Postpartum Haemorrhage (PPH)

Definition

• Primary (Early) PPH: Blood loss exceeding 500 mL after vaginal delivery or 1000 mL after caesarean delivery, occurring within the first 24 hours of delivery.
• Secondary (Late) PPH: Significant bleeding occurring 24 hours to 6 weeks after delivery.

• Textbook of Family Medicine, p. 923
• Tintinalli's Emergency Medicine, p. 2131

Incidence and Global Significance

• Miller's Anesthesia, p. 8906

Classification

The "4 Ts" - Causes of Postpartum Haemorrhage

1. TONE (Uterine Atony) - >70% of cases

• Uterine overdistension: polyhydramnios, multiple gestation, fetal macrosomia
• High parity (grand multiparity)
• Prolonged or precipitate labour
• Use of oxytocin, tocolytics, or general anaesthetics (uterine-relaxing agents)
• Intraamniotic infection (chorioamnionitis)
• Preeclampsia
• Previous PPH
• Uterine fibroids (structural abnormality)
• Obesity

2. TRAUMA - ~20% of cases

• Perineal, vaginal, and cervical lacerations (especially after instrumental delivery)
• Episiotomy extension
• Uterine rupture (especially in women with previous uterine surgery, particularly caesarean section)
• Uterine inversion (rare but dramatic - occurs from fundal implantation of placenta, excessive cord traction, or fundal pressure)

3. TISSUE - ~10% of cases

• Retained placenta or placental fragments
• Placenta accreta (invasion into myometrium - most common, 84%)
• Placenta increta (invasion to serosa, 13%)
• Placenta percreta (invasion beyond serosa into bladder/adjacent structures, 3%)
• Note: Abnormal placentation has increased 10-fold in incidence over 50 years, primarily due to rising caesarean section rates combined with placenta praevia

4. THROMBIN (Coagulopathy) - uncommon

• Disseminated intravascular coagulation (DIC)
• Pre-existing coagulation disorders (von Willebrand disease, haemophilia carrier)
• HELLP syndrome, pre-eclampsia
• Amniotic fluid embolism
• Placental abruption (consumption coagulopathy)
• Anticoagulant use
• Dilutional coagulopathy from massive transfusion
• Tintinalli's Emergency Medicine, p. 2132-2133
• Textbook of Family Medicine, p. 927-929

Pathophysiology

• Tintinalli's Emergency Medicine, p. 2131

Clinical Features

• Excessive vaginal bleeding (may be concealed intra-abdominally)
• Dizziness, syncope, anxiety
• Progressive weakness

• Tachycardia (early and sensitive sign)
• Hypotension (late sign - implies >30% blood loss)
• Pallor, cold clammy skin (signs of shock)
• Uterus: soft/boggy (atony) vs. well-contracted (laceration/retained tissue)
• Per speculum: visible lacerations, continuing active bleeding
• Inability to palpate uterine fundus abdominally (suggests uterine inversion)
• "Beefy-red mass" at vaginal introitus = complete uterine inversion

Diagnosis and Initial Assessment

• Assess uterine tone by fundal palpation (soft and boggy = atony)
• Inspect vagina and cervix with speculum for lacerations
• Check placenta is complete after delivery
• Check for uterine inversion if fundus not palpable

• Full blood count with platelets
• Blood type and crossmatch
• Coagulation screen: fibrinogen, fibrin split products, PT, aPTT
• Renal/liver function, electrolytes
• Point-of-care viscoelastic tests (TEG/ROTEM) - increasingly used to guide coagulation product therapy
• Ultrasound: identifies retained placenta, blood clots within uterus, excludes intra-abdominal bleeding
• Creasy & Resnik's Maternal-Fetal Medicine, p. 947
• Miller's Anesthesia, p. 8907

