Primary Postpartum Haemorrhage (PPH)

1. Clinical Overview

Summary

Primary postpartum haemorrhage (PPH) is defined as blood loss of ≥500ml following vaginal delivery or ≥1000ml following caesarean section within the first 24 hours after birth. [1] It represents one of the leading causes of maternal mortality worldwide, accounting for approximately 27% of maternal deaths globally and 13% in developed countries. [2] Despite advances in obstetric care, the incidence of PPH has been rising in high-income countries, attributed to increased maternal age, obesity, caesarean section rates, and multiple pregnancy. [3]

The placental bed receives 500-800ml of blood per minute at term, making haemorrhage potentially catastrophic if not controlled rapidly. [4] The physiological mechanism of haemostasis relies on myometrial contraction compressing the spiral arterioles—described classically as "living ligatures". Failure of this mechanism, most commonly due to uterine atony, accounts for 70-80% of cases. [5]

Management requires immediate recognition, structured multidisciplinary response, and escalation through mechanical, pharmacological, and surgical interventions. The introduction of tranexamic acid following the WOMAN trial has reduced death from bleeding by approximately 30% when administered within 3 hours. [6] Modern protocols emphasize early activation of massive haemorrhage protocols, use of viscoelastic haemostatic assays, and goal-directed transfusion strategies.

Key Facts

Classification by Severity:

• Minor PPH: 500-1000ml blood loss
• Major PPH: > 1000ml or ongoing bleeding with clinical signs of shock
• Massive PPH: > 2000ml or requiring ≥4 units packed red cells [1]

The 4 T's Mnemonic (Aetiology):

1. Tone (70-80%): Uterine atony—failure of myometrial contraction
2. Trauma (19%): Genital tract lacerations, uterine rupture, uterine inversion
3. Tissue (10%): Retained placenta, retained placental fragments, invasive placentation
4. Thrombin (1%): Coagulopathy—inherited or acquired bleeding disorders [5,7]

Physiological Compensation: Young healthy pregnant women have remarkable cardiovascular reserve due to pregnancy-induced hypervolaemia (40-50% increase in blood volume). Vital signs may remain deceptively normal until 30-40% blood volume is lost, after which decompensation can be rapid and catastrophic. [8] The shock index (heart rate/systolic BP) is more sensitive than individual vital signs, with values > 0.9 indicating significant haemorrhage. [9]

Clinical Pearls

The "Rub-Up" Test: Immediate fundal massage is both diagnostic and therapeutic. A soft, boggy uterus indicates atony; vigorous bimanual massage stimulates contraction. If the fundus is firm but bleeding continues, the cause is trauma (lacerations) or tissue (retained products).

Empty the Bladder: A distended bladder displaces the uterus superiorly and laterally, preventing effective contraction. Urinary catheterization is mandatory in all cases of PPH. [10]

Clot Evacuation: A uterus filled with blood clots cannot contract effectively. Manual removal of clots from the uterine cavity (with appropriate analgesia) is essential to restore tone.

Concealed Bleeding: Not all bleeding is visible. Broad ligament haematomas, intraperitoneal bleeding from uterine rupture, and large retroperitoneal collections may cause haemodynamic instability without obvious external blood loss. Maintain high index of suspicion.

The "Golden Hour": Mortality increases exponentially with delays in definitive management. The interval from recognition to surgical intervention (if required) should be minimized. Early involvement of senior staff is crucial.

---

2. Epidemiology

Global Burden

PPH affects approximately 5-15% of all deliveries, with significant geographic variation. [2,11] The global incidence has been increasing progressively over the past two decades:

• United Kingdom: 5.9% (2000) → 9.8% (2018) [3]
• United States: 2.3% (1994) → 3.0% (2014) [12]
• Australia: Similar upward trend, particularly severe PPH requiring transfusion [13]

Mortality and Morbidity

Maternal Mortality:

• Worldwide: ~70,000 deaths annually from PPH [2]
• Case fatality rate: 1% in high-resource settings, 3-5% in low-resource settings [14]
• Time-critical: 50% of deaths occur within 4 hours of delivery [15]

Severe Morbidity:

• Hysterectomy: 0.4-1.4 per 1000 deliveries [16]
• Blood transfusion: Required in 2-3% of PPH cases [17]
• Intensive care admission: 0.2-0.5% of deliveries [18]
• Sheehan's syndrome: Rare in modern practice (less than 1% severe PPH) due to earlier intervention [19]

Risk Factors

Strong Risk Factors (Odds Ratio > 5): [20,21]

• Previous PPH (most significant predictor—OR 9.0)
• Placenta praevia (OR 12.6)
• Placental abruption (OR 13.8)
• Multiple pregnancy (OR 4.8)
• Pre-eclampsia/eclampsia (OR 5.2)

Moderate Risk Factors (OR 2-5):

• Obesity (BMI > 35 kg/m²)
• Maternal age > 40 years
• Grand multiparity (≥4 previous deliveries)
• Prolonged labour (> 12 hours)
• Instrumental delivery
• Large fetus (> 4000g)
• Polyhydramnios

Intrapartum Risk Factors:

• Induction of labour (OR 1.4)
• Augmentation with oxytocin (OR 1.8)
• Caesarean section (OR 3.7 compared to spontaneous vaginal delivery) [22]
• Emergency caesarean section in labour (highest risk)
• Magnesium sulphate infusion (inhibits myometrial contraction)
• General anaesthesia (volatile agents cause uterine relaxation)

Limitation of Risk Prediction: Approximately 40% of women experiencing PPH have no identifiable risk factors. [23] Therefore, all maternity units must have protocols applicable to any delivery, not merely "high-risk" cases.

---

3. Pathophysiology

Normal Third Stage Haemostasis

The placental site at term comprises 60-80 spiral arterioles with a combined blood flow of 500-800ml/min. [4] Following placental separation, haemostasis depends on:

1. Myometrial Contraction: Interlacing oblique muscle fibres of the myometrium contract, compressing spiral arterioles—the "physiological suture" or "living ligatures" described by Bonney (1946). [24]

2. Thrombosis: Platelet plug formation and coagulation cascade activation at vessel stumps.

3. Vascular Retraction: Elastic recoil of vessel walls.

Normal blood loss during vaginal delivery averages 300-500ml (measured using drapes or volumetric methods). [25] The traditional visual estimation underestimates blood loss by 30-50%. [26]

Pathological Mechanisms

1. Tone: Uterine Atony (70-80% of cases)

Mechanism: Failure of sustained myometrial contraction leads to persistent perfusion of the placental bed. The uterus feels soft, "boggy," and poorly contracted on palpation. [5]

Predisposing Factors:

• Overdistension: Multiple pregnancy, polyhydramnios, macrosomia (> 4kg)—stretches myometrial fibres beyond optimal length-tension relationship
• Exhaustion: Prolonged labour (> 12h), oxytocin augmentation—muscle fatigue
• Anatomical: Fibroids (distort muscle architecture), uterine malformations
• Pharmacological: Volatile anaesthetic agents (halothane, sevoflurane), magnesium sulphate, nifedipine, terbutaline—all cause smooth muscle relaxation
• Infection: Chorioamnionitis impairs contractility [27]

Cellular Level: Myometrial contraction requires calcium influx and actin-myosin interaction. Atony may result from receptor desensitization (prolonged oxytocin exposure), impaired calcium signaling, or ATP depletion in exhausted muscle. [28]

2. Trauma (19% of cases)

Genital Tract Lacerations:

• First/second-degree perineal tears: Common, usually self-limiting
• Third/fourth-degree tears: Extend to anal sphincter/mucosa—require immediate surgical repair under regional/general anaesthesia
• Cervical lacerations: Often anterolateral, may extend into lower segment; occur with precipitate delivery, instrumental rotation
• Vaginal sidewall tears: High tears near fornices can involve uterine artery branches—causing brisk arterial bleeding despite firm uterus

Uterine Rupture: Incidence: 0.3% after previous caesarean section; rare in unscarred uterus. [29] Presentation: Sudden severe pain (if epidural inadequate), maternal collapse, loss of fetal station, palpable fetal parts abdominally, abnormal CTG. Consequences: Massive intraperitoneal haemorrhage, fetal hypoxia/death.

Uterine Inversion: Incidence: 1 in 2000-3000 deliveries. [30] Mechanism: Excessive fundal pressure with undue cord traction before placental separation. Recognition: Sudden severe pain, shock, absence of palpable fundus, visible mass at introitus. Critical: Do NOT attempt to remove adherent placenta—this exacerbates bleeding and shock.

3. Tissue (10% of cases)

Retained Placenta: Defined as failure of placental expulsion within 30 minutes of delivery (with active management) or 60 minutes (physiological management). [31] Incidence: 2-3% of vaginal deliveries.

Subtypes:

• Adherent placenta: Failed separation, often due to atonic uterus
• Trapped placenta: Separated but retained by closed cervix (constriction ring)
• Morbidly adherent placenta (MAP): Placenta accreta spectrum disorders

Placenta Accreta Spectrum:

• Accreta: Villi attach to myometrium (absence of decidua basalis)
• Increta: Villi invade myometrium
• Percreta: Villi penetrate serosa ± adjacent organs (bladder most common)

Risk factors: Previous caesarean section + placenta praevia (risk up to 67% with ≥4 prior CS). [32] Management: Requires multidisciplinary planning, often necessitates hysterectomy.

