Amniotic fluid embolism

Surgical approach (obstetric team actions)

Call for help: senior obstetrician, anaesthetist, haematology, transfusion, ICU, neonatology, activate major obstetric haemorrhage (MOH) protocol
Immediate uterine management if ongoing bleeding/atony: bimanual compression, uterotonics, uterine balloon tamponade
- Escalate to surgical haemostasis: B-Lynch/compression sutures, uterine artery ligation/internal iliac ligation (selected cases)
If bleeding uncontrolled or placenta accreta spectrum suspected/confirmed: proceed to hysterectomy (damage-control approach may be required)
If maternal cardiac arrest with fetus in utero: perimortem caesarean delivery (resuscitative hysterotomy)
- Aim to start within 4 minutes of arrest and deliver by 5 minutes (improves maternal venous return and fetal outcome)

Anaesthetic management (procedural context)

Type of anaesthesia: usually requires immediate conversion to full resuscitation/GA (even if neuraxial in situ), treat as maternal collapse
- If arrest/impending arrest: RSI with cricoid, 100% O2, avoid delays to chest compressions/defibrillation
Airway: cuffed ETT preferred, SGA only as a temporary rescue if intubation delayed/failed
Duration: unpredictable, acute resuscitation minutes, but haemorrhage control and stabilisation often hours, anticipate ICU transfer
How painful: not a pain-driven condition, analgesia is secondary to oxygenation, haemodynamics, and haemostasis
Monitoring/lines: immediate A-line, large-bore IV/rapid infuser, consider central access, continuous ETCO2 (marker of perfusion/ROSC)
Vasoactive support: early noradrenaline, add adrenaline if profound shock, consider vasopressin as adjunct, inotropes for RV failure
Coagulopathy: early balanced blood products guided by viscoelastic testing (TEG/ROTEM) if available, treat DIC aggressively

Definition and epidemiology

Syndrome of sudden maternal cardiovascular collapse and/or respiratory compromise with coagulopathy occurring during labour, caesarean delivery, or within ~30 minutes postpartum (can be later)
Rare but high mortality/morbidity, incidence commonly quoted ~1–2 per 100,000 maternities (varies by definition/registry)
Often a diagnosis of exclusion, may be classified as “definite/probable/possible” depending on case definition (clinical features + timing + exclusion of alternatives)

Pathophysiology (current model)

Not a simple mechanical embolus: thought to be an anaphylactoid/inflammatory response to fetal material entering maternal circulation → pulmonary vasoconstriction, V/Q mismatch, RV failure, hypoxia
Biphasic haemodynamic pattern described: early acute pulmonary hypertension/RV failure → later LV failure/cardiogenic shock
Coagulopathy: activation/consumption of clotting factors and platelets → DIC, uterine atony and massive haemorrhage common
Triggers/risk associations (not diagnostic): induction/augmentation, operative delivery, placental abruption/previa, uterine rupture, eclampsia, advanced maternal age, multiparity

Clinical presentation

Classical triad: hypoxia + hypotension/cardiac arrest + coagulopathy/bleeding (often within minutes)
Prodromal features: dyspnoea, chest pain, agitation/confusion, sense of doom, nausea/vomiting, seizures
Signs: sudden desaturation, bronchospasm, cyanosis, hypotension, arrhythmias, PEA/asystole, later massive PPH with oozing from puncture sites
Fetal compromise: sudden fetal bradycardia/late decelerations may be first sign

Differential diagnosis of peripartum collapse (must be actively excluded)

Massive haemorrhage (atony, abruption, uterine rupture), high/total spinal, local anaesthetic systemic toxicity (LAST)
Pulmonary thromboembolism, air embolism, aspiration, anaphylaxis, sepsis
Eclampsia/ICH, MI/aortic dissection, cardiomyopathy (PPCM), magnesium toxicity

Immediate management (maternal resuscitation priorities)

Recognise maternal collapse, call for help, allocate roles, activate MOH, bring defib, airway trolley, rapid infuser, blood fridge access
A: 100% O2, early intubation/ventilation, suction, consider aspiration, maintain left uterine displacement until delivery
B: ventilate to normocapnia, consider high PEEP cautiously (RV failure risk), treat bronchospasm if present
C: follow ALS with obstetric modifications, high-quality CPR, early defibrillation if shockable, adrenaline per ALS, treat reversible causes
Haemodynamics: rapid volume resuscitation while avoiding overload, early vasopressors, consider inotropes for RV dysfunction
If arrest and pregnancy ≥20 weeks or uterus at/above umbilicus: perimortem caesarean delivery at 4 minutes if no ROSC