Management

Step 1: Resuscitation and Initial Measures

• Call for help - activate massive haemorrhage/obstetric emergency protocol immediately
• Establish 2 large-bore IV lines (14-16G)
• Oxygen supplementation
• IV fluid resuscitation: Hartmann's/Lactated Ringer's initially
• Monitor: continuous pulse oximetry, ECG, urine output via catheter
• Blood type and crossmatch
• Alert blood bank, activate massive transfusion protocol (MTP) early if severe
• Position: lithotomy for examination; avoid Trendelenburg (may worsen respiratory compromise)

Step 2: Identify and Treat the Cause

• Uterine massage: bimanual uterine massage and compression - one fist in anterior fornix, hand compressing fundus suprapubically
• Fundal massage alone if bimanual not possible

• Miller's Anesthesia, p. 8908

• Manual removal of placenta under anaesthesia
• Uterine exploration and curettage
• Ultrasound guidance helpful
• For placenta accreta/percreta: may require hysterectomy (see surgical management)

• Thorough perineal, vaginal, and cervical examination under adequate lighting and anaesthesia
• Repair all lacerations with absorbable sutures
• Uterine rupture: surgical repair or hysterectomy

• Treat underlying cause
• Massive transfusion protocol: packed red blood cells (pRBCs), fresh frozen plasma (FFP), cryoprecipitate, platelets
• Fibrinogen concentrate early (fibrinogen falls rapidly in obstetric haemorrhage)
• Point-of-care TEG/ROTEM to guide targeted product transfusion
• Recombinant factor VIIa: NOT routinely recommended due to adverse event reports; reserved for life-threatening bleeding refractory to all other measures

Step 3: Intrauterine Tamponade

• Bakri balloon or large Foley catheter tamponade - success rates up to 91% reported
• Uterine gauze packing - retrospective evidence supports effectiveness in atony
• Jada System (intrauterine vacuum device) - shown to achieve definitive control in >90% of patients at median 3 minutes
• Grainger & Allison's Diagnostic Radiology, p. 279

Step 4: Interventional Radiology

• Uterine artery embolisation (UAE) - should not be a last resort but is not first-line either
• Performed via bilateral common femoral artery approach, catheterisation of anterior divisions of internal iliac arteries, embolisation of uterine artery with Gelfoam
• Aims to stop bleeding AND preserve the uterus
• Success rates high; bilateral embolisation typically required (excellent pelvic collateral circulation)
• Empirical embolisation performed even with negative angiogram (accepted practice in atony)
• Recurrent bleeding can be treated with repeat embolisation
• Less effective with abnormal placentation (accreta/percreta)
• Grainger & Allison's Diagnostic Radiology, p. 282-285

Step 5: Surgical Management

1. Uterine compression sutures:
   • B-Lynch suture: "brace" suture technique compressing the uterine body and closing off blood supply. Uterine-conserving.
   • Hayman technique: Simpler vertical brace suture variant.
2. Uterine artery ligation (O'Leary suture): Bilateral ligation of uterine arteries at their origin from the internal iliac. Simple, fast, effective.
3. Internal iliac (hypogastric) artery ligation:
   • Reduces pulse pressure in pelvic vessels by ~85%, creating conditions for clot formation
   • Transient decreases in blood pressure and flow allow haemostasis
   • Ample collateral circulation means no long-term ischaemic consequences
   • Subsequent pregnancies have been reported after this procedure
   • Temporary bladder dysfunction and buttock pain may occur postoperatively
4. Peripartum hysterectomy: Life-saving definitive measure when all other options have failed. Most commonly performed for uterine atony unresponsive to all measures, or uterine rupture unrepairable. The peripartum hysterectomy rate is used as an audit measure for PPH algorithm effectiveness.