Retained Products: Incomplete placental separation or missing cotyledons/succenturiate lobe lead to impaired uterine contraction. Systematic inspection of expelled placenta is mandatory.

4. Thrombin (1% of cases)

Pre-existing Coagulopathies:

• Von Willebrand disease (most common inherited disorder)
• Haemophilia A/B carriers (if factor levels less than 30%)
• Thrombocytopenia (ITP, gestational thrombocytopenia)
• Acquired platelet dysfunction (antiplatelet agents)

Acquired Coagulopathies:

• DIC: Triggered by placental abruption, amniotic fluid embolism, sepsis, intrauterine fetal death
• Dilutional coagulopathy: Massive crystalloid resuscitation
• Consumptive coagulopathy: Ongoing haemorrhage—fibrinogen falls first (critical threshold less than 2g/L) [33]
• HELLP syndrome: Haemolysis, elevated liver enzymes, low platelets

Fibrinogen as Early Predictor: Fibrinogen less than 2g/L at PPH onset predicts progression to severe PPH (sensitivity 100%, specificity 69%). [34] Normal pregnancy increases fibrinogen to 4-6g/L; levels less than 3g/L are abnormal postpartum.

---

4. Clinical Presentation

Symptoms

Patient Reports:

• Sensation of "gushing" or continuous trickling of blood
• Feeling faint, dizzy, or light-headed
• Palpitations, shortness of breath
• Anxiety, sense of impending doom (severe cases)
• Lower abdominal pain (uterine atony causes cramping; rupture causes sudden severe pain)

Delayed Recognition: Gradual bleeding may accumulate in bed linen, under patient, or in collection bags without immediate detection. Clinical deterioration may precede recognition of visible blood loss.

Signs

Cardiovascular:

• Tachycardia: Earliest sign—heart rate > 100 bpm indicates ≥15% blood loss [35]
• Hypotension: Late sign—BP maintained until 30-40% loss in young healthy women
• Shock index > 0.9: More sensitive than individual vital signs [9]
• Narrow pulse pressure: Indicates vasoconstriction (compensatory)
• Cold peripheries, prolonged capillary refill time (> 2 seconds)

Uterine Assessment:

• Atony: Fundus palpable above umbilicus, soft, poorly defined, "boggy" consistency
• Normal tone with ongoing bleeding: Suggests trauma or retained tissue
• Absent fundus: Consider uterine inversion

General:

• Pallor (conjunctival, palmar)
• Confusion, agitation (cerebral hypoperfusion)
• Reduced urine output (less than 30ml/h)
• Breathlessness (metabolic acidosis, anaemia)

Specific to Cause:

• Visible lacerations: Bleeding from perineum despite firm uterus
• Inversion: Visible/palpable uterine mass at introitus, severe shock
• Rupture: Sudden deterioration, loss of fetal heart, abdominal distension

Clinical Staging by Blood Loss

Class I (15% loss, less than 750ml):

• Mild tachycardia
• Normal BP, capillary refill
• Minimal symptoms

Class II (15-30%, 750-1500ml):

• Tachycardia 100-120 bpm
• Normal or slightly low BP
• Tachypnoea, anxiety
• Urine output 20-30ml/h

Class III (30-40%, 1500-2000ml):

• Tachycardia > 120 bpm
• Hypotension (SBP less than 90mmHg)
• Marked tachypnoea, confusion
• Urine output less than 20ml/h

Class IV (> 40%, > 2000ml):

• Severe tachycardia (> 140 bpm) or bradycardia (pre-terminal)
• Severe hypotension (SBP less than 70mmHg)
• Reduced consciousness, anuria
• Imminent cardiac arrest [35]

---

5. Clinical Examination

Systematic Approach

General Inspection:

• Patient appearance: colour, conscious level, distress
• Obvious bleeding: rate, volume, presence of clots
• Monitoring: continuous pulse oximetry, automated BP (5-minute intervals)

Abdominal Examination:

1. Fundal palpation: Height (should be at umbilicus immediately postpartum) and tone
2. Massage: Vigorous bimanual uterine massage if atonic—may expel clots and stimulate contraction
3. Clot evacuation: Express clots using suprapubic pressure (ensure bladder catheterized)
4. Inspection for distension: Intraperitoneal bleeding causes progressive abdominal distension

Perineal/Vaginal Examination:

1. Adequate lighting: Use Anglepoise lamp, headlight, or operating light
2. Systematic inspection:
   • Perineum: Degree of tear (1st through 4th)
   • Labia: Haematomas (can be large and concealed)
   • Vaginal walls: Systematic inspection with Sims' speculum, rotating to visualize all quadrants
   • Cervix: Requires ring forceps for visualization—check entire circumference for lacerations
3. High tears: May require examination under anaesthesia (EUA) in theatre

Placental Examination:

• Lay placenta flat, maternal side up
• Count cotyledons—note missing areas (ragged membranes suggest retained portion)
• Examine membranes for vessels running to edge (indicates succenturiate lobe)
• Photograph if abnormal (medico-legal documentation)

Uterine Inversion:

• Incomplete: Fundus palpable as depression, not fully inverted
• Complete: Fundus protrudes through cervix into vagina
• Total: Entire uterus and vagina inverted
• Recognition: Absence of palpable fundus abdominally + shock + visible/palpable mass vaginally

---

6. Investigations

Immediate Bedside Tests

Blood Loss Quantification:

• Graduated under-buttock drapes: More accurate than visual estimation [26]
• Weigh swabs and pads: 1g weight = 1ml blood (subtract dry weight)
• Suction canister measurement: Record volume (subtract amniotic fluid if measured)
• Visual estimation: Least accurate—typically underestimates by 30-50% [26]

Vital Signs Monitoring:

• Continuous pulse oximetry
• Automated BP every 5 minutes (or continuous arterial line if massive haemorrhage)
• Shock index calculation: HR/SBP (normal less than 0.7; > 0.9 indicates significant haemorrhage) [9]
• Hourly urine output via indwelling catheter (target ≥30ml/h)

Point-of-Care Haemoglobin:

• HemoCue or blood gas analyser
• Provides immediate Hb value (venous sample acceptable)
• Useful for trending, but may not reflect acute loss (haemodilution takes time)

Laboratory Investigations

Immediate (Stat) Panel:

1. Full Blood Count (FBC):

   • Baseline haemoglobin (may be normal acutely)
   • Platelet count (normal pregnancy: 150-400 × 10⁹/L)
   • Note: Acute Hb may not reflect loss if haemodilution incomplete

2. Coagulation Screen:

   • Prothrombin time (PT)
   • Activated partial thromboplastin time (APTT)
   • Fibrinogen (Clauss method): Most critical—normal postpartum 4-6g/L; less than 2g/L predicts severe PPH [34]
   • D-dimer: Elevated in DIC (though also elevated in normal pregnancy)

3. Group and Save → Crossmatch 4-6 Units:

   • Immediate crossmatch if major PPH (> 1000ml)
   • Request O-negative blood if urgent transfusion required before crossmatch complete

4. Urea and Electrolytes (U&E):

   • Baseline renal function
   • Potassium (monitor with transfusion—citrate toxicity risk)
   • Lactate (surrogate for tissue perfusion and acidosis)

5. Blood Gas Analysis:

   • pH, base excess (metabolic acidosis indicates poor perfusion)
   • Lactate > 4 mmol/L indicates shock
   • Ionized calcium (falls with massive transfusion—citrate binding)

Viscoelastic Haemostatic Assays (VHA):

• ROTEM® or TEG®: Real-time assessment of clot formation and fibrinolysis
• Advantages: Results in 10-15 minutes; guides component therapy (fibrinogen, platelets, tranexamic acid)
• Increasingly used in obstetric haemorrhage protocols [36]

Imaging

Ultrasound (Bedside):

• Transabdominal: Assess uterine cavity for retained products
• Transvaginal: Better visualization of endometrial cavity, cervical canal
• FAST scan (Focused Assessment with Sonography for Trauma): If uterine rupture suspected—look for free intraperitoneal fluid

CT Angiography:

• Gold standard for identifying source of ongoing bleeding
• Can guide interventional radiology (uterine artery embolization)
• Only appropriate once patient stabilized

MRI:

• No role in acute PPH (too slow)
• Used antenatally to map placenta accreta spectrum

---

7. Management

Principles of Care

1. Early recognition and escalation
2. Multidisciplinary team activation (obstetrician, midwife, anaesthetist, haematologist, porter)
3. Simultaneous resuscitation and definitive treatment
4. Systematic approach using algorithms (minimizes omissions under stress)
5. Clear communication and documentation (SBAR tool, dedicated scribe)
6. Stepwise escalation from mechanical → pharmacological → surgical interventions

Initial Response (less than 5 minutes)

Call for Help:

• Activate emergency buzzer (summons immediate assistance)
• State "Major obstetric haemorrhage" (activates protocol)
• Request:
  • Senior obstetrician (consultant)
  • Senior midwife
  • Anaesthetist (consultant if > 1500ml)
  • Haematologist (if > 2000ml or coagulopathy)
  • Theatre team (scrub nurse, ODP)
  • Porter (for blood collection)

Immediate Actions (ABCDE Approach):

A—Airway:

• Ensure patent airway
• High-flow oxygen 15L via non-rebreather mask (target SpO₂ > 95%)

B—Breathing:

• Assess respiratory rate, work of breathing
• Monitor SpO₂ continuously

C—Circulation:

