Medical management of Post Partum Haemorrhage

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Post Partum Hemorrhage Medical management By Dr Nandini Joshi MD, D.N.B. Assistant Professor Dept of OBG, KAMS&RC 08-07-2015

Transcript of Medical management of Post Partum Haemorrhage

Page 1: Medical management of Post Partum Haemorrhage

Post Partum Hemorrhage Medical management

ByDr Nandini Joshi

MD, D.N.B.Assistant Professor

Dept of OBG, KAMS&RC08-07-2015

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OUTLINE INTRODUCTION INCIDENCE DEFINITION PHYSIOLOGY CLASSIFICATION ETIOLOGY RISK FACTORS PREVENTION MEDICAL MANAGEMENT

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Is Postpartum Hemorrhage a legacy of our Evolutionary

Past? PPH : “An Enigma” An unfortunate side effect for natural

selection for Larger brain The complimentary increase in neonatal

brain Extremely Invasive pattern of placenta

Second contributory factor “Bipedalism” resulting into narrow pelvis , more invasiveness of placenta and extreme remodelling of maternal vasculature

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PPH: Historical Aspects

Mughal Emperor Shah Jahan had 14 children with his wife, the Empress Mumtaz. In 1630, she died of postpartum hemorrhage.He ordered the building of the most beautiful tomb on Earth for her.

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The Swedish Approach

A different approach in the same century (17th century) in Sweden

Queen Ulrika Eleonora also lost people close to her in childbirth

She mandated one or two women from each town to come to Stockholm for midwifery training.

Maternal Mortality transformed

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Postpartum Hemorrhage Today: Living in the shadow of Taj Mahal

Most common Cause for MMR “PPH” (25%- 55%) Globally 1,40,000 women die every year due to PPH otherwise 1 mother dies every 4 minutes -ACOG practice Bulletin 2006

MMR in India (2011-2012) – 178/100000 live births

PPH accounts for 30% of MMR in India

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Incidence ~ 4.1% of all deliveries & Atonic PPH – 3.4% - BJOG 2012

One of the Millennium Development Goals(MDG -5 in 2000) was to reduce maternal mortality by 75% by 2015.

But so far only 45% reduction has been achieved

INCIDENCE

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DEFINITIONS An estimated blood loss of >

500 ml after vaginal delivery & > 1000 ml after cesarean section. . (Pritchart etal 1962)

A decline in hematocrit level of 10% (WHO1989)

Any amount of blood loss that threatens woman’s hemodynamic stability.

Massive PPH refers to a blood loss of >2000 ml or >30% of blood volume.

Pitfalls in definition :Arbitrary, subjective,& based on visual estimation (Underestimate actual blood loss)

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CLASSIFICATION OF PPH

PRIMARY PPH SECONDARY PPH

Occurring within 24 hrs of delivery

(4-6% of all deliveries)

Occurring after 24hrs to 6 wks postpartum

1-3 % of all deliveries Cochrane Database Sits Rev2002;(1), ACOG Practice Bulletin 2006

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Physiological Adaptations during

Pregnancy Maternal blood volume expands by 40% to 50%

during pregnancy. Blood flow to the gravid uterus at term is 650ml/min,

and large amounts of blood can be lost rapidly from placental bed in the absence of uterine tone

Living Ligature : Myometrial fibers in middle layer, run in criss-cross

manner and have double curvature Contraction of these fibers occludes large (spiral

arterioles) blood vessels that run between them.