• Creasy & Resnik's Maternal-Fetal Medicine, p. 948-949
• Grainger & Allison's Diagnostic Radiology, p. 279

Step 6: Massive Transfusion and ICU

• Massive transfusion protocol: Early activation; balanced ratio of pRBCs:FFP:platelets
• Cryoprecipitate or fibrinogen concentrate should be considered early (fibrinogen depletes rapidly)
• Central monitoring: Central venous pressure line or pulmonary artery catheter (Swan-Ganz) for haemodynamic monitoring in massive haemorrhage, to guide fluid management and prevent pulmonary oedema
• Multidisciplinary team: obstetricians, anaesthesiologists, interventional radiologists, haematologists, blood bank, ICU
• Creasy & Resnik's Maternal-Fetal Medicine, p. 949

Uterine Inversion (Special Scenario)

• Predisposed by fundal placental implantation (thinner myometrium)
• Precipitated by excessive cord traction or fundal pressure

1. Tocolysis to relax uterus: magnesium sulphate, β-mimetics (terbutaline), or nitroglycerin IV
2. Manual reinversion: gentle but firm continuous pressure applied to fundus, elevating it into the vagina
3. Summon anaesthetist immediately - general anaesthesia may be needed
4. Once reinverted, give uterotonics (oxytocin) to contract uterus
5. If reinversion fails with tocolysis: Huntington or Haultain procedure (surgical) under general anaesthesia

• Creasy & Resnik's Maternal-Fetal Medicine, p. 3297-3300

Prevention (Active Management of Third Stage of Labour - AMTSL)

1. Prophylactic uterotonic (oxytocin 10 IU IM/IV) immediately after delivery of baby
2. Controlled cord traction (Brandt-Andrews manoeuvre)
3. Uterine massage after placental delivery (though evidence for this step is less strong)

• Identify and correct anaemia antenatally
• Screen for placenta praevia/accreta in high-risk women (previous CS + placenta praevia)
• Establish adequate IV access in women with risk factors
• Ensure crossmatched blood available for high-risk patients
• Textbook of Family Medicine, p. 933

Complications of Untreated/Severe PPH

• Hypovolaemic shock (Classes I-IV)
• DIC - consumption coagulopathy worsens bleeding in a vicious cycle
• Acute tubular necrosis / acute kidney injury
• Acute respiratory distress syndrome (ARDS)
• Sheehan's syndrome: anterior pituitary infarction from severe shock; presents later with failure of lactation, amenorrhoea, hypothyroidism, adrenal insufficiency
• Death - PPH is the leading cause of maternal mortality worldwide

Recent Evidence (2024-2026)

• A 2025 Cochrane Network Meta-Analysis (Gallos et al., PMID 40237648) evaluated uterotonic agents for preventing PPH, providing updated evidence on the relative efficacy of different uterotonics.
• A 2025 Cochrane Systematic Review (Williams et al., PMID 39911088) examined transfusion of blood and blood products for management of PPH, supporting early and targeted use of blood products.

Summary Flowchart

PPH Diagnosed
     ↓
Resuscitate (IV access, oxygen, fluids, crossmatch)
     ↓
Identify cause: TONE / TRAUMA / TISSUE / THROMBIN
     ↓
TONE (Atony)?
  → Bimanual massage + Oxytocin IV
  → Methylergonovine IM (if not hypertensive)
  → Carboprost IM (if not asthmatic)
  → Misoprostol
  → Tranexamic acid (within 3 hours)
     ↓ If persistent
Intrauterine balloon tamponade (Bakri/Foley/Jada)
     ↓ If persistent
Interventional radiology: UAE
     ↓ If persistent / abdomen open
Surgical: B-Lynch suture → Uterine artery ligation
  → Internal iliac artery ligation → Hysterectomy

E-MOTIVE Bundle for Postpartum Haemorrhage

What is E-MOTIVE?

The Acronym - E-MOTIVE

Important distinction: The "E" at the start = Early detection. The "E" at the end = Escalation. The middle MOTIV letters are the first-response treatment bundle (the "MOTIVE bundle").

How E-MOTIVE Works - The Trigger System

Step 1: Objective Blood Loss Measurement

• Blood loss reaches 500 mL, OR
• Clinical signs of haemodynamic compromise appear (even at lower volumes)

Step 2: Simultaneous Bundle Administration

Key Principle: Bundle vs. Sequential Approach

The Landmark E-MOTIVE Trial (Gallos et al., NEJM 2023)

Results

WHO Recommendation (December 2023)

1. Use a calibrated drape for objective blood loss measurement after vaginal delivery to detect PPH early.
2. Use the MOTIVE treatment bundle for all women diagnosed with PPH - all components to be administered as soon as possible, ideally within 15 minutes of PPH diagnosis.