Coagulopathy and haemorrhage management

Send urgent labs: FBC, PT/APTT, fibrinogen, group &amp, screen/crossmatch, ABG/lactate, calcium, repeat frequently
Early tranexamic acid for PPH (e.g., 1 g IV then 1 g if bleeding continues/restarts within 24 h) unless contraindicated
Balanced transfusion: RBC + FFP + platelets, target fibrinogen aggressively (cryoprecipitate or fibrinogen concentrate per local protocol)
Correct ionised hypocalcaemia from citrate, warm patient/fluids, avoid dilutional coagulopathy
Use TEG/ROTEM if available to direct products (e.g., low FIBTEM A5 suggests fibrinogen replacement)
Uterine atony management in parallel: uterotonics, tamponade, surgery, consider interventional radiology if stable enough

Cardiorespiratory support and advanced therapies

Echo (POCUS/TOE) can be diagnostic and guide therapy: RV dilation/strain, LV dysfunction, exclude tamponade
Consider pulmonary vasodilators for severe pulmonary hypertension/RV failure (specialist decision): inhaled nitric oxide or prostacyclin
Mechanical circulatory support: ECMO (VA for cardiogenic shock/arrest, VV for refractory hypoxaemia) in selected centres, balance against bleeding/DIC
ICU care: ongoing haemodynamic monitoring, ventilation, renal support, neuroprotection post-arrest, thromboprophylaxis when safe

Investigations and diagnosis (practical FRCA angle)

Diagnosis is clinical + temporal relationship + exclusion of other causes, no single confirmatory bedside test
ABG: hypoxaemia, metabolic acidosis, raised lactate, ETCO2 may fall abruptly during collapse
Coagulation: low fibrinogen is common and can be profound, thrombocytopenia, prolonged PT/APTT in DIC
CXR: pulmonary oedema/ARDS pattern may develop, ECG: non-specific, troponin may rise in shock
“Tests” sometimes discussed (not routine/limited utility): serum tryptase (if anaphylaxis in differential), complement activation markers, fetal squames in pulmonary vessels are non-specific

Prognosis and follow-up

High maternal morbidity: hypoxic brain injury, ARDS, renal failure, massive transfusion complications, fetal outcome depends on speed of maternal resuscitation/delivery
Debriefing, incident review, documentation, counselling regarding recurrence risk (generally low but uncertain), plan for future pregnancy with high-risk obstetric/anaesthetic input

Test yourself…

You are called to labour ward: a woman becomes suddenly breathless, hypotensive and desaturates immediately after delivery. Talk through your immediate management.

Structured maternal collapse response with simultaneous resuscitation, diagnosis, and haemorrhage control.

Call for help and declare maternal collapse, activate MOH, allocate roles (airway, compressions, drugs, lines, documentation, runner)
A/B: 100% O2, airway manoeuvres, prepare RSI and intubation, ventilate, check ETCO2, consider aspiration and suction
C: obtain large-bore IV access, start vasopressor early (noradrenaline), fluid bolus judiciously, if arrest start ALS immediately
Simultaneously consider differentials: haemorrhage, high spinal, LAST, anaphylaxis, PTE/air embolus, sepsis, eclampsia, treat reversible causes
Send urgent bloods (FBC, coag, fibrinogen, ABG, calcium) and request blood products, start TXA if bleeding/PPH
Early echo/POCUS if available to guide (RV failure vs LV failure) and tailor inotropes/vasopressors

What are the key clinical features that make you suspect amniotic fluid embolism, and what else must you exclude?

Suspect AFE when there is abrupt onset of hypoxia/respiratory distress, hypotension/cardiac arrest, and coagulopathy/bleeding temporally related to labour/delivery/early postpartum
Often fetal distress occurs early (sudden bradycardia) and maternal DIC/PPH follows
Exclude: massive obstetric haemorrhage (atony/abruption/rupture), high/total spinal, LAST, anaphylaxis, pulmonary thromboembolism/air embolism, aspiration, sepsis, eclampsia/ICH, PPCM/MI/aortic dissection

Explain the pathophysiology of AFE and how it influences your haemodynamic management.

Likely an anaphylactoid/inflammatory response to fetal material → acute pulmonary vasoconstriction and pulmonary hypertension → RV failure and reduced LV preload → hypotension/collapse
Later LV dysfunction/cardiogenic shock may occur, management must be dynamic (vasopressors + inotropes guided by echo)
Avoid excessive PEEP/overdistension that worsens RV afterload, consider pulmonary vasodilators in specialist settings

How would you manage the coagulopathy associated with AFE?