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s

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ETIOLOGY OF PPH 4 ‘T’s TONE : Uterine atony (70%), Full Bladder

TISSUE: Retained tissue ,clots

TRAUMA: Uterine, cervical or vaginal laceration

THROMBIN: Coagulopathy (Pre-existing / Aquired)

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ETIOLOGY OF PPHPRIMARY PPH SECONDARY PPH

Uterine atony (80%) Retained products (placenta,membranes,clots) Vaginal/cervical lacerations or haematoma Rupture uterus Broad ligament hematoma Uterine inversion.Defects in coagulation

Subinvolution of placental siteRetained products of conceptionInfectionInherited coagulation defects

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RISK FACTORS FOR PPH: Antenatal

Past history of hemorrhage( risk in 1st ,2nd & 3rd

pregnancy is 5.8%, 14.8%, 21.7% respectively)

Placental abruption & Placenta praevia

Multiple pregnancy (3.3%), macrosomia(2%)

Hypertension in pregnancy (pre eclamptic

state, eclampsia, HELLP) (2.2%)

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…Antepartum Chorioamnionitis (2.7%)

Polyhydramnios & Multiparity

Fetal death

Anemia

Uterine myoma, or Manual Removal

of placenta

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RISK FACTORS FOR PPH- Intrapartum Operative / Instrumental delivery- cesarean or

assisted vaginal.

Prolonged labour (7.6%)

Precipitate labour (rapid labour),

Induction or augmentation

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…Intrapartum

Chorioamnionitis

Shoulder dystocia

Internal podalic version & extraction of 2nd

twin

Acquired coagulopathy(e.g. HELLP, DIC)

General anaesthesia with inhaled agents

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RISK FACTORS FOR PPH – Postpartum

Lacerations or episiotomy (4.7%) Retained placenta (7.8%) Placental abnormalities Uterine rupture Uterine inversion Acquired coagulopathy (e.g. DIC)

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But Remember Always that PPH

is a Very unpredictable

condition and Every parturient

women is at risk of having PPH

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CLINICAL CLASSIFICATION ADOPTED FROM BENEDETTI 2002

Hemorrhage class

Acute blood loss (ml)

Blood loss %

Clinical signs & symptoms

Management

1 500-1000 15 % Mild tachycardia , Tachypnea, Diaphoresis

Marks Action line, Observation +/- ReplacementTherapy

2 1200-1500 20-25 %

Postural Hypotension, Tachycardia, Tachypnea, Decrease urine output

Fluid Replacement with oxytocics

3 1800-2100

30-35 %

Overt hypotension, Tachycardia,Tachypnea, Oliguria, Cold clammy extrimities

Urgent active management

4 2400 40% Profound shock Critical active management

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“It is extremely difficult to make complex things simple whereas it is easy to make simple things complex” -Steve JobsThe Passage of time is likely to increase the complexity

of any given case because continuous bleeding, not

appropriately and adequately controlled on a timely basis,

invariably leads to coagulopathy

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The Golden hour ‘ Time by which resuscitation must be initiated to ensure better

survival’. Because,if medical therapy using 3 or 4 uterotonics has not

worked within one hour, there is no logical reason to think they will work in next hour

“Rule of 30” Patient has probably lost >30% blood volume if, Fall in systolic BP by 30mmHg Heart Rate rises by 30bpm RR rises to >30/min Hb or Hct drops by 30% Urine output < 30ml/hr“She is in Moderate to severe Shock”

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The Lethal Triad – Bloody Vicious Cycle

Hypothermia Acidosis Coagulopathy

Plays a major role in the morbidity & mortality of severely injured or exsanguinating patient

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PPH Armamentarium Uterotonics Delayed cord clamping Controlled cord traction Uterine Massage Bimanual compression Balloon tamponade Compression sutures Uterine artery embolization Systematic devascularization Hysterectomy

Components of AMTSL

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PREVENTION OF PPH Identify Predisposing Factors. Treat anemia & educate patients

regarding PPH. High risk patients to be managed in

tertiary care I/V access ,arrange blood if assessed as

at risk AMTSL (Active management of third

stage)

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ACTIVE MANAGEMENT OF THIRD STAGE OF LABOUR (AMTSL)

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MANAGEMENT OF PPH Initial treatment of PPH includes early recognition

followed by prompt attention to the resuscitation & a simultaneous search for the cause of the bleeding.