Implementation Strategies Used in the Trial

• Simulation-based training of all healthcare workers
• PPH trolleys and carry cases - having all medications and equipment pre-stocked and immediately accessible at the bedside
• Change champions within each facility
• Audit and feedback mechanisms
• Clinical protocols enabling midwives to initiate all bundle components independently (without waiting for a doctor)

Practical Notes on TXA in E-MOTIVE

• Dose: 1g IV over 10 minutes
• Can be repeated once after 30 minutes if bleeding continues
• Only effective if given within 3 hours of birth - do not give if >3 hours since delivery
• TXA is used as treatment, not prevention (in this bundle context)
• Very safe - no significant overdose risk at recommended doses

E-MOTIVE and Escalation (When Bundle is Not Enough)

1. Bimanual uterine compression (manual physical tamponade)
2. Uterine balloon tamponade (Bakri balloon, Foley catheter, Jada system)
3. Non-pneumatic Anti-Shock Garment (NASG) - especially in low-resource settings
4. Interventional radiology: Uterine artery embolisation
5. Surgical: B-Lynch suture, uterine/internal iliac artery ligation, peripartum hysterectomy

Summary

PPH Detected (objective drape measurement ≥500 mL or clinical signs)
                         ↓
         ┌───── MOTIVE Bundle (ALL within 15 min) ─────┐
         M - Massage (bimanual uterine massage)
         O - Oxytocic drugs (oxytocin ± others)
         T - Tranexamic acid 1g IV (within 3 hrs of birth)
         I - IV crystalloid fluids
         V - Verify cause (4 Ts: Tone, Trauma, Tissue, Thrombin)
         E - Escalate if bundle fails
         └──────────────────────────────────────────────┘
                         ↓
         60% reduction in severe PPH + laparotomy + death
                (E-MOTIVE NEJM Trial, 2023)

DIC (Disseminated Intravascular Coagulation) in Labour / Obstetrics

Definition

1. The simultaneous generation of thrombin (clot-forming) and plasmin (clot-dissolving)
2. Consumption of coagulation factors, platelets, and inhibitors
3. Paradoxically: both diffuse bleeding AND microvascular thrombosis occurring at the same time

• Henry's Clinical Diagnosis & Management, p. 954
• Rosen's Emergency Medicine, p. 2003

The Fundamental Pathophysiology

Step-by-Step Abnormal Sequence in Obstetric DIC:

TRIGGER (obstetric cause)
        ↓
Massive release of Tissue Factor (TF) / Thromboplastin into circulation
        ↓
Activation of extrinsic coagulation pathway (TF + Factor VIIa)
        ↓
Uncontrolled Thrombin generation
        ↓
Thrombin overwhelms its inhibitors (antithrombin III, protein C, TFPI)
        ↓
   ┌─────────────────────────────────┐
   │                                 │
Fibrin deposition in             Consumption of:
microvasculature                  - Platelets
(→ organ ischaemia:              - Fibrinogen
  renal, brain, lung,             - Factors V, VIII, XIII
  adrenals, liver)               - Protein C, antithrombin III
   │                                 │
   └──────── → Fibrinolysis activated (plasmin formed)
                      ↓
              Fibrin degradation products (FDPs) / D-dimers released
                      ↓
   FDPs inhibit platelet function + inhibit fibrin polymerisation
                      ↓
          UNCONTROLLED DIFFUSE HAEMORRHAGE

• Rosen's Emergency Medicine, p. 210-215
• Henry's Clinical Diagnosis, p. 385

Obstetric Causes of DIC (Triggers in Labour/Delivery)

