Obstetric haemorrhage

Contents

Overview

Obstetric haemorrhage is the leading cause of maternal mortality worldwide and a major contributor in high-income countries. It includes antepartum haemorrhage (APH, bleeding from 24 weeks gestation before delivery) and postpartum haemorrhage (PPH, the most common and most preventable). The physiological changes of pregnancy — including a 40–50% increase in circulating blood volume — may initially mask the severity of haemorrhage, with clinical deterioration occurring precipitously.

Antepartum Haemorrhage

APH complicates 3–5% of pregnancies. The two most important causes requiring ICU involvement are:

Placenta Praevia

The placenta is implanted over or near the internal cervical os. Presents with painless, bright red vaginal bleeding, often recurrent and increasing in severity. Risk factors: prior uterine surgery (caesarean section), multiparity, advanced maternal age.

Management: hospitalisation, fetal surveillance, corticosteroids for fetal lung maturity if preterm, caesarean section (vaginal delivery contraindicated). Massive haemorrhage risk particularly at time of delivery.

Placental Abruption

Premature separation of the normally sited placenta from the uterine wall. Presents with abdominal pain and uterine tenderness, with or without visible bleeding (concealed abruption). Associated with uterine contractions. Risk factors: hypertension (including pre-eclampsia), cocaine use, trauma, polyhydramnios.

Complications: massive haemorrhage (revealed and concealed), DIC (from release of thromboplastic material from the placenta — fibrinogen may be severely depleted), fetal compromise, and stillbirth.

Management: urgent delivery if fetal or maternal compromise; correct coagulopathy; activate massive haemorrhage protocol.

Placenta Accreta Spectrum

Abnormal placental implantation:

  • Accreta: placenta invades but does not penetrate the myometrium
  • Increta: penetrates the myometrium
  • Percreta: penetrates through the myometrium to the serosa or beyond (bladder, bowel)

Risk factors: uterine scarring (previous caesarean section, uterine surgery). Each additional scar increases risk significantly. When placenta praevia coexists with a prior caesarean scar, the risk of accreta approaches 25–50%.

Planned delivery in a multidisciplinary setting (obstetric, surgical, vascular, ICU, haematology, interventional radiology) reduces mortality. Cell salvage and interventional radiology (internal iliac artery balloon occlusion or UAE) may be used perioperatively.

Postpartum Haemorrhage

PPH is defined as blood loss ≥500 mL after vaginal delivery or ≥1000 mL after caesarean section. Major PPH is ≥1000 mL. Estimated blood loss is consistently underestimated clinically — true losses often exceed estimates by 30–50%.

Causes — 4 Ts:

Tone (most common, ~70%): Uterine atony from failure of the uterus to contract after delivery. Risk factors: prolonged labour, oxytocin augmentation, polyhydramnios, multiple pregnancy, macrosomia, chorioamnionitis, high parity.

Trauma (~20%): Perineal lacerations, episiotomy, cervical tears, uterine rupture, haematoma.

Tissue (~10%): Retained placenta or membranes preventing uterine contraction.

Thrombin (<1%): Pre-existing coagulopathy (e.g., ITP, VWD) or DIC.

Management of Massive Obstetric Haemorrhage

Activate the massive haemorrhage protocol immediately — do not wait for haemodynamic compromise.

Immediate Simultaneous Actions

  • Call for help: senior obstetrician, anaesthetist, midwifery team, haematologist, blood bank
  • IV access: two large-bore cannulae
  • Send bloods: FBC, coagulation (PT, APTT, fibrinogen — fibrinogen is the most sensitive marker of coagulopathy in obstetric haemorrhage), crossmatch, U&E, blood gas
  • Fluid resuscitation: crystalloid as initial bridge; transfuse early
  • Uterotonic therapy (see below)
  • Uterine massage and bimanual compression
  • Identify and treat the cause (4 Ts assessment)

Uterotonic Drugs (for atony)

  • Oxytocin 10 units slow IV bolus, then 40 units in 500 mL at 125 mL/hour. Avoid rapid IV bolus (causes hypotension, tachycardia).
  • Ergometrine 500 micrograms IM (or slow IV): potent uterine contraction; contraindicated in hypertension and pre-eclampsia.
  • Syntometrine = oxytocin + ergometrine combined: used in many units for routine third stage management; avoids IV access.
  • Carboprost (15-methyl PGF2α) 250 micrograms IM (or intramyometrial), repeat every 15 minutes up to 8 doses: potent; contraindicated in asthma.
  • Misoprostol 800–1000 micrograms sublingually or rectally: useful when IV access not available (community setting, resource-limited settings).
  • Tranexamic acid 1 g IV: reduces PPH mortality from haemorrhage when given within 3 hours of delivery (WOMAN trial). Repeat dose at 30 minutes if ongoing haemorrhage. Give early — do not wait.

Haemostatic Interventions

Blood product resuscitation: Use a balanced transfusion strategy (as in trauma): red cells, FFP, and platelets in a 1:1:1 or 1:1:0.5 ratio. In obstetric haemorrhage, fibrinogen is the critical coagulation factor — fibrinogen falls to critically low levels early and correlates with severity. Target fibrinogen above 2 g/L; replace with cryoprecipitate (two pools) or fibrinogen concentrate.