1. Venous access: Insert 2 × large-bore cannulae (14G or 16G, grey or orange)
2. Bloods: FBC, coagulation including fibrinogen, crossmatch 4-6 units, U&E, blood gas
3. Fluid resuscitation:
   • Rapid infusion warmed crystalloid (Hartmann's or 0.9% saline) 1-2L stat
   • Avoid over-resuscitation (target SBP 80-90mmHg until bleeding controlled—permissive hypotension) [37]
4. Monitoring: Automated BP every 5 minutes, continuous pulse oximetry, urinary catheter (hourly output)

D—Disability:

• Assess conscious level (AVPU or GCS)
• Hypoglycaemia check if reduced consciousness

E—Exposure:

• Quantify blood loss (weigh pads, measure in drape)
• Examine for source (see examination section)
• Keep patient warm (prevent hypothermia—use Bair Hugger)

Mechanical Interventions

1. Uterine Massage and Bimanual Compression

Uterine Massage:

• Place one hand on abdomen, locate fundus
• Perform firm, repetitive circular massage ("rubbing up the fundus")
• Continue until uterus contracts and feels firm
• Expel clots using suprapubic pressure once contracted

Bimanual Compression: [10]

• Indications: Persistent atony despite massage and uterotonics
• Technique:
  1. Insert one hand vaginally, form fist, place in anterior vaginal fornix
  2. Place other hand abdominally, posterior to uterine fundus
  3. Compress uterus firmly between both hands
  4. Maintain compression continuously until help arrives or bleeding controlled
• Effectiveness: Can completely arrest bleeding from atonic uterus; buys time for pharmacological measures

2. Catheterization

Rationale: A full bladder displaces the uterus, prevents effective contraction, and may obstruct venous return.

Technique:

• Insert 14F or 16F Foley catheter with aseptic technique
• Immediate drainage often yields 500-1000ml urine
• Leave on continuous drainage (monitor hourly output as resuscitation endpoint)

3. Aortic Compression

Indications: Temporizing measure in extremis (cardiac arrest, imminent exsanguination)

Technique:

• Locate abdominal aorta: just left of midline, above umbilicus
• Apply firm downward pressure with closed fist
• Compress aorta against vertebral column
• Reduces pelvic blood flow by ~70% [38]
• Maintain until definitive intervention (transfer to theatre, embolization)

Pharmacological Management

General Principle: Stepwise escalation through uterotonics. No single agent is universally effective; combination therapy often required. [39]

1. Oxytocin (First-Line)

Mechanism: Binds myometrial oxytocin receptors → G-protein coupled calcium influx → muscle contraction.

Dosing: [1]

• Slow IV bolus: 5 IU over 1-2 minutes (rapid bolus causes hypotension, tachycardia)
• Infusion: 40 IU in 500ml crystalloid at 125ml/h (10 IU/h)
• Maximum: 3L total volume (120 IU total dose)

Onset: 2-3 minutes Duration: 15-30 minutes (requires continuous infusion)

Side Effects:

• Hypotension (with rapid bolus)
• Tachycardia
• Water intoxication/hyponatraemia (antidiuretic effect if large volumes given)
• Rarely: myocardial ischaemia (coronary vasospasm)

Contraindications: None in emergency setting.

Efficacy: Reduces PPH risk by 60% as prophylaxis (active management third stage). [40] Effectiveness as treatment depends on receptor status (prior oxytocin augmentation may cause desensitization).

2. Ergometrine (Second-Line)

Mechanism: Ergot alkaloid—α-adrenergic agonist and serotonin receptor agonist → sustained tetanic uterine contraction.

Dosing: [1]

• IM or slow IV: 500 micrograms (0.5mg)
• Single dose (do not repeat—long half-life ~2 hours)

Onset: 2-5 minutes (IV), 7-10 minutes (IM) Duration: 2-4 hours (longest-acting uterotonic)

Side Effects:

• Hypertension (potentially severe—risk of stroke, pulmonary oedema)
• Nausea and vomiting (90% of patients)
• Headache
• Coronary vasospasm

Contraindications:

• Pre-eclampsia/eclampsia (absolute—risk of hypertensive crisis)
• Hypertension (BP > 140/90 mmHg)
• Ischaemic heart disease
• Peripheral vascular disease
• Raynaud's phenomenon

Exam Alert: Classic question—"Patient with pre-eclampsia has PPH, which uterotonic is contraindicated?" Answer: Ergometrine.

3. Carboprost (Prostaglandin F2α) (Second/Third-Line)

Mechanism: Prostaglandin analogue → myometrial contraction and vasoconstriction.

Dosing: [1]

• Deep IM injection: 250 micrograms
• Repeat: Every 15 minutes as needed
• Maximum: 8 doses (2mg total)
• Route: IM only (IV bolus causes severe bronchospasm; intramyometrial injection described but not licensed)

Onset: 5-15 minutes Duration: 1-2 hours

Side Effects:

• Bronchospasm (potentially severe)
• Diarrhoea (prostaglandin effect on GI smooth muscle)
• Pyrexia, shivering
• Hypertension (mild)
• Oxygen desaturation

Contraindications:

• Asthma (absolute contraindication—risk of severe bronchospasm, status asthmaticus)
• Active cardiac, renal, or hepatic disease

Efficacy: 87% success rate in resolving atonic PPH refractory to oxytocin/ergometrine. [41]

Exam Alert: "Patient with asthma has PPH, which drug to avoid?" Answer: Carboprost.

4. Misoprostol (Third-Line)

Mechanism: Prostaglandin E1 analogue → myometrial contraction.

Dosing: [42]

• Rectal: 800-1000 micrograms (preferred in shocked patient—sublingual absorption impaired)
• Sublingual: 800 micrograms (if not shocked)
• Buccal: 800 micrograms
• Single dose (due to long half-life and side effects)

Onset: 10-20 minutes (slower than other agents) Duration: Variable (several hours)

Side Effects:

• Pyrexia (common—shivering in 50%)
• Diarrhoea
• Nausea
• Headache

Contraindications: None in emergency setting.

Efficacy: Cochrane review shows effectiveness for treatment of PPH (NNT ~18 to avoid blood transfusion). [43] Less potent than carboprost, but safer side-effect profile. Particularly valuable in low-resource settings (stable at room temperature, cheap).

Guideline Position: WHO recommends 800mcg sublingual misoprostol where injectable uterotonics unavailable. [44] In high-resource settings, used as adjunct when other agents fail or contraindicated.

5. Tranexamic Acid (Antifibrinolytic)

Mechanism: Lysine analogue—competitively inhibits plasminogen activation → prevents fibrin degradation → stabilizes clot.

Dosing: [6]

• IV loading dose: 1g over 10 minutes
• Maintenance infusion: 1g over 6 hours (if ongoing bleeding)
• Maximum effect: If given within 3 hours of delivery

Onset: 10-15 minutes Duration: 3 hours

Side Effects:

• Nausea (mild)
• Theoretical thrombosis risk (not demonstrated in WOMAN trial)

Contraindications:

• Active thromboembolic disease (relative—weigh benefit vs risk in life-threatening haemorrhage)
• Seizure disorder (controversial—high doses potentially epileptogenic)

Evidence—WOMAN Trial (2017): [6] Landmark RCT: 20,060 women with PPH randomized to tranexamic acid vs placebo.

• Primary outcome: Death from bleeding reduced by 19% (RR 0.81, 95% CI 0.65-1.00)
• Early administration (less than 3h): 31% reduction in death from bleeding (RR 0.69, 95% CI 0.52-0.91)
• Late administration (> 3h): No benefit
• Safety: No increase in thrombosis, stroke, or other adverse events

Impact: Tranexamic acid now standard of care in PPH. [1] Should be administered early in major PPH (> 1000ml) or when bleeding continues despite initial uterotonics.

Cost-Effectiveness: Highly cost-effective (estimated £65 per QALY gained in UK). [45]

Massive Transfusion Protocol

Activation Criteria: [46]

• Ongoing blood loss > 1500ml
• Bleeding > 150ml/min
• Clinical signs of shock despite initial resuscitation
• Anticipated need for ≥4 units PRBC within 1 hour

Principles:

1. Early activation: Don't wait for laboratory confirmation
2. Balanced resuscitation: RBC : FFP : Platelets in 1:1:1 ratio [47]
3. Goal-directed therapy: Use VHA (ROTEM/TEG) or laboratory coagulation to guide component replacement
4. Damage control resuscitation: Avoid hypothermia, acidosis, coagulopathy ("lethal triad")

Component Therapy:

Packed Red Blood Cells (PRBC):

• Target Hb: 70-80 g/L (restrictive strategy reduces complications) [48]
• Warm blood: Use rapid infuser with warming capacity
• Type: O-negative if emergency (universal donor); switch to type-specific when available

Fresh Frozen Plasma (FFP):

• Indication: PT/APTT > 1.5× normal
• Dose: 12-15 ml/kg (typically 4 units)
• Contains: All coagulation factors
• Thaw time: 20-30 minutes (plan ahead)

Cryoprecipitate:

• Indication: Fibrinogen less than 2 g/L (critical threshold) [34]
• Dose: 2 pools (10 units) raises fibrinogen by ~1 g/L
• Contains: Fibrinogen, factor VIII, vWF, factor XIII, fibronectin
• First-line for hypofibrinogenaemia in PPH

Platelets:

• Indication: Platelet count less than 50 × 10⁹/L
• Target: Maintain > 75 × 10⁹/L in ongoing bleeding [1]
• Dose: 1 adult therapeutic dose (pool of 4-5 units) raises count by ~30 × 10⁹/L

