Amniotic Fluid Embolus

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

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.

Algorithm for Sudden Peri-partum Collapse

  1. Call for help early – activate obstetric emergency / code blue. Ensure airway, breathing, circulation.
  2. If no pulse → start CPR with manual uterine displacement. Attach monitors (ECG, SpO₂, NIBP).
  3. Provide high-flow oxygen; secure airway early (rapid sequence intubation) if not in arrest.
  4. Large-bore IV/IO access; start fluid resuscitation and vasopressors for hypotension as per shock protocols.
  5. Simultaneously consider differential: haemorrhage, eclampsia, PE, anaphylaxis, sepsis, cardiomyopathy.
  6. If cardiac arrest and pregnancy ≥ 20–24 weeks → perimortem caesarean section within 4–5 minutes of arrest.
  7. Send urgent bloods: FBC, coag profile, fibrinogen, ABG, lactate, cross-match, LFT/U&E.
  8. Recognise AFE pattern: sudden hypoxia + hypotension/collapse + bleeding/DIC in temporal relationship to labour/delivery/uterine procedure.
  9. Commence massive transfusion protocol if ongoing bleeding and coagulopathy.

Foundations

Pathophysiology

  • 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

Classic description: two-phase presentation – first cardiopulmonary collapse, then haemorrhagic phase with DIC.

Think AFE if: sudden hypoxia + hypotension or arrest + coagulopathy/bleeding in a peripartum patient with no other obvious cause.

Differential Diagnosis

AFE is a diagnosis of exclusion – rule out:

Investigations

Do not delay resuscitation for investigations. Send targeted tests once ABC is underway.

Definitive diagnosis is often made post-mortem (fetal squames/debris in pulmonary circulation). In practice, we treat presumptively based on the clinical syndrome.

Management

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

Circulation

Haemorrhage & Coagulopathy

Obstetric Management

Post-resuscitation Care

Disposition & Family Communication

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