Postpartum haemorrhage

Surgical approach (what the obstetric team typically does)

  • Call for help early: senior obstetrician, senior anaesthetist, midwife-in-charge, haematology, blood bank; activate major obstetric haemorrhage protocol
  • Immediate measures
    • Bimanual uterine massage; empty bladder; assess uterine tone and ongoing loss
    • Exclude retained products: inspect placenta; consider manual uterine exploration; ultrasound if uncertain
    • Inspect/repair genital tract trauma (cervix/vagina/perineum); consider theatre for examination under anaesthesia
  • Escalation for uterine atony (stepwise)
    • Uterotonics (oxytocin/ergometrine/carboprost/misoprostol) + tranexamic acid
    • Intrauterine balloon tamponade (e.g., Bakri) ± vaginal packing
    • Surgical haemostasis: compression sutures (e.g., B-Lynch), uterine artery ligation, internal iliac artery ligation (variable success, technically demanding)
    • Interventional radiology: uterine artery embolisation (if haemodynamically stable and available)
    • Peripartum hysterectomy (life-saving; do not delay in refractory bleeding/placenta accreta spectrum)
  • If suspected uterine inversion
    • Immediate manual replacement (Johnson manoeuvre) + tocolysis to facilitate reduction (e.g., GTN) then uterotonics after reduction
  • If placenta accreta spectrum suspected/confirmed
    • Avoid forcible placental removal; planned approach often includes leaving placenta in situ and proceeding to hysterectomy with senior team

Anaesthetic management (overview for PPH/theatre)

  • Type of anaesthesia: often conversion to GA if ongoing major haemorrhage, shock, need for laparotomy/hysterectomy, or inadequate neuraxial block; neuraxial may be continued/extended if stable and surgery limited
  • Airway: usually cuffed ETT for major haemorrhage (aspiration risk, need for controlled ventilation, prolonged surgery); SGA only as short-term rescue/bridge in selected stable cases
  • Duration: variable; 30–60 min for EUA/repair/balloon; 1–3+ h for laparotomy, embolisation transfer, or hysterectomy
  • How painful: high if laparotomy/hysterectomy; moderate for EUA/repair; ensure multimodal analgesia and consider neuraxial/abdominal wall blocks if coagulation allows and time permits
  • Immediate anaesthetic priorities
    • Simultaneous resuscitation and haemostasis: two large-bore IV cannulae (14–16G) + rapid infuser/warming; consider arterial line early; central access if poor peripheral access/vasopressors required
    • Activate massive transfusion/obstetric haemorrhage protocol; early TXA; targeted blood component therapy guided by labs/viscoelastic testing
    • Prevent the lethal triad: hypothermia, acidosis, coagulopathy (active warming, warmed fluids/blood, adequate ventilation/perfusion, calcium replacement)
    • Vasopressors: treat vasodilation/anaesthetic-induced hypotension but prioritise volume/blood; noradrenaline infusion often appropriate in ongoing shock after initial volume

Definition and classification

  • Primary PPH: bleeding within 24 h of birth; Secondary PPH: 24 h to 6–12 weeks postpartum (definitions vary)
  • Quantification: cumulative blood loss ≥500 mL after vaginal birth or ≥1000 mL after caesarean often used; any blood loss causing haemodynamic instability is clinically significant
  • Major PPH commonly defined as ≥1000 mL; severe/life-threatening often ≥2000 mL or requiring massive transfusion

Aetiology: the 4 Ts

  • Tone (uterine atony) — most common
    • Risk factors: overdistension (multiple pregnancy, polyhydramnios, macrosomia), prolonged/precipitate labour, chorioamnionitis, oxytocin use, uterine fatigue, high parity, uterine fibroids, GA/volatile agents
  • Tissue (retained placenta/products; placenta accreta spectrum)
    • Placenta accreta spectrum risk: placenta praevia + previous caesarean, uterine surgery/curettage, Asherman’s
  • Trauma (genital tract lacerations, uterine rupture, uterine inversion)
    • Consider if uterus well-contracted but bleeding continues
  • Thrombin (coagulopathy: pre-existing or acquired)
    • Causes: placental abruption, severe pre-eclampsia/HELLP, sepsis, amniotic fluid embolism, massive haemorrhage/dilutional coagulopathy, anticoagulants, inherited bleeding disorders

Recognition and initial actions (first minutes)