1. Placental Abruption (Most Common Obstetric Cause)

• The injured placenta releases thromboplastin into the maternal circulation, triggering the coagulation cascade
• The damaged uterus releases plasminogen activator, triggering fibrinolysis simultaneously
• Severity of DIC is directly proportional to the degree of placental separation
• Severe clotting disorders rarely occur unless separation is large enough to cause fetal demise
• DIC is haemorrhagic in type (bleeding predominates)
• Rosen's Emergency Medicine, p. 3406

2. Amniotic Fluid Embolism (AFE)

• Amniotic fluid contains powerful procoagulants: activated coagulation factors II, VII, X, and tissue factor
• Entry of amniotic fluid into maternal circulation triggers immediate, massive DIC
• One of the most catastrophic and rapidly fatal obstetric emergencies
• Presents with sudden cardiovascular collapse + DIC + acute respiratory distress
• Robbins Pathology, p. 553

3. Retained Dead Fetus / Intrauterine Fetal Demise (IUFD)

• Dead fetal tissue contains excess thromboplastin which is gradually released
• Unlike other causes, this is associated with a prothrombotic (not haemorrhagic) form of DIC - i.e., microthrombosis predominates over bleeding
• Develops slowly over days to weeks if dead fetus is retained
• Henry's Clinical Diagnosis, p. 387

4. Pre-eclampsia / Eclampsia

• Endothelial damage activates coagulation
• HELLP syndrome (Haemolysis, Elevated Liver enzymes, Low Platelets) can coexist and overlap with DIC
• Can trigger haemorrhagic DIC
• Rosen's Emergency Medicine, p. 3022

5. Postpartum Haemorrhage (PPH) - Secondary DIC

• Massive blood loss and aggressive volume resuscitation → dilutional coagulopathy (depletion of clotting factors by dilution)
• Contributes to and worsens a DIC-like consumptive picture
• The DIC further worsens PPH - a vicious cycle

6. Sepsis / Chorioamnionitis / Postpartum Infection

• Gram-negative (and gram-positive) organisms activate the coagulation cascade via endotoxin/exotoxin-mediated TF expression
• Septic abortion is a classic cause

7. Retained Products of Conception (RPOC)

• Retained placental tissue and decidua contain thromboplastin - gradual release triggers DIC

8. Uterine Rupture

• Massive haemorrhage and tissue factor release trigger consumptive coagulopathy

Summary Table

Clinical Features of DIC in Labour

Bleeding Manifestations (when haemorrhagic component dominates)

• Persistent oozing from IV sites, venepuncture sites, and wounds
• Uncontrolled vaginal/uterine haemorrhage not responding to uterotonics
• Petechiae, purpura, ecchymoses (spontaneous bruising)
• Haematuria, haemoptysis, GI bleeding
• Bleeding from episiotomy/laceration repair sites
• Oozing from caesarean section wound

Thrombotic/Ischaemia Manifestations (when thrombotic component dominates)

• Acute Kidney Injury (AKI): oliguria/anuria from renal cortical necrosis - most common organ affected
• Neurological: confusion, seizures (CNS microvascular thrombosis)
• Respiratory: ARDS (pulmonary microvascular fibrin deposition)
• Skin necrosis: acral ischaemia, purpura fulminans
• Adrenal haemorrhage: Waterhouse-Friderichsen syndrome
• Sheehan syndrome: pituitary infarction (contributes postpartum)

Signs

• Tachycardia, hypotension (haemorrhagic shock)
• Soft/boggy uterus if atony coexists
• Petechiae and purpura on skin
• Jaundice (haemolysis from microangiopathic haemolytic anaemia - MAHA)

Diagnosis - Laboratory Tests

Key Tests and Findings in DIC

Key point: In obstetric DIC, fibrinogen is the most sensitive early marker. In normal pregnancy, fibrinogen is elevated (400-600 mg/dL). A "normal" fibrinogen of 200 mg/dL in a pregnant woman may already represent significant consumption. A level <150 mg/dL signals overt DIC; <100 mg/dL is critical.