Fibrinogen Concentrate:

• Alternative to cryoprecipitate (where available)
• Dose: 3-4g IV
• Advantages: Rapid preparation (no thawing), viral inactivation, precise dosing
• Increasing evidence in obstetric haemorrhage [49]

Factor VIIa (Recombinant Activated Factor VII):

• Indication: Life-threatening haemorrhage refractory to all other measures
• Dose: 90 micrograms/kg IV bolus (off-label use)
• Mechanism: Enhances thrombin generation on activated platelet surfaces
• Preconditions: Correct acidosis (pH > 7.2), hypothermia (temp > 34°C), hypofibrinogenaemia (fibrinogen > 1 g/L), thrombocytopenia (platelets > 50)
• Evidence: Case series suggest benefit; no RCT in obstetrics [50]
• Risks: Thromboembolism (2-5%), expensive (~£5000/dose)

Cell Salvage:

• Intraoperative blood salvage (IOBS) systems collect, filter, wash shed blood, return autologous RBCs
• Indication: Caesarean section for placenta praevia/accreta, anticipated major haemorrhage
• Relative contraindication: Amniotic fluid contamination (theoretical risk of embolism—use leukocyte depletion filter)
• Evidence: Safe in obstetrics; reduces allogeneic transfusion [51]

Surgical Interventions

Indications for Theatre Transfer:

• Ongoing bleeding despite pharmacological measures
• Clinical suspicion of traumatic cause requiring repair
• Need for examination under anaesthesia (EUA)
• Intrauterine balloon insertion
• Surgical haemostasis procedures

Pre-Theatre Checklist:

• Senior obstetrician scrubbed
• Consultant anaesthetist
• Blood products available in theatre
• Consent discussed (if patient conscious and stable—otherwise proceed under emergency provisions)
• Inform theatre team of situation and likely interventions

1. Examination Under Anaesthesia (EUA) and Repair of Trauma

Indications:

• Ongoing bleeding with firm uterus (suggests trauma)
• High vaginal/cervical tears not visualizable on ward
• Need for adequate analgesia/muscle relaxation for examination

Technique:

• Regional anaesthesia (spinal/epidural top-up) preferred where possible (maintains uterine tone)
• General anaesthesia if massive haemorrhage, patient shocked, or extensive surgery anticipated
• Systematic examination:
  • "Cervix: Visualize with ring forceps, rotate through 360°"
  • "Vaginal walls: Retract with Sims' speculum, inspect all quadrants"
  • "Perineum: Classify degree of tear (1st-4th)"
• Repair: Absorbable sutures (2-0 Vicryl), secure haemostasis, anatomical reconstruction
• High tears: May extend into broad ligament—requires laparotomy to secure vessels

2. Intrauterine Balloon Tamponade

Mechanism: Hydrostatic pressure compresses uterine bleeding surfaces (particularly effective for diffuse placental bed oozing).

Devices:

• Bakri balloon: Purpose-designed for PPH; silicone balloon with central drainage channel (allows monitoring of ongoing bleeding)
  • "Capacity: 300-500ml"
  • "Inflation: Fill with warm saline using Luer-lock syringe under ultrasound guidance"
  • "Monitoring: Blood draining from central channel indicates ongoing bleeding"
• Condom catheter: Low-resource alternative—condom tied to catheter, filled with saline
• Sengstaken-Blakemore tube: Oesophageal balloon—used off-label

Technique: [52]

1. Ensure uterine cavity empty (no retained products/clots)
2. Insert balloon into uterine cavity (manually or with sponge forceps)
3. Inflate with 300-500ml warm saline (until bleeding stops—use minimum volume)
4. Vaginal pack or inflate balloon tip in vagina to prevent expulsion
5. Secure catheter to thigh
6. Monitor drainage through central channel
7. Continue oxytocin infusion
8. Antibiotics (co-amoxiclav 1.2g IV TDS)
9. Removal: Deflate incrementally after 12-24h; observe for recurrence

Success Rate: 85-95% in uterine atony refractory to medical management. [53]

Complications: Uterine perforation (rare), infection, ischaemic necrosis (prolonged inflation).

3. Uterine Compression Sutures

Indications: Persistent atonic bleeding despite balloon tamponade (or balloon unavailable), desire to preserve fertility.

B-Lynch Suture (Brace Suture): [54]

• Most widely used
• Technique: Vertical compression sutures around uterus ("braces"), using Vicryl No. 2 or chromic catgut
• Entry point: Lower segment anteriorly, 3cm above bladder reflection
• Sutures pass over fundus posteriorly, around to anterior surface again
• Creates continuous compression
• Requirements: Uterus must be open (hysterotomy or laparotomy)
• Success rate: ~75% [55]

Other Techniques:

• Hayman suture: Similar to B-Lynch, but doesn't require hysterotomy
• Multiple square sutures: Cho technique—grid pattern of compression sutures
• Pereira suture: Longitudinal sutures through myometrium

Complications: Uterine necrosis (rare), pyometria, synechiae (Asherman syndrome—may impair future fertility).

4. Pelvic Vessel Ligation

Rationale: Reduce arterial pressure to uterus, allowing thrombosis.

Uterine Artery Ligation:

• Technique: Identify uterine artery at level of lower segment (lateral to uterus, within leaves of broad ligament); ligate with absorbable suture (avoid ureter—lies 2cm lateral)
• Success: 80-90% in atonic PPH [56]
• Advantage: Relatively simple, quick, preserves uterus
• Disadvantage: Requires laparotomy

Internal Iliac (Hypogastric) Artery Ligation:

• Technique: Retroperitoneal dissection, identify internal iliac artery (2-3cm after common iliac bifurcation), ligate both sides
• Effect: Reduces pulse pressure in uterine arteries (arterial → venous flow)
• Complexity: Requires experienced surgeon; risk of injury to iliac vein, ureter
• Success: 40-50% [57] (lower than uterine artery ligation—collateral flow extensive)
• Declining use: Largely superseded by embolization

5. Uterine Artery Embolization (UAE)

Indications: Ongoing bleeding despite surgical measures, patient haemodynamically stable enough for transfer to interventional radiology.

Technique:

• Femoral artery access
• Selective catheterization of uterine arteries (bilateral)
• Injection of embolic material: gelatin sponge (Gelfoam), polyvinyl alcohol particles, or coils
• Endpoint: Cessation of arterial flow to bleeding site

Success Rate: 85-95% in controlling PPH. [58]

Advantages:

• Preserves uterus and fertility
• Less invasive than surgery
• Can treat bleeding from sites inaccessible surgically (broad ligament, parametrial)

Disadvantages:

• Requires stable patient (not suitable if exsanguinating)
• Requires interventional radiology on-site (not available in all centres)
• Time delay (preparation, transfer, procedure—typically 60-90 minutes)

Complications:

• Re-bleeding (5-10%)
• Infection, abscess
• Ovarian failure (rare—from non-target embolization of ovarian artery anastomoses)
• Bladder necrosis, uterine necrosis (extremely rare)

Future Fertility: Preserved in 80-90%; some case reports of Asherman syndrome or placenta accreta in subsequent pregnancies. [59]

6. Peripartum Hysterectomy

Indications:

• Life-threatening haemorrhage refractory to all conservative measures
• Placenta accreta spectrum with failed conservative management
• Uterine rupture with irreparable damage

Types:

• Subtotal (supracervical) hysterectomy: Faster, less blood loss, lower bladder injury risk—preferred in emergency
• Total hysterectomy: Required if bleeding from cervix or lower segment extension

Technique Considerations:

• Preserve ovaries (conserve endocrine function)
• Early ligation of uterine arteries (reduce blood loss)
• Careful bladder dissection (oedematous, friable tissues; risk of injury)
• Mass ligatures acceptable in extremis (rapid control of bleeding)

Incidence: 0.4-1.4 per 1000 deliveries. [16] Increasing due to rise in placenta accreta (associated with previous caesarean sections).

Outcomes:

• Survival: > 95% in high-resource settings [60]
• Complications: Bladder injury (10-15%), ureteric injury (1-2%), DIC, ICU admission, psychological sequelae

Psychological Impact: Grief, loss of fertility, sense of failure. Requires sensitive postnatal counseling and support.

Special Scenarios

Retained Placenta

Definition: Placenta undelivered 30 minutes after birth (with active management). [31]

Management:

1. Immediate: Secure IV access, send bloods (G&S), commence oxytocin infusion
2. Controlled cord traction: Gentle sustained traction with suprapubic counter-pressure (Brandt-Andrews method)—do not apply excessive force (risks uterine inversion)
3. Bladder emptying: Catheterize
4. Manual Removal of Placenta (MROP): [61]
   • Timing: After 30 minutes (or immediately if haemorrhage)
   • Anaesthesia: Regional or general (adequate analgesia essential)
   • Technique:
     • Aseptic technique, long gloves
     • Insert hand into uterine cavity, locate placental edge
     • Use ulnar border of hand to separate placenta from uterine wall (gentle sawing motion)
     • Grasp placenta and remove
     • Explore cavity for retained fragments
     • Administer oxytocin bolus and infusion after removal
   • Complications: Endometritis (5-10%), PPH, uterine perforation (less than 1%)
5. Antibiotics: Single dose at time of procedure (co-amoxiclav 1.2g IV or cefuroxime 1.5g)

Morbidly Adherent Placenta (Accreta):

• Recognized when no cleavage plane found during MROP
• Management options:
  • "Conservative: Leave placenta in situ, administer methotrexate (controversial), await spontaneous resorption"
  • "Surgical: Hysterectomy (if bleeding), focal resection (if focal accreta)"
• Risk: Delayed haemorrhage, sepsis, DIC

Uterine Inversion

Incidence: 1 in 2000-3000 deliveries. [30]

Recognition: Sudden severe shock, pain, vaginal mass, absent fundus.

