Amniotic Fluid Embolus (AFE)
Rare, catastrophic obstetric emergency. Sudden cardiovascular collapse, hypoxia, and coagulopathy during labour or shortly postpartum.
Peri-partum collapse
Hypoxia + hypotension + DIC
Diagnosis of exclusion
Resuscitate first, label later
ED / Labour Ward Priorities
Overview
Key concept: Amniotic Fluid Embolus (AFE) is an anaphylactoid syndrome of pregnancy, not a classic embolus. It
presents with sudden hypoxia, hypotension or cardiac arrest, and rapidly evolving coagulopathy in association with labour,
delivery, or uterine procedures.
- AFE is rare but one of the leading causes of sudden maternal collapse in labour or immediately postpartum.
- Clinical diagnosis – there is no rapid test. Exclude more common causes (haemorrhage, PE, anaphylaxis, eclampsia, sepsis).
- Management is supportive: high-quality resuscitation, ventilation, vasopressors, and aggressive correction of DIC.
- Requires immediate multidisciplinary response (ED, obstetrics, anaesthetics, ICU, blood bank).
Algorithm for Sudden Peri-partum Collapse
Flow- Call for help early – activate obstetric emergency / code blue. Ensure airway, breathing, circulation.
- If no pulse → start CPR with manual uterine displacement. Attach monitors (ECG, SpO₂, NIBP).
- Provide high-flow oxygen; secure airway early (rapid sequence intubation) if not in arrest.
- Large-bore IV/IO access; start fluid resuscitation and vasopressors for hypotension as per shock protocols.
- Simultaneously consider differential: haemorrhage, eclampsia, PE, anaphylaxis, sepsis, cardiomyopathy.
- If cardiac arrest and pregnancy ≥ 20–24 weeks → perimortem caesarean section within 4–5 minutes of arrest.
- Send urgent bloods: FBC, coag profile, fibrinogen, ABG, lactate, cross-match, LFT/U&E.
- Recognise AFE pattern: sudden hypoxia + hypotension/collapse + bleeding/DIC in temporal relationship to labour/delivery/uterine procedure.
- Commence massive transfusion protocol if ongoing bleeding and coagulopathy.
Foundations
Pathophysiology & Risk FactorsPathophysiology
- Entry of amniotic fluid, fetal cells or other debris into maternal circulation.
- Triggers a massive inflammatory / anaphylactoid response with pulmonary vasospasm and right heart failure.
- Release of mediators (histamine, leukotrienes, endothelin, complement) → acute pulmonary hypertension, hypoxia, myocardial depression.
- Secondary phase: profound coagulopathy and DIC, leading to severe obstetric haemorrhage.
When & Where It Occurs
- Typically during labour or within minutes–hours after delivery (vaginal or C-section).
- Can occur with:
- Induction/augmentation of labour.
- Instrumentation, manual removal of placenta.
- Uterine trauma or rupture.
- Second–third trimester terminations or miscarriages.
- Invasive procedures (e.g. amniocentesis).
- Risk factors may include multiparity, advanced maternal age, placenta praevia/accreta, abruptio placentae – but AFE can occur in women with no risk factors.
Clinical Features
PresentationClassic description: two-phase presentation – first cardiopulmonary collapse, then haemorrhagic phase with DIC.
- Phase 1 – Cardiopulmonary:
- Sudden onset dyspnoea, chest tightness, sense of impending doom.
- Rapid hypoxia: cyanosis, low SpO₂ despite oxygen.
- Tachycardia, hypotension, arrhythmias, pulmonary oedema.
- Seizures or altered consciousness; up to 20% present primarily with a seizure.
- Cardiac arrest can be the first sign.
- Phase 2 – Haemorrhagic / DIC:
- Massive uterine bleeding and/or bleeding from IV sites, wounds, mucosa.
- Laboratory evidence of consumptive coagulopathy (prolonged PT/aPTT, low fibrinogen, thrombocytopenia).
- Uterine atony and postpartum haemorrhage.
Think AFE if: sudden hypoxia + hypotension or arrest + coagulopathy/bleeding in a peripartum patient with no other obvious cause.