ISTH Scoring System for Overt DIC

• Henry's Clinical Diagnosis & Management, p. 363-375

Management of Obstetric DIC

The Golden Principle: Treat the Underlying Cause FIRST

• Placental abruption → Deliver the baby and placenta promptly
• Retained dead fetus → Expedite delivery/evacuation
• Sepsis → Antibiotics and source control
• PPH → Control haemorrhage (uterotonics, surgical, etc.)
• Eclampsia → Deliver, manage BP, magnesium sulphate

Resuscitation - Simultaneous with Treating the Cause

• Two large-bore IV lines
• Blood and blood products ordered EARLY
• Activate Massive Transfusion Protocol (MTP) promptly
• Oxygen, urinary catheter (monitor renal output)

Key point: Give cryoprecipitate / fibrinogen concentrate EARLY in obstetric DIC. Fibrinogen depletes fastest and is the rate-limiting factor in haemostasis. Do not wait for all labs to return before starting.

• 1g IV over 10 minutes
• Antifibrinolytic - inhibits plasmin, reduces fibrin degradation
• Reduces death from bleeding in PPH (WOMAN trial)
• Use within 3 hours of delivery/PPH onset

• TEG (Thromboelastography) or ROTEM (Rotational Thromboelastometry)
• Allows rapid, targeted assessment of which component of the coagulation process is failing
• Guides specific product replacement rather than "blind" empirical transfusion
• Reduces unnecessary transfusion and improves outcomes

• Heparin is occasionally used when thrombosis predominates (e.g., retained dead fetus with prothrombotic DIC and evidence of venous thromboembolism)
• Generally avoided in obstetric DIC where haemorrhage is the primary problem
• Only considered when thrombotic manifestations clearly outweigh bleeding

• Reserved for life-threatening haemorrhage refractory to all other measures
• Not universally recommended - multiple adverse events (arterial thromboembolism) reported
• Off-label use; considered a last resort before/alongside hysterectomy

DIC in the Context of Each Major Obstetric Trigger

Placental Abruption + DIC

• DIC severity correlates with degree of separation
• If fetal demise = severe DIC virtually certain
• Deliver promptly; vaginal delivery preferred if safe (avoids surgery on coagulopathic patient)
• Correct coagulopathy simultaneously

Amniotic Fluid Embolism + DIC

• Sudden cardiovascular collapse → DIC → haemorrhage
• Management: aggressive resuscitation, intubation/ventilation, ECMO in severe cases, treat DIC with FFP + platelets + cryoprecipitate
• Mortality remains very high (25-50%)

PPH + DIC (The Vicious Cycle)

PPH → Loss of clotting factors → DIC
DIC → More bleeding → Worse PPH
                ↑___________|

Complications of Untreated/Inadequately Treated DIC

• Acute Kidney Injury / Renal cortical necrosis - permanent renal failure
• ARDS - from pulmonary fibrin microemboli
• Multi-organ failure - liver, CNS, adrenals
• Sheehan's syndrome - anterior pituitary infarction from hypotension
• Maternal death - DIC in haemorrhaging patients with placental implantation abnormalities is the highest-risk scenario for maternal mortality
• Waterhouse-Friderichsen syndrome - adrenal haemorrhage in sepsis-related DIC

Summary Diagram

OBSTETRIC TRIGGER
(Abruption / AFE / Retained dead fetus / Sepsis / PPH / Pre-eclampsia)
                    ↓
        Massive Tissue Factor release
                    ↓
    Uncontrolled Thrombin generation
         ↙                    ↘
Fibrin microthrombi       Consumption of Factors,
in organs                 Fibrinogen, Platelets
(Ischaemia: kidney,              ↓
 brain, lungs)          Fibrinolytic activation
                                 ↓
                        FDPs/D-dimers released
                         ↓              ↓
                   Inhibit platelets  Inhibit fibrin
                         ↓
               UNCONTROLLED HAEMORRHAGE

MANAGEMENT:
1. Treat trigger (deliver/evacuate/antibiotics)
2. FFP + Cryoprecipitate (fibrinogen) + Platelets + pRBCs
3. Tranexamic acid (within 3 hrs)
4. TEG/ROTEM-guided therapy
5. Consider heparin only if thrombosis >> bleeding