Postpartum Haemorrhage: Recognition and Management

Introduction

Postpartum haemorrhage (PPH) is defined as blood loss of 500 mL or more from the genital tract within 24 hours of a vaginal birth, or 1000 mL or more after caesarean section.¹ It is graded as minor (500-1000 mL) or major (over 1000 mL), and major PPH is further divided into moderate (1000-2000 mL) and severe (over 2000 mL).¹

PPH is the most common cause of major obstetric haemorrhage and remains the leading direct cause of maternal death worldwide, though maternal mortality from PPH in the UK is low because of early recognition and structured escalation protocols.² Every maternity unit runs regular PPH drills because outcomes depend on speed - blood loss is very frequently underestimated by eye, and delay in recognising ongoing bleeding is one of the most consistently identified avoidable factors in maternal deaths.³

Primary PPH occurs within 24 hours of birth and is the focus of this article. Secondary PPH occurs from 24 hours to 12 weeks postpartum, is usually caused by retained products of conception or endometritis, and typically presents with persistent bleeding, offensive lochia and fever rather than a sudden catastrophic loss.¹

Aetiology: the four Ts

The causes of primary PPH are traditionally remembered as the four Ts, and thinking through them in order at the bedside is the fastest way to find a treatable cause.¹

Tone

Uterine atony is by far the most common cause. After delivery, the interlacing myometrial fibres normally contract around the spiral arteries supplying the placental bed, acting as a physiological tourniquet - this is sometimes called the 'living ligature' effect. Anything that overstretches the uterus (multiple pregnancy, polyhydramnios, macrosomia), exhausts it (prolonged labour, grand multiparity) or leaves tissue behind prevents this mechanism from working.

Trauma

Genital tract trauma includes perineal and vaginal tears, cervical lacerations, and episiotomy. Instrumental delivery (forceps or ventouse) and precipitate labour increase the risk. Uterine rupture is rare but catastrophic, and should be suspected in a woman with a previous caesarean scar who develops sudden abdominal pain, scar tenderness, cessation of contractions or fetal distress.

Tissue

Retained placenta or fragments of membrane prevent adequate uterine contraction. Risk is increased by a placenta accreta spectrum disorder, a succenturiate lobe, or a previous history of retained placenta. The placenta and membranes should always be examined for completeness immediately after delivery.

Thrombin

Coagulopathy is the least common primary cause but should be suspected when bleeding is disproportionate to visible trauma, does not clot, or continues despite a well-contracted uterus. It may be pre-existing (von Willebrand disease, ITP, anticoagulant therapy) or acquired - placental abruption, pre-eclampsia/HELLP syndrome and amniotic fluid embolism can all precipitate disseminated intravascular coagulation.⁴

Risk factors

Risk factors can be present before labour or emerge during it, which is why risk should be reassessed continuously rather than only at booking.¹

Antenatal

• Previous PPH or retained placenta
• Multiple pregnancy
• Polyhydramnios or macrosomia
• Grand multiparity (parity ≥4)
• Maternal obesity (BMI ≥35)
• Placenta praevia or a low-lying placenta
• Antepartum haemorrhage
• Pre-eclampsia or hypertensive disease
• Known coagulopathy or anticoagulant use

Intrapartum

• Prolonged first, second or third stage of labour
• Induced or augmented labour (oxytocin use)
• Precipitate labour (under 3 hours)
• Instrumental delivery or caesarean section
• Episiotomy or extensive perineal trauma
• Chorioamnionitis or pyrexia in labour
• Retained placenta

Clinical features

The presentation is visible bleeding from the genital tract after birth, but the clinical picture depends heavily on the cause and on how much blood loss has already occurred by the time it is recognised. Visual estimation of blood loss is notoriously inaccurate and tends to underestimate large volumes, particularly when blood is mixed with amniotic fluid or pooled under drapes, so clinical signs of hypovolaemia matter as much as the volume on the swab count.³

Tachycardia is often the earliest sign of significant blood loss because healthy pregnant women compensate well and maintain blood pressure until a large volume has been lost - a normal blood pressure does not exclude major haemorrhage. Look for a soft, poorly contracted ('boggy') uterus on abdominal palpation suggesting atony, visible perineal or vaginal lacerations, an incomplete placenta on inspection, and bleeding that fails to clot suggesting coagulopathy.

Immediate management

PPH is a medical emergency and management follows simultaneous communicate, resuscitate, monitor and investigate, and arrest the bleeding rather than a strict sequence - several people should be acting at once.¹

Call for help and communicate

Call for senior obstetric and anaesthetic help early, alert the on-call haematologist and blood bank, and activate the major obstetric haemorrhage protocol if bleeding is ongoing or exceeds 1000-1500 mL. Note the time bleeding started.