Fibrinogen level as a guide: In the OBS2 study, a fibrinogen ≤2 g/L at the time of PPH diagnosis was strongly predictive of progression to severe PPH. Proactive fibrinogen replacement is recommended.

Recombinant Factor VIIa (rFVIIa): Reserved for life-threatening haemorrhage refractory to conventional therapy. Expensive and associated with thromboembolic risk. Used as rescue therapy.

Thromboelastography (TEG/ROTEM): Point-of-care coagulation assessment guides targeted product replacement in real time and is particularly useful in obstetric haemorrhage where standard coagulation tests are slow.

Surgical and Interventional Options

Uterine balloon tamponade: Bakri balloon or Sengstaken-Blakemore tube inserted into the uterus and inflated to tamponade bleeding. Effective for atony as a bridge to further intervention or as definitive management in minor cases.

B-Lynch suture: Compression suture applied around the uterus to reduce blood supply to the myometrium and promote mechanical contraction.

Uterine artery ligation: Reduces flow to the uterus; can be combined with ovarian artery ligation.

Interventional radiology: Uterine artery embolisation (UAE) effectively controls PPH in centres with 24-hour IR availability. Preserves uterine and ovarian function. Internal iliac artery balloon occlusion can be placed prophylactically before delivery in placenta accreta.

Peripartum hysterectomy: Definitive treatment for uncontrolled PPH. Associated with significant morbidity (bladder and ureteric injury, massive blood loss). Consent should ideally be obtained preoperatively in planned high-risk cases.

ICU Care

ICU admission is required for:

  • Haemodynamic instability or shock requiring vasopressor support
  • Massive transfusion and ongoing coagulopathy
  • Respiratory failure (ARDS from massive transfusion or amniotic fluid embolism)
  • Renal failure from hypovolaemia
  • Post-surgical monitoring
  • DIC

Obstetric patients are generally young and physiologically resilient — aggressive resuscitation and early intervention are rewarded with good outcomes if haemorrhage control is achieved. The risk of adverse fetal/neonatal outcome must be considered in decisions about delivery timing.

Viva Questions

What are the 4 Ts of postpartum haemorrhage and how do you approach their management?

The 4 Ts framework provides a systematic approach to identifying the cause of PPH. Tone refers to uterine atony — the most common cause, responsible for approximately 70% of PPH. Management is with uterotonic agents (oxytocin, ergometrine, carboprost, misoprostol) and uterine massage or bimanual compression. Trauma describes perineal or genital tract lacerations, episiotomy extensions, cervical tears, or uterine rupture. Management requires direct visualisation of the birth canal under good light and surgical repair. Tissue refers to retained placental tissue or membranes preventing the uterus from contracting down. Examination of the placenta for completeness, and manual removal or surgical evacuation of retained products, is required. Thrombin refers to coagulopathy — either pre-existing (ITP, VWD, anticoagulant therapy) or secondary (DIC from abruption or amniotic fluid embolism). Management targets the underlying disorder and replaces coagulation factors. In practice, multiple causes often coexist and are assessed and treated simultaneously.

What is the role of tranexamic acid in obstetric haemorrhage?

Tranexamic acid (TXA) is an antifibrinolytic agent that inhibits the activation of plasminogen to plasmin, thereby preventing fibrin clot breakdown. In PPH, fibrinolysis is an early and important contributor to haemorrhage. The WOMAN trial (Lancet 2017) was a large randomised placebo-controlled trial of TXA 1 g IV (with a second dose at 30 minutes if bleeding continued) versus placebo in women with PPH from all causes. TXA significantly reduced death from PPH (1.5% vs 1.9%; risk ratio 0.81) and reduced the need for laparotomy. Crucially, benefit was greatest when TXA was given within 3 hours of delivery — after 3 hours, there was no significant benefit. TXA should now be given promptly as part of the initial management of PPH, alongside uterotonic drugs, resuscitation, and cause-identification. It is safe, cheap, and widely available. Concerns about thromboembolic risk are not supported by the WOMAN trial data.

How does coagulopathy develop in obstetric haemorrhage and how do you manage it?

Obstetric haemorrhage causes coagulopathy through several mechanisms. Haemorrhage leads to dilutional coagulopathy as the intravascular volume is replaced with crystalloid and packed red cells that contain no clotting factors. Activated fibrinolysis occurs early in PPH — fibrin clots at the placental site are rapidly degraded, worsening bleeding before a replacement coagulopathy develops. Placental abruption and amniotic fluid embolism can cause acute consumption coagulopathy (DIC) from release of thromboplastic material. Of the coagulation factors, fibrinogen falls first and most steeply in obstetric haemorrhage and is the best early predictor of severity — a fibrinogen below 2 g/L at the onset of PPH strongly predicts progression to severe haemorrhage. Management requires aggressive fibrinogen replacement with cryoprecipitate (two pools, each providing approximately 3–4 g fibrinogen) or fibrinogen concentrate, targeting a level above 2 g/L. FFP provides a broader range of clotting factors and should be given in balanced ratio with red cells (1:1 or close to it). Platelets should be maintained above 50–75 × 10⁹/L. Point-of-care coagulation monitoring (ROTEM or TEG) guides targeted replacement and allows faster decision-making than standard laboratory turnaround times.