  • PPH is often underestimated: use quantitative blood loss (weigh swabs, measure suction) and clinical signs; remember pregnancy physiology masks shock until late
  • Immediate actions: call for help; left uterine displacement if still pregnant (e.g., at CS); high-flow oxygen; keep warm; secure IV access; send bloods
    • Bloods: FBC, coagulation (PT/APTT/fibrinogen), group & screen/crossmatch; consider VBG/ABG with lactate, calcium, base deficit
  • Early communication: blood bank for emergency O negative / group-specific blood; consider cell salvage if in theatre and not already set up

Resuscitation principles (anaesthetic focus)

  • A–E with parallel haemorrhage control; treat as major trauma physiology
  • Airway/breathing: anticipate aspiration; early RSI if deteriorating, ongoing major bleeding, reduced consciousness, or need for laparotomy
  • Circulation: permissive hypotension is NOT appropriate in obstetrics (uteroplacental perfusion and maternal end-organ perfusion); aim for adequate MAP and mental status while haemostasis achieved
  • IV access and monitoring
    • 2 × large-bore cannulae; pressure bags/rapid infuser; consider arterial line early (beat-to-beat BP, sampling) and urinary catheter for output
    • ECG, SpO2, NIBP (until art line), capnography if intubated, temperature, hourly urine output
  • Fluids and blood: avoid large volumes of crystalloid; early balanced blood component therapy; warm everything
  • Calcium: citrate toxicity common with massive transfusion; give calcium chloride/gluconate guided by ionised calcium (aim normal iCa)
  • Hypothermia prevention: forced-air warming, fluid warmers, warmed blood; target normothermia

Uterotonics and key drugs (doses, cautions)

  • Oxytocin
    • First-line: small IV boluses (e.g., 1–3 IU slow IV) then infusion (e.g., 10–40 IU in 500–1000 mL crystalloid at appropriate rate; local protocols vary)
    • Adverse effects: hypotension, tachycardia, myocardial ischaemia (rare), water intoxication with prolonged high-dose infusion
  • Ergometrine (or Syntometrine where used)
    • Dose often 0.5 mg IM/slow IV (check local guidance)
    • Contraindications/cautions: hypertension, pre-eclampsia, ischaemic heart disease; causes nausea/vomiting, bronchospasm (rare), coronary vasospasm
  • Carboprost (15-methyl PGF2α)
    • Dose often 250 micrograms IM/intramyometrial, repeat every 15–20 min to max 2 mg (protocol dependent)
    • Contraindications/cautions: asthma (bronchospasm), pulmonary hypertension; adverse effects: diarrhoea, vomiting, fever
  • Misoprostol (PGE1 analogue)
    • Often 800–1000 micrograms PR (or SL/oral per protocol)
    • Adverse effects: pyrexia, shivering, diarrhoea
  • Tranexamic acid (TXA)
    • Give early: 1 g IV as soon as PPH diagnosed; consider second 1 g if bleeding continues after 30 min or restarts within 24 h (per WOMAN trial approach; align with local guideline)
    • Best within 3 hours of birth; avoid delay
  • Fibrinogen replacement
    • Fibrinogen falls early in obstetric haemorrhage; low fibrinogen predicts severity; replace with cryoprecipitate or fibrinogen concentrate per protocol/viscoelastic testing

Blood products and haemostatic strategy (exam-ready)

  • Activate major haemorrhage protocol early: aim for timely RBC + FFP + platelets in balanced ratios until guided therapy available
  • Targets (typical; follow local policy)
    • Hb: pragmatic target often ≥80 g/L during active bleeding (higher if ongoing shock/cardiac disease)
    • Platelets: keep >75 ×10^9/L (many aim >100 ×10^9/L if ongoing massive bleeding)
    • Fibrinogen: keep ≥2.0 g/L (often aim ≥2.0–3.0 g/L in obstetrics due to high baseline)
    • PT/APTT: aim <1.5 × normal
    • Temperature >36°C; ionised Ca2+ normal; pH >7.2
  • Viscoelastic testing (TEG/ROTEM) can speed targeted therapy
    • Common pattern: early low fibrinogen (e.g., low FIBTEM A5/A10) → give cryo/fibrinogen concentrate
  • Cell salvage
    • Recommended/accepted in obstetrics (including CS) with leucocyte depletion filter per local practice; ensure anti-D prophylaxis for RhD-negative mothers if fetal blood exposure possible
  • Recombinant factor VIIa: rescue therapy only after correction of fibrinogen/platelets/pH/temperature/calcium and surgical control attempted; thrombosis risk