Resuscitate

• Two large-bore (14G) cannulae and send bloods: full blood count, coagulation screen, fibrinogen, group and save/crossmatch, and urea and electrolytes
• Lie the woman flat and keep her warm
• High-flow oxygen
• Warmed crystalloid while awaiting blood products
• Transfuse red cells early in major haemorrhage rather than waiting for a crossmatch result - use O-negative or group-specific blood if crossmatched blood is not yet available

Arrest the bleeding: mechanical measures

Bimanual uterine massage stimulates contraction and is the first physical step - one hand is placed on the abdomen over the fundus and rubbed to stimulate contraction, or, if bleeding continues, one hand is placed in the vagina to compress the uterus against the other hand on the abdomen. Ensure the bladder is empty (catheterise) as a full bladder prevents adequate uterine contraction.

Arrest the bleeding: medical (uterotonic) management

Uterotonics are used in an escalating sequence if the uterus remains atonic.^1,5

Arrest the bleeding: surgical management

If bleeding continues despite mechanical and medical measures, escalate to surgical intervention.¹

1. Intrauterine balloon tamponade: a Bakri balloon inflated within the uterine cavity applies direct pressure to the placental bed and is often used as a 'tamponade test' - if bleeding stops, definitive surgery may be avoided
2. Haemostatic brace suturing (B-Lynch suture): compresses the uterus longitudinally, usually performed at laparotomy or during caesarean section
3. Uterine artery or internal iliac artery ligation: reduces pelvic blood flow to the uterus
4. Interventional radiology - uterine artery embolisation: an option in a stable patient with access to the service
5. Hysterectomy: the definitive, life-saving last resort when all other measures fail

For trauma, direct repair of lacerations under adequate analgesia (or in theatre if extensive) is definitive. For tissue, manual removal of the placenta under regional or general anaesthesia is required if it has not delivered, with prophylactic antibiotics given because of infection risk. For thrombin causes, correct coagulopathy with fresh frozen plasma, cryoprecipitate and platelets guided by laboratory results and haematology advice, alongside treating the underlying cause.

Prevention: active management of the third stage

Active management of the third stage of labour is standard practice in the UK and substantially reduces the incidence and severity of PPH compared with physiological (expectant) management.⁷ It comprises prophylactic uterotonic administration with delivery of the anterior shoulder or immediately after birth, deferred cord clamping (unless immediate resuscitation is needed), and controlled cord traction to deliver the placenta once signs of separation are seen.

The standard prophylactic uterotonic after vaginal birth is oxytocin 10 units IM; at caesarean section, oxytocin 5 units is given by slow IV injection. Syntometrine (oxytocin 5 units combined with ergometrine 500 micrograms) is a more effective alternative at preventing PPH, but causes considerably more nausea, vomiting and hypertension, and is contraindicated in women with hypertensive disease - so it is reserved for those at higher risk of PPH without a contraindication.

Women at higher risk of PPH (previous PPH, multiple pregnancy, macrosomia, grand multiparity, known coagulopathy) should be identified antenatally, advised to deliver in an obstetric unit rather than a midwife-led unit or at home, and have IV access secured in labour.

Secondary postpartum haemorrhage

Secondary PPH occurs between 24 hours and 12 weeks after birth and most commonly results from endometritis (infection of the uterine lining), retained products of conception, or a combination of both. It presents with persistent or worsening vaginal bleeding, offensive-smelling lochia, lower abdominal pain, fever and an enlarged, tender uterus.¹

Investigation includes a high vaginal swab and endocervical swab for infection, full blood count and CRP, and a pelvic ultrasound to look for retained products. Management combines broad-spectrum antibiotics for suspected endometritis with surgical evacuation of retained products of conception if these are seen on scan and bleeding is significant, though ultrasound findings can be difficult to interpret in the immediate postpartum period and should be considered alongside the clinical picture.

Complications

Major PPH can lead to hypovolaemic shock, disseminated intravascular coagulation, and multi-organ failure if resuscitation is inadequate or delayed. Sheehan's syndrome - pituitary infarction secondary to severe obstetric haemorrhage and hypotension - is a rare but important late complication, presenting with failure of lactation, amenorrhoea and features of hypopituitarism. Transfusion carries its own risks (transfusion reactions, fluid overload), and hysterectomy performed as a life-saving measure ends future fertility, which has a significant psychological impact that should be addressed in follow-up.

Red flags

Prognosis

With prompt recognition and structured escalation, most women with PPH make a full recovery. The overall risk of maternal death from PPH in high-income settings is low, but PPH remains a leading cause of severe maternal morbidity, including the need for blood transfusion, critical care admission, and, rarely, hysterectomy.² Women who have had a PPH are at increased risk of recurrence in future pregnancies and should be counselled about planning delivery in a consultant-led unit with active management of the third stage next time.