Once PPH has been identified, management involves four components, all of which must be undertaken SIMULTANEOUSLY:

Communication, Resuscitation, Arresting the bleeding, Monitoring & investigation. - RCOG 2009

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JOINT STATEMENT & ACTION PLANLAUNCHED IN 2004 BY ICM/FIGO

An algorithm has been suggested for the management of PPH H.A.E.M.O.S.T.A.S.I.S.

General medicalH: Ask for helpA: Assess (vitals, blood loss) & resuscitateE: Establish etiology & check Ecbolics (syntometrine, ergometrine, bolus syntocinon) & Ensure availability of bloodM: Massage uterusO: Oxytocin infusion, prostaglandins (i/v,rectal,i/m, intra-myometrial)Specific surgicalS: Shift to operating room, exclude retained products & trauma, bimanual compression, antishock Garment if transfer requiredT: Tissue & Trauma to be excluded , proceed for Tamponade balloon, uterine packingA: Apply compression suturesS: Systematic pelvic devascularization (uterine, ovarian, quadruple, internal iliac)I: Intervention radiologist, uterine artery embolization if appropriateS: Subtotal or total abdominal hysterectomy

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H – Ask for Help Multidisciplinary ApproachAlert – Senior obstetrician Anaesthetists Midwives/ Nursing Staff Theatre staff Haematologists Blood Bank Hospital Porters Intensive care units

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A – Assess & Resuscitate

Assess Vital signs & Estimate Blood Loss

Adequate venous access : 2 large bore I/V

cannulas(16-18G)

Draw Blood sample (~20ml) for CBP, Group,

Cross Match, Coagulation screen, RFT & LFT

Foley’s catheter : Monitoring adequate renal

perfusion.

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ESTIMATION OF BLOOD LOSS Visual Estimation: underestimates

blood loss by 30-50%.

Clinical Symptoms : changes in clinical

status may lag behind blood loss.

PPH bags

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A conical calibrated drape BRASSS V DRAPE: For objective assessment of blood loss (decreases error by 15-33%)

BRASSS V DRAPE is being used in low resource setting

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Volume replacement

Fluid of Choice – Crystalloid over colloids

Crystalloid of choice – Ringer Lactate

Crystalloid, 3- 5ml / ml of blood loss to maintain

urine output at > 30 ml /hr

Loss of 1l of blood requires replacement with 4-

5l of crystalloids (NS or RL) or colloids until

Cross – matched blood is available

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In class III – class IV haemorrhage : CAB of

basic life support should be provided

C Circulation – circulatory blood volume must

be restored & maintained. Infuse 1 litre

crystalloid solution with in 15-20 min, at least 2-3

litres of fluid in first hour to be given.

A Ensure Airway is patent

B Breathing- If respiration is not adequate,

involve anaesthesiologist and intesivist

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Shock Index : Heart rate/ Systolic BP

Normal value – 0.5-0.7

In significant Haemorrhage – 0.9- 1.1

Change in SI – A better correlate in

identifying acute blood loss

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E – establish etiology, ecbolics, ensure availability of blood

Rule out 4 ‘T’s and act - Tone – Start Massage & uterotonics Trauma – EUA & Repair or Pressure

pack Tissue – manual removal under

anaesthesia Thrombin (coagulopathy) : correction

with FFP, cryoprecipitate

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M – Massage the uterus Manually Bimanually

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BIMANUAL COMPRESSIONForm a fist. Place the fist in anterior fonix & apply pressure against the anterior wall of uterusWith the other hand press deeply into the abdomen behind the uterus, applying pressure against the posterior wall of uterusMaintain pressure until bleeding is controlled & uterus contracts while continuing resuscitate measures

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O – Oxytocin infusion, And Other ecbolics

For management of PPH, oxytocin should be preferred over other uterotonics.

If oxytocin is not available or alone is not effective, ergometrine or oxytocin-ergometrine fixed-dose combination should be offered as 2nd line treatment.

If the above 2nd line treatments are not available or not effective, a prostaglandin should be offered as the 3rd line of treatment.

