🌪️ Amniotic Fluid Embolism (AFE)

🔷 INTRODUCTION

Amniotic Fluid Embolism (AFE) is a rare but catastrophic obstetric emergency, characterized by sudden cardiovascular collapse, respiratory failure, and coagulopathy, often occurring during labor, delivery, or immediately postpartum.

Though once thought to result from mechanical obstruction by amniotic fluid, current understanding recognizes it as a disseminated anaphylactoid-like response, triggered by amniotic fluid components entering maternal circulation.

🧠 Incidence: 1 in 15,000 to 1 in 40,000 deliveries
💀 Mortality: 11–44% (maternal), ~30% (fetal)
🆘 One of the leading causes of maternal death in developed countries

🔷 PATHOPHYSIOLOGY

AFE is believed to occur in 2 phases:

🔹 Phase 1 – Acute Pulmonary Vasospasm

  • Amniotic fluid or fetal antigens enter maternal circulation (e.g., via uterine veins).
  • Pulmonary vasoconstriction acute right heart failure cardiac output
  • Hypoxia and cyanosis appear rapidly
  • Reflex pulmonary hypertension causes left heart failure secondarily

🔹 Phase 2 – Hemorrhagic Phase

  • Systemic inflammatory response Cytokine storm, complement activation
  • Disseminated Intravascular Coagulation (DIC)
  • Massive hemorrhage (uterine atony, oozing from all puncture sites)

🔬 Key Triggers:

  • Amniotic fluid components: squamous cells, lanugo, bile salts, meconium, prostaglandins
  • Strong immunological response: like anaphylaxis or septic shock

🔷 RISK FACTORS

Maternal

Obstetric

Advanced age

Cesarean section

Multiparity

Instrumental delivery

Obesity

Uterine rupture

Cardiovascular disease

Placenta previa/accreta

Eclampsia or preeclampsia

Induction of labor

Chorioamnionitis

Polyhydramnios

Trauma

Amnioinfusion

🧠 Note: AFE can still occur in absence of any identifiable risk factors.

🔷 CLINICAL FEATURES

🩸 Classic Triad

  1. Sudden hypoxia
  2. Hypotension Cardiovascular collapse
  3. DIC and coagulopathy

⏱️ Typical Onset

  • During labor
  • Immediately after delivery
  • During cesarean or second stage of labor
  • Within 30 minutes postpartum

🚨 Detailed Presentation

  • Sudden dyspnea, cyanosis
  • Seizures or agitation
  • Pulmonary edema
  • Cardiac arrest (PEA/asystole)
  • Bleeding from IV sites, uterus
  • Fetal bradycardia or death in utero

🧠 AFE mimics anaphylaxis, massive PE, eclampsia, sepsis — must be diagnosed clinically (diagnosis of exclusion).

🔷 INVESTIGATIONS

Supporting Investigations (Non-specific)

  • ABG: Severe hypoxemia, metabolic acidosis
  • ECG: Right heart strain
  • CXR: Pulmonary edema
  • Coagulation profile: Low fibrinogen, prolonged PT/aPTT, platelets
  • Serum tryptase (mast cell degranulation)
  • Pulmonary artery catheter: PA pressures, cardiac output

🧬 Postmortem or pathology: Fetal squames in maternal pulmonary vasculature
🧠 But note: fetal debris may also be found in normal deliveries – not diagnostic.

Condition

Differentiating Feature

Pulmonary embolism

No coagulopathy, often postpartum

Eclampsia

Hypertension, proteinuria, seizure history

Anaphylaxis

History of allergen exposure

Septic shock

Fever, leukocytosis

Uterine rupture

Abdominal pain, abnormal fetal tracing

🔷 MANAGEMENT – ANESTHETIC & CRITICAL CARE

📍Immediate Goals:

  • Support oxygenation & ventilation
  • Maintain hemodynamics
  • Control coagulopathy
  • Ensure fetal survival

🔹 Step-wise Management (ACLS modified for pregnancy)

🛌 Positioning

  • Left uterine displacement (prevent aortocaval compression)

💉 Airway and Breathing

  • 100% O₂ by mask Intubate early
  • Mechanical ventilation with PEEP
  • Correct hypoxia and respiratory acidosis

❤️ Circulation

  • Immediate CPR if cardiac arrest
  • Avoid delay in perimortem cesarean if no ROSC in 4 minutes
  • Volume resuscitation (crystalloids + blood products)
  • Vasopressors (norepinephrine, phenylephrine), inotropes (dobutamine)

🧬 Coagulopathy Management

  • Treat DIC aggressively:
    • FFP
    • Platelets
    • Cryoprecipitate
    • Tranexamic acid (early use)
  • Uterine massage and uterotonics for atony
  • Consider Recombinant Factor VIIa or fibrinogen concentrate if available

🧠 Neurological Support

  • Control seizures with magnesium sulfate
  • Monitor for cerebral hypoxia, seizures, encephalopathy

🔷 OBSTETRIC CONSIDERATIONS

  • Immediate delivery if fetal distress or maternal cardiac arrest
  • Perimortem Cesarean Section:
    • If maternal arrest persists beyond 4 min
    • Goal: Deliver fetus 
  • Hysterectomy may be life-saving if uterine atony continues

🔷 POST-ACUTE CARE

  • ICU care mandatory
  • Neurological assessment
  • Ventilator weaning
  • Psychosocial support
  • Family counseling
  • Monitor for multiorgan dysfunction

🔷 MCQ PEARLS

Question

Answer

Triad of AFE?

Hypoxia, hypotension, DIC

Definitive diagnostic test?

None (clinical diagnosis)

Immediate management?

ABCs + Left lateral tilt + early intubation

Commonest time of onset?

During or shortly after delivery

AFE is mediated by?

Anaphylactoid reaction to fetal antigens

Role of amniotic fluid components in pathogenesis?

Trigger SIRS-like cascade