifiable,
underlying pathological process against which treatment must be directed to the cause
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Pregnancy Hypercoagulability
coagulation factors I (fibrinogen), VII, IX, X
plasminogen; plasmin activity fibrinopeptide A, b-
thromboglobulin, platelet factor 4, fibrinogen
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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
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Significance of Consumptive CoagulopathyBleedingCirculatory obstructionorgan
hypoperfusion and ischemic tissue damage
Renal failure, ARDSMicroangiopathic hemolysis
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Causes
Abruptio placentae (most common cause in obstetrics)
Sever Hemorrhage (Postpartum hge)Fetal Death and Delayed Delivery
>2wksAmniotic Fluid EmbolusSepticemia
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Treatment
Identify and treat source of coagulopathy
Correct coagulopathy– FFP, cryoprecipitate, platelets
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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
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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”
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Amniotic Fluid Embolus
Pathophysiology: brief pulmonary and systemic hypertensiontransient, profound oxygen desaturation (neurological injury in survivors) secondary phase: lung injury and coagulopathy
Diagnosis is clinical
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Amniotic Fluid Embolus
Management: supportive
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Amniotic Fluid Embolus
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
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Septicemia
Due to septic abortion, antepartum pyelonephritis, puerperal infection
Endotoxin activates extrinsic clotting mechanism through TNF (tumor necrosis factor)
Treat cause
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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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Thank you.