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EMERGENCY

Amniotic Fluid Embolism (AFE)

High EvidenceUpdated: 2025-12-24

On This Page

Red Flags

  • Sudden Cardiorespiratory Collapse
  • Unexplained Seizure
  • Profound Hypoxia (Cyanosis)
  • Coagulopathy (Bleeding from IV sites)
Overview

Amniotic Fluid Embolism (AFE)

1. Clinical Overview

Summary

Amniotic Fluid Embolism (AFE) is a rare but catastrophic obstetric emergency involving the entry of amniotic fluid (laden with fetal cells, hair, vernix) into the maternal circulation. This triggers a massive biphasic anaphylactoid reaction leadng to rapid cardiorespiratory collapse and Disseminated Intravascular Coagulation (DIC). It remains a leading direct cause of maternal death in the developed world. Diagnosis is clinical and often one of exclusion. [1,2]

Key Facts

  • Mechanism: The pathophysiology is Immune-mediated, not obstructive. Fetal antigens trigger:
    1. Phase 1: Pulmonary Vasospasm (Severe Pulmonary Hypertension) -> RV Failure -> Hypoxia.
    2. Phase 2: LV Failure (Myocardial suppression) + DIC (Consumptive Coagulopathy).
  • Timing: 70% occur during labour, 19% during C-section, 11% postpartum.
  • Mortality: Historically 60-80%, now 13-30% with modern ICU care, but neurological morbidity in survivors is high.

Clinical Pearls

The "Sense of Doom": Premonitory symptoms appear in 50% of cases up to 4 hours before collapse. Agitation, confusion, "I feel like I'm going to die", or tingling fingers. TAKE THIS SERIOUSLY.

Resuscitative Hysterotomy: (Perimortem C-Section). If maternal cardiac arrest occurs, you must deliver the baby within 5 minutes. This is primarily to save the Mother (empty uterus = no aortocaval compression = effective CPR).

Atypical Presentation: Not all collapse. Some present purely as massive haemorrhage (DIC) with no obvious cause (Atony/Trauma excluded). Suspect AFE in unexplained resistant coagulopathy.

2. Epidemiology

Incidence

  • 1 in 20,000 to 1 in 40,000 deliveries.
  • Unpredictable and unpreventable.

Risk Factors

  • Placenta Praevia / Abruption.
  • Induction of Labour.
  • Multiple Pregnancy.
  • Maternal Age > 35.
  • Eclampsia.
  • Note: Can occur in completely low-risk spontaneous labour.
3. Pathophysiology

The "Anaphylactoid" Reaction

  1. Breach: Fluid enters uterine veins via endocervical veins or placental site.
  2. Pulmonary Hit: Vasoconstriction + V/Q Mismatch -> Hypoxia (Sats less than 80%).
  3. Cardiac Hit: RV Failure (Acute Cor Pulmonale) -> Septum pushes left -> LV Failure -> Hypotension.
  4. Haematological Hit: Thromboplastin-like effect of amniotic fluid -> Consumes factors -> DIC.
4. Clinical Presentation

Classic Triad

  1. Acute Hypoxia: Dyspnoea, Cyanosis, Gasping.
  2. Hypotension: Collapse, Cardiac Arrest (PEA common).
  3. Coagulopathy: Following within 30 mins. Oozing from puncture sites, gums, uterus.

Differential Diagnosis

Pulmonary Embolism (PE)
Usually no immediate DIC.
Eclampsia
Seizure, but high BP (AFE has low BP).
Uterine Rupture
Pain, loss of contractions.
Sepsis
Slower onset.
Total Spinal Block
If regional anaesthesia used.
5. Clinical Examination
  • General: Cyanosed, grey, unconscious.
  • Vitals: Tachycardia, Hypotension, Desaturation.
  • Uterus: May be hypertonic or atonic.
  • Sites: Check IV lines/Catheter for blood (DIC).
6. Investigations

Bedside

  • ABG: Profound Hypoxia. Acidosis.
  • ECG: RV Strain (S1Q3T3), Tachycardia.

Lab (Stat)

  • FBC: Low Platelets.
  • Coagulation: Prolonged PT/APTT, Low Fibrinogen (less than 1.5 g/L is critical), High D-Dimer.
  • Tryptase: Sometimes elevated (confirms anaphylactoid nature) but normal does not exclude.

Imaging

  • CXR: Pulmonary Oedema (ARDS picture).
  • Echo (TOE): Acute RV dilation, Septal bowing.
7. Management

Management Algorithm

           MATERNAL COLLAPSE
     (Hypoxia + Hypotension + Fetal Distress)
                    ↓
          CALL FOR HELP (2222)
(Obstetrician, Anaesthetist, ODP, Paeds, Haematology)
                    ↓
           START CPR (ABCDE)
  - Left Lateral Tilt (15 degrees)
  - 100% Oxygen / Intubate early
  - IV Access x2 (Grey/Orange)
                    ↓
        IS UTERUS GRAVID? (>20w)
          ↓                  ↓
         YES                 NO
          ↓                  ↓
    PERIMORTEM        CONTINUE ALS
    C-SECTION         Treat reversible causes
  (Start by 4m)
  (Baby out by 5m)
                    ↓
        MANAGE COAGULOPATHY (DIC)
  - Massive Haemorrhage Protocol
  - Fibrinogen Concentrate / Cryoprecipitate
  - Tranexamic Acid
  - Platelets / FFP / RBCs (1:1:1 ratio)
                    ↓
          INTENSIVE CARE
  - Vasopressors (Noradrenaline/Vasopressin)
  - Ventilatory Support
  - Echocardiography

1. Resuscitation (A-B-C)

  • Airway: Secure early (Intubation). Aspiration risk is high.
  • Breathing: 100% Oxygen.
  • Circulation:
    • High quality chest compressions.
    • Left Lateral Tilt (manual displacement of uterus) is mandatory to relieve IVC compression.
    • Recombinant Factor VIIa: Considered in intractable bleeding (last resort due to thrombosis risk).

