Category: Education

Presentation Description

No description available.


By: drapande (97 month(s) ago)

u can do it now...

By: kondadasula (97 month(s) ago)

i need to download this presentation sir so please let me download it.

Presentation Transcript

Postpartum Hemorrhage : 

Postpartum Hemorrhage DR. AJANTA PANDE (SAMANTA)

Slide 2: 

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: : 

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 : 

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.

Slide 5: 

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 : 

Proposed classification. adapted from Benedetti,2002

Types of PPH : 

Types of PPH Immediate/primary PPH- occurs within 24 hrs of delivery) Third stage hemorrhage 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 : 

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 : 

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 : 

Uterine atony It is responsible for upto 80% of primary PPH. Predisposing factors- Grand 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 : 

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 : 

Secondary PPH Retained bits of placenta Placental polyp Subinvolution of placental site Endometritis Infected sloughing from cervicovaginal wound Puerperal inversion of uterus

Slide 14: 

Prepare Handle management of PPH postpartum Hemorrhage (PPH) Predict

Slide 15: 

- Prepare for PPH - Timing of Delivery - proper labor management -exploration of cervicovaginal canal -intense monitoring upto 1hr - Increased postpartum/postoperative surveillance Patients at risk Prevention of PPH

Slide 16: 

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

Slide 17: 

2.- Timing of Delivery - Placenta previa - Previous classical cs Previous myomectomy Fibroid uterus Avoids uterine rupture Avoids significant hemorrhage Elective C/S after completion of 37 weeks Prevention of PPH

Proper labor management : 

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) Placental delivery by controlled cord traction Uterine massage after placental delivery

Diagnosis & Management : 

Diagnosis & Management



Soakage characteristics of 10×10cm pads : 

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 : 

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 : 

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 loss : 

Stages of shock:clinical assessment of bl loss

HAEMOSTASIS algorithm : 

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

Slide 27: 

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 : 

“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.

Slide 29: 

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: : 

Intravenous fluids: CRYSTALLOIDS



Establishment of etiology : 

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 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.

Slide 34: 

Ergot alkaloids-0.2mg methyl ergonovine IM C/I: Hypertension, S/E:Hypertension,M.Ischaemia Prostaglandins- Carboprost /15methylPGF28:80-90% 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.

Slide 35: 

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)

Slide 36: 

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.

Blood replacement in PPH : 

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.

Slide 38: 

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 : 

Blood products commonly transfused

Coagulopathies : : 

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 : 

Treatment of secondary PPH sonographic evaluation if retained product if cavity empty& patient stable Gentle 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 : 

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 : 

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.

Slide 44: 

“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- : 


authorStream Live Help