Anaesthesia technique considerations

  • If neuraxial in situ (epidural/spinal)
    • Assess haemodynamic stability and block adequacy; top-up epidural cautiously if stable and surgery limited
    • Convert to GA early if major haemorrhage, high likelihood of laparotomy/hysterectomy, agitation, or airway/ventilation concerns
  • General anaesthesia
    • RSI with cricoid (as per local practice); use haemodynamically stable induction (ketamine/etomidate where appropriate; reduce propofol dose)
    • Volatile agents reduce uterine tone; consider minimising volatile concentration and using adjuncts (opioid, ketamine, TIVA) once baby delivered; balance against need for anaesthesia depth
    • Early invasive monitoring, active warming, frequent blood gases and coagulation checks
  • Postoperative care
    • HDU/ICU if massive transfusion, ongoing vasopressors, coagulopathy, hypothermia, acidosis, or after hysterectomy
    • Analgesia: multimodal; consider TAP block/wound infiltration if coagulation acceptable; avoid neuraxial catheter removal until coagulation normal and per ASRA/RA-UK timing guidance
    • Thromboprophylaxis: high VTE risk postpartum and after haemorrhage/surgery; balance against bleeding—start when haemostasis secured

Secondary PPH (late bleeding) — anaesthetic relevance

  • Causes: retained products, endometritis, subinvolution of placental site, coagulation disorders
  • May present for EUA/ERPC; assess sepsis, anaemia, ongoing bleeding; ensure group & screen, coagulation, IV access; consider aspiration risk still increased early postpartum
You are called to a 32-year-old after vaginal delivery with ongoing heavy bleeding. Talk through your immediate management.

Structure: recognise PPH, call for help, resuscitate while facilitating haemostasis, and initiate haemostatic resuscitation early.

  • Call for help and allocate roles; activate major obstetric haemorrhage protocol; inform blood bank
  • A–E assessment; high-flow oxygen; keep warm; left lateral tilt if relevant; continuous monitoring
  • Two large-bore IV cannulae + rapid infuser; send FBC, PT/APTT, fibrinogen, group & crossmatch; ABG/VBG incl lactate and ionised calcium
  • Start uterotonics (oxytocin first-line) and give TXA 1 g IV early; request senior obstetric review for 4 Ts
  • Early blood products rather than crystalloids; consider O negative RBC if unstable; balanced components pending results/ROTEM
  • Escalate monitoring: arterial line early; urinary catheter; consider vasopressors (noradrenaline) after initial volume/blood
  • Prepare for theatre and GA if ongoing major bleeding/need for surgical control; anticipate difficult physiology and aspiration risk
List the causes of PPH and how you would differentiate them clinically.

Use the 4 Ts; clinical clues guide directed treatment.