-WHO 2009

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UTEROTONICS: Oxytocin

Methyl Ergometrine , Syntometrine

Prostaglandins- 15methyl PGF2α, misoprostol (PGE1)

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able 1. Medical Management of Postpartum HemorrhageDrug* Dose/Route Frequency CommentOxytocin (Pitocin) IV: 10–40 units in 1

liter normal saline or lactated Ringer's solution @125ml/hrIM: 10 units

Continuous Avoid undiluted rapid IV infusion, which causes hypotension.

Methylergonovine(Methergine)

IM/IV: 0.2 mg Every 2–4 h upto 5 doses in 24hrs

Avoid if patient is hypertensive.

15-methyl PGF2α

(Carboprost)(Hemabate)

IM: 0.25 mg Every 15min, 8 doses maximum

Avoid in asthmatic patients; relative contraindication if hepatic, renal, and cardiac disease. Diarrhea, fever, tachycardia can occur.

Misoprostol(Cytotec, PGE1)

800–1,000 mcg rectally or sublingually

   

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METHYL ERGOMETRINE

Require very specific storage conditions, as they

deteriorate rapidly with exposure to light, heat, humidity.

Side effects: Nausea, vomiting, paresthesias ,chest pain,

tinitus, headache, increased BP Contraindicated in:

Sepsis, migraineHypertension, heart disease,Peripheral vascular disease, Raynaud’s phenomenon Liver & kidney disease,

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SYNTOMETRINE Combination of oxytocin 5U & Ergometrine 0.5mg Given I/M

No important clinical differences in the effectiveness of syntometrine & oxytocin for the prevention of PPH , (Choy et al , BJOG 2002; 109,173-177)

Associated with a higher risk of hypertension, vomiting

In severe PPH, syntometrine did not demonstrate a benefit rather cause increased side effects such as hypertension & vomiting due to the ergot component . (Cochrane Database of Systematic Reviews. 2004;1)

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PGF2α

It is administered in doses of 0.25 mg IM. Contraindication is asthma due to broncho-

constrictive properties of the F class of prostoglandins.

Produce nausea, vomiting, diarrhea & pyrexia, case report of severe intrapulmonary shunting & hypotension seen. Cardiac , pulmonary ,renal & hepatic disease are contraindications

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MISOPROSTOL Synthetic PGE1 analogue Oral/ Vaginal/ Rectal/Sublingual Oral,sublingual route(faster onset of action).

Rectal & Vaginal routes(greater bioavailability+longer duration of action).

Inexpensive, temprature stability Plasma concentration peaks in 30 min(oral),

1-2 hrs (vaginal)

Adverse factors(dose dependent); nausea, vomiting, diarrhea, chills, shivering, fever.

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TRANEXAMIC ACID IN PPH WHO 2009

Tranexamic Acid may be offered in treatment for PPH if: (i) Uterotonics has failed to stop the bleeding(ii) If bleeding may be partly due to trauma.

(Strength of Recommendation – Strong - WHO 2012)

There is a consensus view that fibrinolytic inhibitors (such as tranexamic acid) seldom, have a place in the management of obstetric haemorrhage. RCOG 2009

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BLOOD COMPONENT THERAPY

MTP – Massive Transfusion Protocol

Involves transfusion of >10PRBCs in 24 hours

Ideal ratio of RBC:FFP is 1:1 Can be combined with PRPs if

thrombocytopenia in 1:1:1 ratio

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Use of Activated Recombinant Factor VII (Novoseven) in Obstetrics(COG 2010)

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S – Shift to OT or higher center If initial medical therapy fails within

Golden Hour, shift to a center where multidisciplinary approach available – “PPH precedes Death by 2 hours”

Two important life savior methods to transfer include

Aortic compression by Skilled Birth Attendant

Non Pneumatic Anti Shock Garment

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NNASG Maintains

circulations to Vital organs – Brain , Heart & Kidney

No time Limit No side effects

like gangrene as it is Non Pneumatic

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“Women are not dying because of a disease we cannot treat.

They are dying because societies have yet to make the decision that

their lives are worth saving”. 

Mohd. Fathalla, President of FIGO- 1997

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