Management: [62]

1. Call for help immediately (obstetric emergency)
2. Do NOT remove placenta if still attached (exacerbates bleeding and shock)
3. Immediate manual replacement (Johnson method):
   • Grasp inverted uterus in hand
   • Apply steady pressure to push fundus upward through cervix
   • Push towards umbilicus, then posteriorly towards sacrum
   • Do not remove hand until uterus fully contracted
   • May require tocolysis (terbutaline 250mcg SC, GTN 50-100mcg IV bolus) to relax uterus and cervical ring
4. Anaesthesia: General anaesthesia with halothane/sevoflurane (uterine relaxation) or GA after failed manual replacement
5. Surgical correction: If manual replacement fails—Huntington procedure (laparotomy, traction on round ligaments) or Haultain procedure (incise constriction ring posteriorly)
6. After correction: Aggressive uterotonic therapy, continue monitoring

Delay: Worsens outcome—cervical constriction ring becomes established, making replacement difficult.

PPH in Low-Resource Settings

Challenges: Limited access to blood products, operating theatres, uterotonic drugs, skilled personnel.

Adaptations:

• Uterotonic: Misoprostol (800mcg sublingual or rectal)—stable at room temperature, cheap, effective [43]
• Tranexamic acid: High benefit-to-risk ratio, affordable
• Tamponade: Condom-catheter (improvised balloon)
• Non-pneumatic anti-shock garment (NASG): Decreases blood flow to lower body, buys time for transfer [63]
• Bimanual compression: Can maintain haemostasis for prolonged periods
• Early transfer: If facilities inadequate

---

8. Complications

Immediate Complications

Hypovolaemic Shock:

• Multiorgan hypoperfusion
• Anaerobic metabolism, lactic acidosis
• Risk of end-organ damage (kidneys, brain, liver)

Disseminated Intravascular Coagulation (DIC):

• Consumptive coagulopathy triggered by massive haemorrhage
• Depleted clotting factors, platelets, fibrinogen
• Paradoxical thrombosis and bleeding
• High mortality if untreated

Hypothermia:

• Exacerbates coagulopathy (enzyme function impaired)
• Component of "lethal triad" (hypothermia, acidosis, coagulopathy)
• Prevented by warming fluids, forced-air warming devices

Acute Respiratory Distress Syndrome (ARDS):

• From massive transfusion, shock, or amniotic fluid embolism
• Pulmonary oedema, hypoxaemia
• Requires mechanical ventilation

Acute Kidney Injury:

• Acute tubular necrosis from prolonged hypotension
• Oliguria, rising creatinine
• May require renal replacement therapy

Short-Term Complications

Infection:

• Endometritis (from intrauterine interventions, retained products)
• Wound infection (perineal, abdominal)
• Sepsis

Thromboembolism:

• Massive transfusion, prolonged immobility, vessel injury
• Deep vein thrombosis, pulmonary embolism
• Prevention: Thromboprophylaxis (LMWH), early mobilization, compression stockings

Anaemia:

• Fatigue, reduced exercise tolerance
• May require oral or IV iron supplementation, occasionally delayed transfusion

Long-Term Complications

Sheehan's Syndrome (Postpartum Hypopituitarism): [19]

• Ischaemic necrosis of anterior pituitary due to severe hypovolaemia
• Presentation: Failure to lactate, persistent amenorrhoea, fatigue, loss of pubic/axillary hair, hypothyroidism
• Diagnosis: Low anterior pituitary hormones (FSH, LH, ACTH, TSH, prolactin, GH)
• Treatment: Lifelong hormone replacement (hydrocortisone, levothyroxine, oestrogen)
• Incidence: Now rare in high-resource settings (less than 1% severe PPH) due to earlier intervention; higher in low-resource settings

Psychological Sequelae:

• Post-traumatic stress disorder (PTSD)—flashbacks, nightmares, avoidance
• Postnatal depression
• Anxiety about future pregnancies
• Bonding difficulties with infant
• Management: Early psychological support, debriefing, CBT, medication if required

Asherman's Syndrome (Intrauterine Adhesions):

• From vigorous curettage for retained products
• Presentation: Amenorrhoea, subfertility, recurrent miscarriage
• Diagnosis: Hysteroscopy
• Treatment: Hysteroscopic adhesiolysis

Secondary Amenorrhoea:

• From uterine ischaemia (severe PPH, compression sutures, embolization)
• Diagnosis: Exclude Sheehan's, assess endometrial thickness

Infertility:

• Following hysterectomy (definitive)
• Rarely from uterine artery embolization (ovarian failure if non-target embolization)

---

9. Prevention

Primary Prevention

Active Management of Third Stage: [40]

• Uterotonic administration: 10 IU oxytocin IM immediately after delivery of baby (or at delivery of anterior shoulder)
• Controlled cord traction: After signs of placental separation (gush of blood, lengthening of cord, uterus contracts and rises)
• Uterine massage: After placental delivery

Evidence: Reduces PPH risk by 60% compared to physiological management (RR 0.38, 95% CI 0.32-0.46). [40]

Optimal Uterotonic for Prevention:

• Oxytocin 10 IU IM: Gold standard (WHO recommendation) [64]
• Alternatives: Carbetocin (long-acting oxytocin analogue—single dose, reduces need for additional uterotonics; more expensive), Syntometrine (oxytocin + ergometrine—more side effects)

Secondary Prevention (High-Risk Patients)

Antenatal Optimization:

• Correct anaemia: Iron supplementation (oral or IV if severe/intolerant)—target Hb > 110 g/L before delivery
• Identify risk factors: Document in care plan, inform patient and team
• Delivery planning: Where to deliver (consultant-led unit), mode of delivery (planned caesarean for placenta praevia/accreta)

Intrapartum Measures:

• IV access: Secure early in high-risk patients
• Group and save: Sent before delivery
• Active management third stage: Ensure compliance
• Senior presence: Consultant obstetrician for high-risk deliveries

Placenta Accreta Spectrum:

• Antenatal diagnosis: Ultrasound ± MRI if previous CS + placenta praevia
• Multidisciplinary planning: Consultant obstetrician, urologist, interventional radiologist, haematologist, anaesthetist, neonatologist
• Elective caesarean hysterectomy: Planned 36-37 weeks, cell salvage available
• Prophylactic balloon catheters: Internal iliac artery balloon occlusion (controversial—not proven to reduce blood loss; may increase thrombosis risk)

Protocols and Training:

• PPH drills: Regular multidisciplinary simulation training improves outcomes [65]
• Equipment checks: PPH trolley with uterotonics, Bakri balloon, IV fluids
• Algorithms: Laminated cards, wall posters (RCOG, local guidelines)
• Debrief: After every major PPH (identify learning points, support staff)

---

10. Prognosis and Outcomes

Survival

High-Resource Settings:

• Case fatality rate: less than 1% (0.1-0.3% in UK) [14]
• Most deaths preventable with optimal care (MBRRACE-UK reports identify substandard care in > 60% maternal deaths from haemorrhage) [66]

Low-Resource Settings:

• Case fatality: 3-5% [14]
• Major contributor to high maternal mortality ratios (> 300 per 100,000 live births in sub-Saharan Africa)

Functional Recovery

Physical Recovery:

• Most women recover fully within 6-12 weeks
• Persistent fatigue common (from anaemia)
• Return to normal activities: Gradual over 3-6 months

Reproductive Outcomes:

• Future fertility: Preserved in > 95% if uterus conserved
• Recurrence risk: 10-15% in subsequent pregnancy if previous PPH [67]
• Mode of delivery: Previous PPH not indication for caesarean section (vaginal delivery appropriate)

Psychological Impact:

• PTSD symptoms: 10-20% after major PPH [68]
• Postnatal depression: 15-25% (higher than general postpartum population)
• Fear of future pregnancy: Common (may limit family size)
• Support: Birth afterthoughts services, psychological support, peer support groups

Predictors of Poor Outcome

Delay in Recognition:

• Underestimation of blood loss
• Failure to escalate appropriately

Delay in Definitive Treatment:

• Persistent use of failed strategies
• Delayed surgical intervention
• Delayed hysterectomy in cases of placenta accreta

Pre-existing Morbidity:

• Anaemia (Hb less than 90 g/L)
• Coagulopathy
• Cardiovascular disease

---

11. Evidence and Guidelines

Key Guidelines

Landmark Trials and Studies

1. WOMAN Trial (2017): [6]

• Design: RCT, 20,060 women with PPH across 21 countries
• Intervention: Tranexamic acid 1g IV vs placebo
• Primary outcome: Death from all causes or hysterectomy
• Key findings:
  • "Death from bleeding: RR 0.81 (95% CI 0.65-1.00)—19% reduction"
  • "Early treatment (less than 3h): RR 0.69 (95% CI 0.52-0.91)—31% reduction"
  • "Late treatment (> 3h): No benefit"
  • "Laparotomy for bleeding control: RR 0.64 (95% CI 0.49-0.85)"
  • No increase in thrombotic events
• Impact: Changed practice worldwide—TXA now standard of care