Differential Diagnosis
Don’t MissAFE is a diagnosis of exclusion – rule out:
- Massive obstetric haemorrhage (e.g. uterine atony, placenta accreta, uterine rupture).
- Pulmonary embolism (thromboembolic).
- High spinal / epidural block, local anaesthetic toxicity.
- Drug-induced anaphylaxis (e.g. antibiotics, oxytocin, anaesthetic agents).
- Septic shock (chorioamnionitis, puerperal sepsis).
- Eclampsia / severe pre-eclampsia (hypertension, proteinuria, seizures).
- Peripartum cardiomyopathy, myocardial infarction, air embolism.
Investigations
SupportDo not delay resuscitation for investigations. Send targeted tests once ABC is underway.
- ABG: severe hypoxia, respiratory/metabolic acidosis, raised lactate.
- FBC: anaemia from bleeding, thrombocytopenia.
- Coagulation profile & fibrinogen: prolonged PT/INR, aPTT, low fibrinogen consistent with DIC.
- Cross-match and prepare blood products (RBCs, FFP, cryoprecipitate, platelets).
- U&E, LFTs: assess organ dysfunction.
- ECG & CXR: evaluate for pulmonary oedema, other cardiac causes.
- Point-of-care echo (if available) may show acute right ventricular strain or global dysfunction.
Definitive diagnosis is often made post-mortem (fetal squames/debris in pulmonary circulation). In practice, we treat presumptively based on the clinical syndrome.
Management
Emergency
Principles: aggressive resuscitation (ACLS), optimise oxygen delivery, support the failing heart, and
correct coagulopathy/haemorrhage while obstetric team manages delivery and uterine bleeding.
Airway & Breathing
- High-flow oxygen via non-rebreather mask initially.
- Early intubation and mechanical ventilation for severe hypoxia, respiratory distress or decreased level of consciousness.
- Consider PEEP for pulmonary oedema; titrate to SpO₂ and haemodynamics.
Circulation
- Rapid IV fluid resuscitation, balanced crystalloids initially.
- Vasopressors (e.g. noradrenaline) for persistent hypotension after fluids.
- Inotropes may be required for myocardial dysfunction (guided by echo/ICU team).
- Continuous monitoring: invasive arterial line and central access if feasible and not delaying resus.
Haemorrhage & Coagulopathy
- Activate massive transfusion protocol early if bleeding and coagulopathy are evident.
- Administer:
- Packed red cells to maintain adequate Hb and oxygen carrying capacity.
- Fresh frozen plasma for clotting factors.
- Cryoprecipitate or fibrinogen concentrate to correct low fibrinogen.
- Platelets if thrombocytopenic or heavy bleeding.
- Coordinate closely with laboratory/blood bank; repeat coagulation studies and fibrinogen levels.
Obstetric Management
- Continuous involvement of obstetric and anaesthetic teams.
- Uterine atony and postpartum haemorrhage require:
- Uterine massage, uterotonics (e.g. oxytocin, misoprostol; avoid ergometrine if severe hypertension).
- Mechanical methods (balloon tamponade), surgical haemostasis if required.
- Perimortem C-section if cardiac arrest and pregnancy ≥ 20–24 weeks – improves both maternal and neonatal outcomes.
Post-resuscitation Care
- All survivors require ICU admission for ongoing respiratory, cardiovascular and coagulation support.
- Monitor urine output (indwelling catheter) and organ function carefully.
Disposition & Family Communication
Support- Any suspected or confirmed AFE → ICU level care if the patient survives initial resuscitation.
- Ensure thorough documentation of:
- Timeline of events (onset of symptoms, delivery time, arrest and resuscitation details).
- Vitals, interventions, drugs and blood products given.
- Discussions with obstetric, anaesthetic, ICU and blood bank teams.
Family communication: AFE is sudden and often devastating. Provide clear explanations in simple language,
acknowledge uncertainty, and ensure early psychological and bereavement support where needed.
Treat first, diagnose later
Early team activation
Think DIC & massive haemorrhage
ICU for all survivors