  • Tone (atony): boggy/enlarged uterus, diffuse bleeding; responds to massage/uterotonics
  • Tissue: placenta incomplete, continued bleeding with subinvoluted uterus; ultrasound may help; consider accreta if risk factors and placenta not separating
  • Trauma: uterus firm but bleeding persists; visible tears/haematoma; consider uterine rupture (pain, shock, loss of station) or inversion (mass, shock out of proportion)
  • Thrombin: oozing from puncture sites, mucosal bleeding; abnormal coagulation/fibrinogen; consider abruption/HELLP/sepsis/AFE
What uterotonic drugs do you use in PPH and what are the key contraindications/side effects relevant to anaesthesia?
  • Oxytocin: hypotension/tachycardia if bolused; water intoxication with prolonged high-dose infusion
  • Ergometrine: contraindicated in hypertension/pre-eclampsia; can cause severe hypertension, nausea/vomiting, coronary vasospasm
  • Carboprost: contraindicated in asthma; bronchospasm, diarrhoea, fever
  • Misoprostol: pyrexia/shivering/diarrhoea
  • TXA: give early; consider repeat dose if ongoing bleeding; be mindful of seizure risk at very high doses and thrombosis risk in predisposed patients (overall benefit in PPH)
Explain why fibrinogen is important in obstetric haemorrhage and how you would replace it.
  • Fibrinogen falls early in PPH and low levels predict progression to severe haemorrhage; pregnancy baseline fibrinogen is high so a ‘normal non-pregnant’ value may be inadequate
  • Measure fibrinogen early and repeat; use ROTEM/TEG if available (e.g., low FIBTEM suggests hypofibrinogenaemia)
  • Replace with cryoprecipitate or fibrinogen concentrate per local protocol; aim fibrinogen ≥2.0 g/L (often ≥2–3 g/L in ongoing bleeding)
Describe your approach to anaesthesia for a patient with PPH requiring examination under anaesthesia and possible laparotomy.
  • Assess haemodynamic status, ongoing blood loss, and existing neuraxial block; decide early if GA likely needed
  • If unstable/major haemorrhage anticipated: GA with RSI and cuffed ETT; invasive monitoring (arterial line); active warming; rapid access to blood products
  • Induction: haemodynamically stable technique (reduce propofol; consider ketamine/etomidate); have vasopressors ready
  • Maintenance: minimise volatile if uterine atony; balance depth and uterine tone; continue haemostatic resuscitation and correct calcium/temperature
  • If stable with effective epidural/spinal and limited procedure: consider continuing neuraxial with close monitoring, but have a low threshold to convert to GA
What are the key physiological reasons PPH can deteriorate rapidly, and what are your resuscitation end-points?
  • Pregnancy: increased blood volume and cardiac output can mask early shock; once compensation fails, collapse can be sudden
  • Coagulopathy develops early (especially low fibrinogen), worsened by dilution, hypothermia, acidosis
  • End-points: improving mental state, capillary refill, HR/BP/MAP, urine output, falling lactate/base deficit, normothermia, corrected coagulation including fibrinogen and platelets, normal ionised calcium
How would you manage uterine inversion presenting with haemorrhage and shock?
  • Recognise: severe pain, haemorrhage, shock often out of proportion; uterine fundus absent abdominally, mass in vagina
  • Call for help; resuscitate; immediate manual replacement (Johnson manoeuvre) — do not delay for theatre if possible
  • Tocolysis to aid reduction (e.g., GTN) and then uterotonics after successful replacement to maintain tone
  • Prepare for GA if needed for relaxation and rapid control; treat haemorrhage with blood products and TXA
Outline an obstetric massive transfusion strategy and the complications you must anticipate.
  • Early activation; early RBC + FFP + platelets in balanced approach until results/ROTEM; early fibrinogen replacement
  • Give TXA early; monitor and correct ionised calcium; warm patient and fluids
  • Complications: hypocalcaemia, hypothermia, acidosis, hyperkalaemia, transfusion reactions, TRALI/TACO, dilutional coagulopathy, DIC, thrombosis
A woman with placenta praevia and previous caesarean is bleeding at caesarean delivery. What is your concern and how does it change your plan?
  • High suspicion for placenta accreta spectrum → risk of catastrophic haemorrhage and hysterectomy
  • Plan: senior multidisciplinary team; large-bore access, arterial line, crossmatched blood available, cell salvage, TXA, clear triggers for conversion to GA and hysterectomy
  • Avoid forcible placental removal; anticipate prolonged surgery and ICU need
Describe the anaesthetic implications of using volatile agents during management of uterine atony.
  • Volatile agents cause dose-dependent uterine relaxation and may worsen atony; consider minimising MAC and using alternative adjuncts once baby delivered
  • Balance against need for anaesthesia depth and haemodynamic stability; communicate with obstetric team about uterine tone and drug effects
Discuss the causes, recognition, and management of postpartum haemorrhage.
  • Structure answer: definition/classification → 4 Ts → recognition/quantification → immediate actions → resuscitation → uterotonics/TXA → blood products/targetsescalation to theatre/GA → postoperative care
Outline a major obstetric haemorrhage protocol and the role of viscoelastic testing.
  • Include: activation criteria, communication, pack-based delivery of RBC/FFP/platelets, early fibrinogen replacement, TXA, calcium/temperature management, lab/ROTEM triggers, deactivation and debrief
Discuss the pharmacology and contraindications of uterotonic agents used to treat PPH.
  • Oxytocin (hypotension), ergometrine (hypertension/coronary spasm), carboprost (asthma/bronchospasm), misoprostol (pyrexia), TXA (early antifibrinolytic)
Explain the pathophysiology of coagulopathy in obstetric haemorrhage and how you would treat it.
  • Early fibrinogen depletion + dilution + consumption (DIC triggers) + hypothermia/acidosis; treat with targeted components, warming, calcium, and definitive haemostasis

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