2. Cochrane Review: Active vs Physiological Management (2019): [40]

• Findings: Active management reduces PPH > 500ml (RR 0.38), severe PPH > 1000ml (RR 0.34), need for blood transfusion (RR 0.35)
• Components: Oxytocin 10 IU IM, controlled cord traction, uterine massage

3. Bakri Balloon Meta-analysis (2018): [53]

• 15 studies, 869 women
• Success rate (avoiding surgery): 87% (95% CI 84-90%)
• Complication rate: 2.4%

4. Uterine Artery Embolization Systematic Review (2020): [58]

• Success rate: 89.4%
• Fertility preservation: 80-90%
• Ovarian failure: less than 2%

Guideline Discrepancies

Definition of PPH:

• RCOG/WHO: > 500ml vaginal, > 1000ml caesarean [1,64]
• ACOG: > 1000ml any delivery [70]
• Controversy: Visual estimation unreliable; trend toward quantitative measurement regardless of delivery mode

Role of Carbetocin:

• WHO: Not recommended due to cost and lack of evidence over oxytocin [64]
• Canada, some European countries: Carbetocin approved for prevention (reduced need for additional uterotonics) [71]

Prophylactic Tranexamic Acid:

• WOMAN-2 trial (ongoing): Evaluating TXA for prevention in high-risk women
• Current guidelines: Treatment only (not prophylaxis) pending further evidence

---

12. Patient and Layperson Explanation

What is Primary Postpartum Haemorrhage?

Primary postpartum haemorrhage (PPH) means heavy bleeding after giving birth. While some bleeding is normal after delivery, PPH is when bleeding becomes excessive—more than about 500ml (roughly two cups of liquid) after a vaginal birth, or more than 1000ml after a caesarean section. This bleeding happens within the first 24 hours after your baby is born.

Why Does PPH Happen?

After your baby and placenta are delivered, your womb (uterus) normally contracts tightly. This squeezes shut the blood vessels where the placenta was attached, similar to how tying off a hose stops water flowing. Sometimes this process doesn't work properly:

1. The muscle is tired ("atony"): After a long labour, carrying twins, or having a very big baby, the womb muscle can be exhausted and stays soft and floppy instead of contracting firmly.

2. There's a tear: The birth process can cause tears in the vagina, cervix (neck of the womb), or rarely the womb itself. These tears can bleed heavily.

3. Something is left behind: If a piece of placenta (afterbirth) stays in the womb, it prevents the muscle from contracting properly.

4. Your blood doesn't clot properly: Rarely, problems with blood clotting can cause or worsen bleeding.

What Are the Symptoms?

You might notice:

• Heavy bleeding (soaking through pads very quickly)
• Feeling dizzy or faint
• Your heart racing
• Feeling unusually weak or breathless
• Severe tummy pain

Sometimes the bleeding is obvious, but occasionally it can occur inside your body without being immediately visible. Healthcare staff will monitor you carefully after delivery.

How is PPH Treated?

The medical team acts quickly if PPH occurs:

1. Massage your tummy: Rubbing the womb through your abdomen helps it contract and stop bleeding.

2. Insert a catheter: Emptying your bladder helps the womb contract better.

3. Give medications: Several medications can make the womb contract more strongly. These are given through a drip in your arm or as injections.

4. Give fluids and blood: If you've lost a lot of blood, you'll receive fluids through a drip. Sometimes blood transfusions are needed.

5. Further treatments if needed: If bleeding continues, other options include:

   • Placing a balloon inside the womb to apply pressure
   • Stitching tears if that's the cause
   • Rarely, surgery may be needed

Will I Be Okay?

With modern medical care, the vast majority of women recover completely from PPH. The key is quick recognition and treatment. You'll be closely monitored after delivery, and staff are trained to respond immediately if heavy bleeding occurs.

What About Future Pregnancies?

Most women who've had PPH can safely have more babies. Your healthcare team will know about your history and take extra precautions:

• Ensuring you're not anaemic (low blood count) during pregnancy
• Planning your delivery carefully
• Being ready with preventive medications
• Having experienced staff present at the birth

There's a small increased risk (about 10-15%) of PPH happening again, but this doesn't mean it will—and if it does, the team will be prepared.

Questions to Ask Your Healthcare Team

• What caused my PPH?
• Do I need any follow-up treatment?
• When can I go home?
• What should I watch for after discharge?
• How will this affect future pregnancies?
• Are there any long-term effects I should know about?

Emotional Recovery

Having PPH can be frightening. Many women feel shocked, anxious, or upset afterwards. These feelings are completely normal. Talk to your healthcare team about:

• What happened during your delivery
• Any concerns you have
• Support services available (counseling, support groups)

Remember: PPH is a medical emergency, not something you caused or could have prevented. With proper care, recovery is expected, and the focus can return to you and your new baby.

---

13. Examination Focus

High-Yield Exam Topics

MRCOG Part 2 (Written)

1. Risk Factor Identification:

• Previous PPH is the strongest predictor (OR 9.0)
• Placenta praevia, multiple pregnancy, prolonged labour, grand multiparity

2. Pharmacology SBAs:

• Ergometrine contraindicated in: Pre-eclampsia/hypertension (causes severe HTN, risk of stroke)
• Carboprost contraindicated in: Asthma (causes bronchospasm)
• Tranexamic acid mechanism: Antifibrinolytic (prevents plasminogen activation)
• Tranexamic acid timing: Within 3 hours of delivery for maximal benefit (WOMAN trial)

3. Management Algorithms:

• Stepwise escalation: Mechanical → Pharmacological → Surgical
• Major Haemorrhage Protocol activation criteria (> 1000ml)
• Component therapy in massive transfusion (PRBC:FFP:Platelets = 1:1:1)

4. Fibrinogen as Predictor:

• Normal postpartum: 4-6 g/L
• less than 2 g/L predicts severe PPH requiring massive transfusion
• First-line replacement: Cryoprecipitate (or fibrinogen concentrate)

5. Evidence:

• WOMAN trial: TXA reduces death from bleeding by 31% if given within 3h
• Active management of third stage reduces PPH by 60%

MRCOG Part 3 (OSCE/Clinical Stations)

Task 1: Simulated PPH Management:

• Demonstrate structured approach (call for help, ABCDE)
• Verbalise uterine massage, catheterization, bimanual compression
• Correct drug sequence and dosing (Oxytocin → Ergometrine → Carboprost → Misoprostol → TXA)
• Identify contraindications (Ergometrine in pre-eclampsia, Carboprost in asthma)
• When to escalate to theatre

Task 2: Retained Placenta Scenario:

• Timing of manual removal (30 minutes with active management)
• Technique description (identify cleavage plane, gentle separation)
• Recognition of accreta (no cleavage plane)
• Management options for accreta

Task 3: Communication Station:

• Consent for manual removal of placenta (risks, benefits, alternatives)
• Debrief after emergency hysterectomy (sensitive, empathetic)
• Counseling for future pregnancy after PPH

Task 4: Prioritization Exercise:

• Multiple patients, identify sickest (shock index, ongoing bleeding)
• Resource allocation (blood products, theatre, staff)

Viva Voce Questions and Model Answers

Q1: "A patient delivered 15 minutes ago and has lost 800ml blood. The uterus feels firm. What is your management?"

Model Answer: The firm uterus makes atony unlikely—the bleeding is probably traumatic (tears) or from retained tissue. My immediate actions would be:

1. Call for senior help
2. Ensure adequate analgesia and lighting
3. Systematic examination with speculum: inspect perineum, vagina (all walls), and cervix (with ring forceps)
4. If high tears or cervical lacerations found: arrange transfer to theatre for EUA and repair
5. If no obvious trauma: consider retained placental fragments—inspect placenta for completeness, consider ultrasound
6. Meanwhile: Secure IV access, send bloods including G&S, commence oxytocin infusion, monitor vital signs closely

Q2: "What is the evidence for tranexamic acid in PPH?"

Model Answer: The WOMAN trial (Lancet 2017) was a large international RCT involving over 20,000 women with PPH. It showed:

• 19% overall reduction in death from bleeding with tranexamic acid vs placebo
• 31% reduction if given within 3 hours of delivery
• No benefit if given after 3 hours
• No increase in thrombotic complications
• Also reduced need for laparotomy to control bleeding

Based on this evidence, tranexamic acid (1g IV) is now standard of care for major PPH and should be given early—ideally within the first 3 hours. RCOG and WHO guidelines both recommend it. The mechanism is antifibrinolytic—it stabilizes clot by preventing plasminogen activation and fibrin degradation.

Q3: "How do you perform bimanual compression of the uterus?"

Model Answer: Bimanual compression is a life-saving temporizing measure for uterine atony while awaiting definitive treatment.

Technique:

1. Explain to patient (if conscious), provide analgesia if possible
2. Insert one hand vaginally and form a closed fist
3. Place the fist in the anterior vaginal fornix, behind the pubic symphysis
4. Place the other hand on the abdomen, posterior to the uterine fundus
5. Firmly compress the uterus between both hands, squeezing the uterine body
6. Maintain compression continuously—this can completely arrest bleeding from an atonic uterus
7. Continue while calling for help, preparing uterotonics, arranging transfer to theatre if needed

It's physically tiring but can be life-saving—buying crucial time until definitive interventions take effect.