2. Surgical

  • Perimortem C-Section:
    • Do not move to theatre. Do it where you are.
    • No anaesthesia needed if cardiac arrest.
    • Emptying uterus improves venous return by 60-80%.
  • Hysterectomy: May be needed to control uterine bleeding if atony/DIC persists.

3. Supportive

  • ECMO: Extracorporeal Membrane Oxygenation may be life-saving for reversible heart/lung failure.
8. Complications
  • Maternal: Anoxic Brain Injury. Multi-organ failure (Renal/Hepatic). Sheehan's Syndrome.
  • Fetal: Hypoxic Ischaemic Encephalopathy (HIE). Cerebral palsy. Death.
9. Prognosis and Outcomes
  • Current survival ~70-80% (improved from historic lows).
  • Neurological intact survival is lower (~50% of survivors have deficits).
  • Recurrence: Unknown. Most are advised against future pregnancy.
10. Evidence and Guidelines

Key Guidelines

GuidelineOrganisationKey Recommendations
Maternal CollapseRCOG GTG 56 (2011)Algorithm for collapse. Hysterotomy timing (4 mins).
AFESMFM (USA)Diagnostic criteria: Hypotension + Hypoxia + Coagulopathy + Onset during/30min post labour.

Landmark Data

1. UKOSS (UK Obstetric Surveillance System)

  • AFE Incidence: 2.0 per 100,000 maternities.
  • Mortality: 19% case fatality.
  • Key learning: Early recognition and aggressive correction of coagulopathy improves survival.
11. Patient and Layperson Explanation

What is Amniotic Fluid Embolism?

It is a very rare emergency where some of the fluid surrounding the baby enters the mother's bloodstream.

Why is it dangerous?

It's not just that the fluid "blocks" a vessel. It triggers a massive allergic-like reaction in the mother. Her blood vessels clamp down (stopping blood flow to the lungs), her heart struggles to pump, and her blood loses the ability to clot.

Did the doctors do something wrong?

No. AFE is unpredictable and unpreventable. It can happen in completely normal labours.

What is the treatment?

The medical team rushes to support her heart and lungs (CPR, ventilators) and gives lots of blood products to fix the clotting. Sometimes, the baby must be delivered immediately (even if the mother's heart has stopped) to help the mother's heart restart.

12. References

Primary Sources

  1. RCOG Green-top Guideline No. 56. Maternal Collapse in Pregnancy and the Puerperium. 2011.
  2. Fitzpatrick KE, et al. Incidence, risk factors, management and outcomes of amniotic-fluid embolism. Lancet. 2016.
  3. Society for Maternal-Fetal Medicine (SMFM). Diagnosis and management of amniotic fluid embolism. 2016.
13. Examination Focus

Common Exam Questions

  1. Diagnosis: "Collapse + Coagulopathy during labour?"
    • Answer: AFE.
  2. Resuscitation: "Time limit for Perimortem C-Section?"
    • Answer: Start at 4 mins, Delivery by 5 mins.
  3. Pathology: "Mechanism of hypoxia?"
    • Answer: Pulmonary Vasospasm / VQ Mismatch.
  4. Investigations: "Diagnostic blood test?"
    • Answer: None. (Tryptase is supportive only, Serum Sialyl Tn antigen is experimental).

Viva Points

  • Fetal Squames: Finding fetal cells in the maternal pulmonary artery (at autopsy or aspirate) is NOT diagnostic. Fetal cells are found in normal women too. The diagnosis is the reaction, not the presence of cells.
  • Factor VIIa: Used off-label for "uncontrollable haemorrhage" in AFE. Costs £3000-5000 a dose.

Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.

Last updated: 2025-12-24

At a Glance

EvidenceHigh
Last Updated2025-12-24
Emergency Protocol

Red Flags

  • Sudden Cardiorespiratory Collapse
  • Unexplained Seizure
  • Profound Hypoxia (Cyanosis)
  • Coagulopathy (Bleeding from IV sites)

Clinical Pearls

  • **The "Sense of Doom"**: Premonitory symptoms appear in 50% of cases up to 4 hours before collapse. Agitation, confusion, "I feel like I'm going to die", or tingling fingers. TAKE THIS SERIOUSLY.
  • **Atypical Presentation**: Not all collapse. Some present purely as massive haemorrhage (DIC) with no obvious cause (Atony/Trauma excluded). Suspect AFE in unexplained resistant coagulopathy.
  • Hypoxia (Sats less than 80%).

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines