Antepartum Haemorrhage

Specific Learning Outcomes

 Enumerate the aetiology of APH
 Internalize the basic clinical assessment, investigations and
complications of APH
 Describe the risk factors, aetiology, diagnosis, management and
complications of the complicated causes of APH

Definition - bleeding from or into the genital tract after the 28th week of
pregnancy and prior to the birth of the baby.

From 22 weeks (foetus>500mg) in developed countries

Different terminologies used

Spotting – Staining, streaking or blood spotting noted on underwear or
sanitary pad
Minor haemorrhage – Blood loss <50ml that has settled
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Major haemorrhage – Blood loss of 50-1000ml with no signs of
clinical shock
Massive haemorrhage – Blood loss>1000 ml and/or signs of clinical
shock
Recurrent APH - > one episode
Epidemiology

 It affects 3-5% of all pregnancies

 Three times commoner in multiparous than in primiparous women
 Leading cause of perinatal and maternal mortality world wide
 Most often unpredictable
 May lead to post-partum haemorrhage

Aetiology
No definite cause in about 40% of cases

Types
Simple
 Local causes
 Vaginal Trauma
 Cervical Erosion or Tumour
 Cervicitis
 Blood Dyscrasia
 Thrombocytopenia
 Anticoagulants
Complicated
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  Placenta Praevia
 Abruptio Placentae
 Vasa praevia (bleeding from fetal vessels in the fetal membranes)
 Uterine rupture

Clinical Assessment of APH

 First and foremost, ensure maternal and foetal welfare with
 Mother as priority
 Establish whether urgent intervention is required to
 Manage maternal or foetal compromise
 Assess extent of vaginal bleeding and
 Maternal cardiovascular status
 Assess foetal wellbeing
 No digital pelvic examination
Investigations
 FBC
 Coagulation profile
 Ultrasound
 D- dimer: Abruptio Placentae
 If Rh negative mother give anti-D
 Continuous foetal heart rate monitoring if feasible otherwise
 After every 15 minutes

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Complications of APH
 Premature delivery
 Foetal distress and death
 IUGR
 Haemorrhagic shock
 DIC
 Uterine atony –Couvelaire uterus
 PPH
 Anaemia
 Acute renal failure
 Acute tubular necrosis
Placenta Praevia
Definition - Placenta which has implanted partially or wholly in the
lower uterine segment
Types
Old Classification
 Grade 1 – Just enters lower segment
 Grade 2 – Enters LUS but does not reach os
 Grade 3 – Partially covers os but not completely
 Grade 4 – Completely covers os

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Types (New classification)
Minor – Enters LUS but does not cover the os
Major – Covers internal os completely

Aetiology
 Unclear
 Any damage to endometrium or myometrium
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  Scar tissue impedes migration away from os
 Multiple pregnancy- large surface area
 Smoking- vasoconstriction
 Cocaine Use – Vasoconstriction-hypertrophy
 Endo/myometrial damage
 Previous C/S
 Spontaneous abortion with curretage
 Uterine damage
 Endometritis
 Manual removal of placenta
 Other Factors
 Previous placenta praevia
 Maternal age – reduced uterine blood flow needs greater
surface area
 Parity - 3 previous deliveries 2.6 fold
 Vessels at site of previous placenta reduced flow
discourage implantation
 Idiopathic
Presentation
 Antepartum Haemorrhage
 Late pregnancy
 Painless bleeding

 Malpresentation
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  Breech/High Head/Unstable lie in 3rd trimester
 Asymptomatic –found at routine U/S scan
Diagnosis
 Ultrasound
 Transabdominal
 Transvaginal
Management
Mahady’s Equation
Intrauterine 37/4037/5Extrauterine
environment environment

Conservative if preterm and

 Mother and foetus stable
 No active bleeding
Entails
 Bed rest
 Keep pad chart
 Foetal kick chart
 Vital signs monitoring
 Ultrasound
 Biophysical profile

 Steroids
 Dexamethazone 12mg, 12hrly. 2 doses if
 Foetus between 24 weeks and 34 weeks 6days
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  Regular Hb
 X-match/Transfuse
 Delivery
 Timing – Mahady’s equation
 Usually 38/52
 Mode of Delivery
 Minor praevia – 2cm from os
 Examination in theatre/ARM/Vaginal delivery
 Major praevia
 Caesarean Section
Associated Complications
 Preterm delivery and its complications
 PPROM
 Increased rate of C/S
 Congenital Abnormality - noted to be higher (6.7%)
 Small for Dates(SGA) with repeated bleeding
 19% - decreased placental perfusion
 Reduced nutrient transfer
 Malpresentation – 3 fold increase
 Breech
 Transverse lie
 Oblique
 Abnormal Placentation – Accreta/Percreta
 Unscarred uterus 5%
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  1 previous C/S 24%; 4 C/S 67%
 Pregnancy Induced Hypertension – reduced
 ½ normal incidence
Abruptio Placentae
Types
Placental Site - Upper Uterine Segment

Presentation
Pain & Vaginal bleeding (Revealed)
 Pain/Shock
 No vaginal bleeding (concealed)
Associated risk factors
 Hypertension/Pre-eclampsia
 Trauma
 RTA /Pelvic #
 Amniocentesis
 External cephalic version
 Cordocentesis
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  Domestic violence
 Smoking – 40% increase for each year smoked
 Cocaine – hypertension/catecholamine release
 Rupture of membranes
 Rapid decompression especially in polyhydramnios
 Delivery of multiple pregnancy
 Thrombophilias
 Factor V leiden, prothrombin gene, protein C &S
 Antiphospholipid syndrome & homocysteinaemia
 Cord complications –short cord
 Foetal abnormality
 Raised alpha feto-protein
 Increased recurrence
 Maternal Age
 Alcohol
 Idiopathic
Symptoms
 Vaginal Bleeding ( Revealed) 80%
 Abdominal /Back Pain (Severe) 70%
 Fetal Distress 60%
 Contractions (Hypertonic) 35%
 Preterm Labour 25%
 Fetal Death in utero 15%
Complications
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 Maternal
 Haemorrhagic /Hypovolaemic SHOCK
 Coagulopathy DIC/Hypofibrinogenaemia
 Couvelaire Uterus / Uterine rupture
 Renal Failure
 Ischaemic Necrosis distal organs –liver, adrenals and pituitary
 Premature labour
 PPH
Fetal
 Hypoxia - Fetal distress
 Anaemia
 Growth Retardation - if treated conservatively and survives
 CNS Abnormalities
 Intra Uterine Death
Investigations
 Blood Group - X match
 Rh – anti D
 Haemoglobin/FBC - Platelets
 Clotting Time / Fibrinogen /FDP /PTT
 Urea /Creatinine
 Ultrasound - exclude Praevia
 Non Stress Test
 Biophysical Profile
Management
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Mahady’s Equation
Intrauterine 37/407/52 Extrauterine
environment environment

Conservative if premature foetus (dexamethazone if <34 weeks) and

 Mother and foetus stable
 Clotting factors not changing rapidly
 If not bleeding much and vital signs are stable
 Very small abruptio

Active management
Principles of management

 Early delivery
 Adequate transfusion
 Adequate analgesia
 Detailed maternal and foetal monitoring

Management

 Correct SHOCK
 I V access – 2 large bore cannulae
 Crystalloids IV – emergency
 Blood as soon as possible preferably fresh
 Correct DIC – Fresh frozen plasma, ? Heparin
 Catheterise - hourly urine output chart
 Assess for delivery

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  FH absent - induce – IV oxytocin
 FH present
 C/S –Foetal distress, severe bleeding, labour not
advanced; consent in case excess bleeding leading to
hysterectomy
 Induce –very low gestation,

Prognosis

 Independent risk factor for perinatal mortality

 Foetal hypoxia causing death
 Perinatal mortality is less than 50 per 1,000.
 Maternal mortality

Vasa Praevia

 Occurs in about 1 of every 1,000 pregnancies

 Rupture of foetal vessels that run in membranes below
 Foetal presenting part unsupported by placenta/umbilical cord

Predisposing factors
 Velamentous insertion of the umbilical cord
 Accesory placental lobes
 Multiple gestations

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Diagnosis
 Painless bleeding at time of spontaneous rupture of membranes or
 Post amniotomy
 Foetal bradycardia
 Foetal shock or death can occur rapidly at time of diagnosis since
 Major bulk of blood volume is foetal (3kg foetus-300ml) so
 Check FHR always after rupture of membranes
 Definitive by inspecting placenta & membranes after delivery

Uterine rupture:
 About 40% of women have had prior uterine surgery
 Other risk factors for uterine rupture are these conditions:
 More than four pregnancies
 Trauma
 Excessive use of oxytocin
 Shoulder dystocia
 Some forceps deliveries

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  Rupture may occur before or during labour or at time of delivery
Management
 Emergency
 Fluids, blood
 Laparatomy
 More often than not subtotal hysterectomy

DR D.K NGOTHO – SL RH

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