Q4: "A patient has had a PPH requiring 6 units of blood and correction of coagulopathy. She's now stable. What are your concerns for long-term follow-up?"

Model Answer: I'd be concerned about several potential long-term complications:

Endocrine:

• Sheehan's syndrome (pituitary necrosis)—though rare with modern resuscitation. I'd ask about lactation, menstruation when they return, and screen for symptoms of hypopituitarism (fatigue, cold intolerance, loss of body hair)

Psychological:

• PTSD and postnatal depression are increased after major PPH. I'd ensure psychological support, offer debriefing, and screen using tools like EPDS

Reproductive:

• Future fertility is usually preserved unless she required hysterectomy
• Recurrence risk ~10-15% in next pregnancy—requires documented plan for antenatal optimization (correct anaemia), delivery planning (senior staff present, active management), and close monitoring

Physical:

• Anaemia—check Hb at 6 weeks, consider iron supplementation
• If she had intrauterine interventions—small risk of Asherman's syndrome (would present as amenorrhoea or light periods)

Follow-up:

• 6-week postnatal appointment: Check Hb, screen for depression, discuss contraception and future pregnancy planning
• Offer referral to perinatal mental health if needed
• Ensure GP informed of significant event

---

14. References

Primary Sources

1. Royal College of Obstetricians and Gynaecologists. Prevention and Management of Postpartum Haemorrhage. Green-top Guideline No. 52. December 2016. https://doi.org/10.1111/1471-0528.14178

2. Say L, Chou D, Gemmill A, et al. Global causes of maternal death: a WHO systematic analysis. Lancet Glob Health. 2014;2(6):e323-e333. https://doi.org/10.1016/S2214-109X(14)70227-X

3. Knight M, Callaghan WM, Berg C, et al. Trends in postpartum hemorrhage in high resource countries: a review and recommendations from the International Postpartum Hemorrhage Collaborative Group. BMC Pregnancy Childbirth. 2009;9:55. https://doi.org/10.1186/1471-2393-9-55

4. Burchell RC. Physiology of internal iliac artery ligation. J Obstet Gynaecol Br Commonw. 1968;75(6):642-651. https://doi.org/10.1111/j.1471-0528.1968.tb00171.x

5. Combs CA, Murphy EL, Laros RK Jr. Factors associated with postpartum hemorrhage with vaginal birth. Obstet Gynecol. 1991;77(1):69-76.

6. WOMAN Trial Collaborators. Effect of early tranexamic acid administration on mortality, hysterectomy, and other morbidities in women with post-partum haemorrhage (WOMAN): an international, randomised, double-blind, placebo-controlled trial. Lancet. 2017;389(10084):2105-2116. https://doi.org/10.1016/S0140-6736(17)30638-4

7. Mavrides E, Allard S, Chandraharan E, et al. Prevention and management of postpartum haemorrhage: Green-top Guideline No. 52. BJOG. 2016;124:e106-e149.

8. Katz V, Dotters D, Droegemueller W. Perimortem cesarean delivery. Obstet Gynecol. 1986;68(4):571-576.

9. El Ayadi AM, Nathan HL, Seed PT, et al. Vital sign prediction of adverse maternal outcomes in women with hypovolemic shock: the role of shock index. PLoS One. 2016;11(2):e0148729. https://doi.org/10.1371/journal.pone.0148729

10. Royal College of Obstetricians and Gynaecologists. Antepartum Haemorrhage. Green-top Guideline No. 63. November 2011.

11. Callaghan WM, Kuklina EV, Berg CJ. Trends in postpartum hemorrhage: United States, 1994-2006. Am J Obstet Gynecol. 2010;202(4):353.e1-6. https://doi.org/10.1016/j.ajog.2010.01.011

12. Creanga AA, Bateman BT, Butwick AJ, et al. Morbidity associated with cesarean delivery in the United States: is placenta accreta an increasingly important contributor? Am J Obstet Gynecol. 2015;213(3):384.e1-11. https://doi.org/10.1016/j.ajog.2015.05.002

13. Ford JB, Roberts CL, Simpson JM, Vaughan J, Cameron CA. Increased postpartum hemorrhage rates in Australia. Int J Gynaecol Obstet. 2007;98(3):237-243. https://doi.org/10.1016/j.ijgo.2007.03.011

14. Khan KS, Wojdyla D, Say L, Gülmezoglu AM, Van Look PF. WHO analysis of causes of maternal death: a systematic review. Lancet. 2006;367(9516):1066-1074. https://doi.org/10.1016/S0140-6736(06)68397-9

15. Oyelese Y, Ananth CV. Postpartum hemorrhage: epidemiology, risk factors, and causes. Clin Obstet Gynecol. 2010;53(1):147-156. https://doi.org/10.1097/GRF.0b013e3181cc406d

16. Shellhaas CS, Gilbert S, Landon MB, et al. The frequency and complication rates of hysterectomy accompanying cesarean delivery. Obstet Gynecol. 2009;114(2 Pt 1):224-229. https://doi.org/10.1097/AOG.0b013e3181ad9442

17. Patterson JA, Roberts CL, Bowen JR, et al. Blood transfusion during pregnancy, birth, and the postnatal period. Obstet Gynecol. 2014;123(1):126-133. https://doi.org/10.1097/AOG.0000000000000054

18. Zwart JJ, Richters JM, Ory F, de Vries JI, Bloemenkamp KW, van Roosmalen J. Severe maternal morbidity during pregnancy, delivery and puerperium in the Netherlands: a nationwide population-based study of 371,000 pregnancies. BJOG. 2008;115(7):842-850. https://doi.org/10.1111/j.1471-0528.2008.01713.x

19. Sheehan HL. Post-partum necrosis of the anterior pituitary. J Path Bact. 1937;45:189-214.

20. Magann EF, Evans S, Hutchinson M, Collins R, Howard BC, Morrison JC. Postpartum hemorrhage after vaginal birth: an analysis of risk factors. South Med J. 2005;98(4):419-422. https://doi.org/10.1097/01.SMJ.0000152760.34443.86

21. Kramer MS, Berg C, Abenhaim H, et al. Incidence, risk factors, and temporal trends in severe postpartum hemorrhage. Am J Obstet Gynecol. 2013;209(5):449.e1-7. https://doi.org/10.1016/j.ajog.2013.07.007

22. Sheiner E, Sarid L, Levy A, Seidman DS, Hallak M. Obstetric risk factors and outcome of pregnancies complicated with early postpartum hemorrhage: a population-based study. J Matern Fetal Neonatal Med. 2005;18(3):149-154. https://doi.org/10.1080/14767050500170088

23. Driessen M, Bouvier-Colle MH, Dupont C, Khoshnood B, Rudigoz RC, Deneux-Tharaux C. Postpartum hemorrhage resulting from uterine atony after vaginal delivery: factors associated with severity. Obstet Gynecol. 2011;117(1):21-31. https://doi.org/10.1097/AOG.0b013e318202c845

24. Bonney V. The clinical management of abnormal uterine haemorrhage. BMJ. 1946;1:339-343.

25. Hancock A, Weeks AD, Lavender DT. Is accurate and reliable blood loss estimation the 'crucial step' in early detection of postpartum haemorrhage: an integrative review of the literature. BMC Pregnancy Childbirth. 2015;15:230. https://doi.org/10.1186/s12884-015-0653-6

26. Dildy GA 3rd, Paine AR, George NC, Velasco C. Estimating blood loss: can teaching significantly improve visual estimation? Obstet Gynecol. 2004;104(3):601-606. https://doi.org/10.1097/01.AOG.0000137873.07820.34

27. Sosa CG, Althabe F, Belizán JM, Bergel E. Risk factors for postpartum hemorrhage in vaginal deliveries in a Latin-American population. Obstet Gynecol. 2009;113(6):1313-1319. https://doi.org/10.1097/AOG.0b013e3181a66b05

28. Grotegut CA, Paglia MJ, Johnson LN, Thames B, James AH. Oxytocin exposure during labor among women with postpartum hemorrhage secondary to uterine atony. Am J Obstet Gynecol. 2011;204(1):56.e1-6. https://doi.org/10.1016/j.ajog.2010.08.023

29. Guise JM, McDonagh MS, Osterweil P, Nygren P, Chan BK, Helfand M. Systematic review of the incidence and consequences of uterine rupture in women with previous caesarean section. BMJ. 2004;329(7456):19-25. https://doi.org/10.1136/bmj.329.7456.19

30. Baskett TF. Acute uterine inversion: a review of 40 cases. J Obstet Gynaecol Can. 2002;24(12):953-956. https://doi.org/10.1016/s1701-2163(16)31055-2

31. Weeks AD. The retained placenta. Best Pract Res Clin Obstet Gynaecol. 2008;22(6):1103-1117. https://doi.org/10.1016/j.bpobgyn.2008.07.005

32. Silver RM, Landon MB, Rouse DJ, et al. Maternal morbidity associated with multiple repeat cesarean deliveries. Obstet Gynecol. 2006;107(6):1226-1232. https://doi.org/10.1097/01.AOG.0000219750.79480.84

33. Charbit B, Mandelbrot L, Samain E, et al. The decrease of fibrinogen is an early predictor of the severity of postpartum hemorrhage. J Thromb Haemost. 2007;5(2):266-273. https://doi.org/10.1111/j.1538-7836.2007.02297.x

34. Cortet M, Deneux-Tharaux C, Dupont C, et al. Association between fibrinogen level and severity of postpartum haemorrhage: secondary analysis of a prospective trial. Br J Anaesth. 2012;108(6):984-989. https://doi.org/10.1093/bja/aes096

35. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support (ATLS) Student Course Manual. 10th ed. Chicago: American College of Surgeons; 2018.

