Postpartum Hemorrhage

DR. AJANTA PANDE (SAMANTA)

2

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.

PPH today living in the shadow of TAJMAHAL

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,2002Hemorrhage class

Estimated blood loss (ml)

Blood volume loss (%)

Clinical signs & symptoms

management

0 <500 <10 none none

1 500-1000 15 minimal Observation+/-RP Tx

2 1200-1500 20-25↓urine output↑pulse rate↑respiratory ratePostural hypotensionNarrow pulse pr

Replacement therapy with oxytocics

3 1800-2100 30-35 HypotensionTachycardia TachypneaCold clammy

Urgent active management

4 >2400 >40 Profound shock Critical active Mx

Types of PPH

Immediate/primary PPH- occurs within 24 hrs of delivery)

1. Third stage hemorrhage

2. PPH after 3rd stage 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 It is responsible for upto 80% of primary PPH. Predisposing factors-1. Grand Multipara2. Over distended uterus(large fetus , twins ,

hydroamnios)3. Malnutrition4. APH5. Anesthesia (general anesthesia)6. Malformed uterus7. Tumor(fibroid uterus)8. Abnormal uterine contraction(Precipitate/prolonged

labor)9. 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. Retained bits of placenta

2. Placental polyp

3. Subinvolution of placental site

4. Endometritis

5. Infected sloughing from cervicovaginal wound

6. Puerperal inversion of uterus

Prepare Handle

management of PPH

postpartum Hemorrhage (PPH)

Predict

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

Patients at risk

Prevention of PPH

Prevention of PPH

1.- Prepare for PPH

-Nursing

-Anesthesia

- Surgical assistance

Drugs/Equipment

-Oxytocin

-Carbetocin

-Methergine

-Prostaglandins

-Crystalloids

-Blood/Bl.products

-Surg. Instruments

-Hemostatic ballons

( Cook, S-B, Foley)

Personnel

2.- Timing of Delivery- Placenta previa

- Previous classical cs

- Previous myomectomy

- Fibroid uterus

Avoids uterine ruptureAvoids significant hemorrhage

Elective C/S

after completion of 37 weeks

Prevention of PPH

Proper labor management

Management of proloned labor Slow delivery of baby Active management of 3rd stage1. Administration of uterotonics (oxytocin

10U/Ergometrine 0.2mg IM)

2. Placental delivery by controlled cord traction

3. Uterine massage after placental delivery

Diagnosis & Management

PPH BOWL AND BAG

Soakage characteristics of 10×10cm 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 pain…rule out intra-abdominal blood loss.

Stages of shock:clinical assessment of bl lossclassification Class I Class II Class III Class IV

Blood loss (% ) 10-15 15-30 30-40 >40

Consciousness alert Anxious, restless Agitated,confused unconscious

Respiratory rate N Mild↑ed raised raised

Complexion N pale pale grey

Extremities N cool cool cold

Capillary refill N slow slow Minimal/absent

Pulse rate N N elevated Fast but thready

SBP N N N/slight↓ed hypotension

Urine output N reduced reduced oligoanuric

HAEMOSTASIS algorithm

H- ask for help A- assess (vitals, blood loss) & resuscitate E -

1. 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-0.5-0.7.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.

HARTMANN’SSOLUTION

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% HUMANALBUMIN

More physiological than gelatin,remains intravascular for 12 hrs

Expensive, no clear advantage over crystalloids

HYDROXY ETHYL STERCH

Remains in intravascular space for 12-24 hrs

Risk of coagulopathy, renal injury

Establishment of etiology

T-tone-thorough assesment of uterine size& tone

T-tissue-manual exploration of uterine cavity ↓anaesthesia

T-trauma-ex↓anaesthesia 4 extended tear in cervix,vagina

T-thrombine-defect in coagulation

Uterine atony

Retained products

lacerations

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 4°C.

Misoprostol/PGE1:tab 400-600µg orally /800µg rectally have been tried.

In a randomised trial(Derman et al,2006)600µg 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

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.

Misoprostol 600µg Misoprostol 400µg

Oxytocin 10IU

Shivering 56/199(28%) 38/198(19%)

25/200(12.5%)

Pyrexia>38°C 15/199(7.5%) 4/195(2%) 6/199(3%)

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/µL 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 restorationClotting 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 if cavity empty& patient stableGentle suction & curettage 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-ßHCG 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