Treat as DIC with massive haemorrhage: activate MOH, rapid lab assessment and frequent reassessment
Give TXA early for PPH, transfuse balanced components (RBC/FFP/platelets) and replace fibrinogen early (cryo or fibrinogen concentrate per protocol)
Use TEG/ROTEM if available, correct calcium, temperature, and acidosis, avoid dilution and maintain uterine tone/surgical haemostasis

A woman arrests on the labour ward at 36 weeks. Describe the obstetric modifications to ALS and the role of perimortem caesarean delivery.

High-quality CPR with manual left uterine displacement, early airway control and 100% oxygen, defibrillation as per standard ALS
If no ROSC rapidly, perform perimortem caesarean (resuscitative hysterotomy) aiming to start by 4 minutes and deliver by 5 minutes
Rationale: improves maternal venous return and cardiac output by relieving aortocaval compression, may improve fetal survival

You suspect AFE but the patient is profoundly hypoxic and hypotensive. What monitoring and bedside investigations will help you guide therapy in real time?

Continuous ETCO2 (perfusion/CPR quality/ROSC), invasive arterial BP, urine output, temperature, frequent ABGs including lactate and ionised calcium
POCUS/echo to assess RV size/function, LV function, volume status, and exclude tamponade, lung ultrasound for oedema/pneumothorax
Viscoelastic testing (TEG/ROTEM) to guide blood products and fibrinogen replacement

Discuss the differential diagnosis of sudden collapse shortly after neuraxial anaesthesia for caesarean section and how you would distinguish them from AFE.

High/total spinal: rapid hypotension, bradycardia, high sensory block, difficulty breathing due to motor block, usually no DIC/oozing
LAST: tinnitus/metallic taste/seizures then arrhythmias, treat with lipid emulsion, timing with local anaesthetic dosing
Anaphylaxis: bronchospasm, urticaria/angioedema, hypotension, tryptase may help later, coagulopathy not typical early
Haemorrhage: visible bleeding/uterine atony, falling Hb, shock, coagulopathy may be dilutional/consumptive later
AFE: sudden hypoxia + hypotension/collapse with early fetal distress and rapid DIC/PPH, often no preceding neuraxial warning signs

What advanced therapies might be considered in refractory AFE, and what are the limitations?

Inhaled pulmonary vasodilators (NO/prostacyclin) for severe pulmonary hypertension/RV failure, requires expertise and monitoring
ECMO (VA for shock/arrest, VV for refractory hypoxaemia) in appropriate centres, major limitation is bleeding risk in DIC and need for anticoagulation
Massive transfusion and damage-control surgery may be required, early ICU involvement is essential

Outline your management of sudden maternal collapse on the labour ward.

Commonly examined as an A–E + obstetric-specific ALS answer with parallel MOH activation and perimortem delivery decision-making.

Immediate actions: call for help, emergency buzzer, bring defib/airway kit, allocate roles, document times, consider reversible causes (4 Hs/4 Ts plus obstetric causes)
A/B: 100% O2, intubate early, ventilate, confirm with capnography, treat bronchospasm, consider aspiration
C: ALS algorithm, IV/IO access, vasopressors, bloods, activate MOH, TXA if bleeding, correct calcium/temperature
Obstetric modifications: left uterine displacement, perimortem caesarean if ≥20 weeks and no ROSC by 4 minutes
Post-ROSC: ICU transfer, targeted temperature management as per local policy, ongoing haemorrhage control, neuroprognostication later

Discuss the causes of coagulopathy in obstetrics and how you would manage DIC in a bleeding parturient.

Causes: placental abruption, severe pre-eclampsia/HELLP, sepsis, retained dead fetus, AFE, massive haemorrhage/dilution, acute fatty liver of pregnancy
Management: treat cause + haemostatic resuscitation (RBC/FFP/platelets) + early fibrinogen replacement, TXA for PPH, viscoelastic-guided therapy where available
Supportive: warming, calcium, correct acidosis, maintain uterine tone and surgical haemostasis, ICU involvement

Describe the anaesthetic considerations for perimortem caesarean delivery.

Priority is maternal resuscitation, procedure is performed where arrest occurs, do not delay for transfer to theatre
Airway: RSI with cuffed ETT if feasible without interrupting compressions, otherwise continue BVM/SGA as bridge
Circulation: ongoing ALS, anticipate massive haemorrhage, MOH activation, rapid infuser, vasopressors, correct coagulopathy
After delivery: expect improved venous return/CPR efficacy, continue resuscitation, neonatal team receives baby