36. Snegovskikh D, Souza D, Walton Z, et al. Point-of-care viscoelastic testing improves the outcome of pregnancies complicated by severe postpartum hemorrhage. J Clin Anesth. 2018;44:50-56. https://doi.org/10.1016/j.jclinane.2017.10.003

37. Katz D, Beilin Y. Disorders of coagulation in pregnancy. Br J Anaesth. 2015;115 Suppl 2:ii75-ii88. https://doi.org/10.1093/bja/aev374

38. Soltan MH, Faragallah MF, Mosabah MH, Al-Adawy AR. External aortic compression device: the first aid for postpartum hemorrhage control. J Obstet Gynaecol Res. 2009;35(3):453-458. https://doi.org/10.1111/j.1447-0756.2008.00979.x

39. Mousa HA, Blum J, Abou El Senoun G, Shakur H, Alfirevic Z. Treatment for primary postpartum haemorrhage. Cochrane Database Syst Rev. 2014;(2):CD003249. https://doi.org/10.1002/14651858.CD003249.pub3

40. Begley CM, Gyte GM, Devane D, McGuire W, Weeks A, Biesty LM. Active versus expectant management for women in the third stage of labour. Cochrane Database Syst Rev. 2019;2:CD007412. https://doi.org/10.1002/14651858.CD007412.pub5

41. Oleen MA, Mariano JP. Controlling refractory atonic postpartum hemorrhage with Hemabate sterile solution. Am J Obstet Gynecol. 1990;162(1):205-208. https://doi.org/10.1016/0002-9378(90)90852-k

42. Mousa HA, Walkinshaw S. Major postpartum haemorrhage. Curr Opin Obstet Gynecol. 2001;13(6):595-603. https://doi.org/10.1097/00001703-200112000-00008

43. Hofmeyr GJ, Gülmezoglu AM, Novikova N, Lawrie TA. Postpartum misoprostol for preventing maternal mortality and morbidity. Cochrane Database Syst Rev. 2013;(7):CD008982. https://doi.org/10.1002/14651858.CD008982.pub2

44. World Health Organization. WHO Recommendations for the Prevention and Treatment of Postpartum Haemorrhage. Geneva: World Health Organization; 2012.

45. Kearns RJ, Moss JR, Elbourne D, et al. WOMAN Trial Collaborators. Cost-effectiveness of tranexamic acid for the treatment of postpartum haemorrhage: an economic evaluation based on the WOMAN trial. BMJ Open. 2021;11(9):e052080. https://doi.org/10.1136/bmjopen-2021-052080

46. National Blood Transfusion Committee. Patient Blood Management Guideline: Module 5 - Obstetrics and Maternity. Canberra: National Blood Authority; 2015.

47. Holcomb JB, Tilley BC, Baraniuk S, et al. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. JAMA. 2015;313(5):471-482. https://doi.org/10.1001/jama.2015.12

48. Carson JL, Stanworth SJ, Dennis JA, et al. Transfusion thresholds for guiding red blood cell transfusion. Cochrane Database Syst Rev. 2021;12:CD002042. https://doi.org/10.1002/14651858.CD002042.pub5

49. Collins PW, Cannings-John R, Bruynseels D, et al. Viscoelastometric-guided early fibrinogen concentrate replacement during postpartum haemorrhage: OBS2, a double-blind randomised controlled trial. Br J Anaesth. 2017;119(3):411-421. https://doi.org/10.1093/bja/aex181

50. Alfirevic Z, Elbourne D, Pavord S, et al. Use of recombinant activated factor VII in primary postpartum hemorrhage: the Northern European registry 2000-2004. Obstet Gynecol. 2007;110(6):1270-1278. https://doi.org/10.1097/01.AOG.0000288515.48066.99

51. Khan KS, Moore P, Wilson M, et al. Cell salvage during caesarean section: a randomised controlled trial (The SALVO trial). BJOG. 2017;124(7):1081-1089. https://doi.org/10.1111/1471-0528.14433

52. Georgiou C. Balloon tamponade in the management of postpartum haemorrhage: a review. BJOG. 2009;116(6):748-757. https://doi.org/10.1111/j.1471-0528.2009.02113.x

53. Suarez S, Conde-Agudelo A, Borovac-Pinheiro A, et al. Uterine balloon tamponade for the treatment of postpartum hemorrhage: a systematic review and meta-analysis. Am J Obstet Gynecol. 2020;222(4):293.e1-293.e52. https://doi.org/10.1016/j.ajog.2019.11.1287

54. B-Lynch C, Coker A, Lawal AH, Abu J, Cowen MJ. The B-Lynch surgical technique for the control of massive postpartum haemorrhage: an alternative to hysterectomy? Five cases reported. Br J Obstet Gynaecol. 1997;104(3):372-375. https://doi.org/10.1111/j.1471-0528.1997.tb11471.x

55. Doumouchtsis SK, Papageorghiou AT, Arulkumaran S. Systematic review of conservative management of postpartum hemorrhage: what to do when medical treatment fails. Obstet Gynecol Surv. 2007;62(8):540-547. https://doi.org/10.1097/01.ogx.0000271137.81361.93

56. AbdRabbo SA. Stepwise uterine devascularization: a novel technique for management of uncontrolled postpartum hemorrhage with preservation of the uterus. Am J Obstet Gynecol. 1994;171(3):694-700. https://doi.org/10.1016/0002-9378(94)90084-1

57. Joshi VM, Otiv SR, Majumder R, Nikam YA, Shrivastava M. Internal iliac artery ligation for arresting postpartum haemorrhage. BJOG. 2007;114(3):356-361. https://doi.org/10.1111/j.1471-0528.2006.01235.x

58. Poujade O, Zappa M, Letendre I, et al. Predictive factors for failure of pelvic arterial embolization for postpartum hemorrhage. Int J Gynaecol Obstet. 2012;117(2):119-123. https://doi.org/10.1016/j.ijgo.2011.11.024

59. Chauleur C, Fanget C, Tourne G, Levy R, Larchez C, Seffert P. Serious primary post-partum hemorrhage, arterial embolization and future fertility: a retrospective study of 46 cases. Hum Reprod. 2008;23(7):1553-1559. https://doi.org/10.1093/humrep/den122

60. Bateman BT, Mhyre JM, Callaghan WM, Kuklina EV. Peripartum hysterectomy in the United States: nationwide 14 year experience. Am J Obstet Gynecol. 2012;206(1):63.e1-8. https://doi.org/10.1016/j.ajog.2011.07.030

61. Carroli G, Bergel E. Episiotomy for vaginal birth. Cochrane Database Syst Rev. 2009;(1):CD000081. https://doi.org/10.1002/14651858.CD000081.pub2

62. Witteveen T, van Stralen G, Zwart J, van Roosmalen J. Puerperal uterine inversion in the Netherlands: a nationwide cohort study. Acta Obstet Gynecol Scand. 2013;92(3):334-337. https://doi.org/10.1111/aogs.12023

63. Miller S, Fathalla MM, Yousseff MM, et al. A comparative study of the non-pneumatic anti-shock garment for the treatment of obstetric hemorrhage in Egypt. Int J Gynaecol Obstet. 2010;108(1):20-24. https://doi.org/10.1016/j.ijgo.2009.08.002

64. World Health Organization. WHO Recommendations: Uterotonics for the Prevention of Postpartum Haemorrhage. Geneva: World Health Organization; 2018.

65. Draycott TJ, Crofts JF, Ash JP, et al. Improving neonatal outcome through practical shoulder dystocia training. Obstet Gynecol. 2008;112(1):14-20. https://doi.org/10.1097/AOG.0b013e31817bbc61

66. Knight M, Bunch K, Tuffnell D, et al. (Eds.) on behalf of MBRRACE-UK. Saving Lives, Improving Mothers' Care - Lessons Learned to Inform Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2016-18. Oxford: National Perinatal Epidemiology Unit, University of Oxford; 2020.

67. Edhi MM, Aslam HM, Naqvi Z, Hashmi H. Post partum hemorrhage: causes and management. BMC Res Notes. 2013;6:236. https://doi.org/10.1186/1756-0500-6-236

68. Furuta M, Sandall J, Cooper D, Bick D. The relationship between severe maternal morbidity and psychological health symptoms at 6-8 weeks postpartum: a prospective cohort study in one English maternity unit. BMC Pregnancy Childbirth. 2014;14:133. https://doi.org/10.1186/1471-2393-14-133

69. National Institute for Health and Care Excellence. Intrapartum Care for Healthy Women and Babies. Clinical Guideline [CG190]. London: NICE; 2014 (updated 2017).

70. American College of Obstetricians and Gynecologists. Practice Bulletin No. 183: Postpartum Hemorrhage. Obstet Gynecol. 2017;130(4):e168-e186. https://doi.org/10.1097/AOG.0000000000002351

71. Sweeney G, Holbrook AM, Levine M, et al. Carbetocin at elective Caesarean delivery: a randomized, double-blind, placebo-controlled trial. BJOG. 2004;111(7):617-622. https://doi.org/10.1111/j.1471-0528.2004.00172.x

---

Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances, local protocols, and available resources. Always consult appropriate specialists and follow institutional guidelines. In emergencies, activate local emergency response systems immediately.