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Amniotic Fluid Embolism (AFE)

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Pathophysiology

1. Phase 1 — Acute right ventricular failure from pulmonary vasospasm/hypertension → hypoxia → cardiac arrest
2. Phase 2 — Left ventricular failure (myocardial depression, likely immune-mediated)
3. Phase 3 — Coagulopathy (DIC) — the classic triad is not always sequential; DIC may dominate the presentation

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Differential Diagnosis

Diagnostic criteria (Society for MFM/SMFM, 2016): Sudden cardiovascular collapse or arrest, respiratory distress, coagulopathy or clinical DIC, all in the absence of any other explainable cause during labor, C-section, or within 30 min postpartum.

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ACLS in the Pregnant Patient (AFE Context)

Anatomical & Physiological Modifications

Algorithm — Maternal Cardiac Arrest (AHA 2020)

1. Call for help — Activate maternal cardiac arrest team (OB, neonatology, anesthesia, nursing)
2. Airway — Early intubation (RSI); 100% O₂
3. Circulation
   • Standard BLS/ACLS chest compressions at full depth
   • Left uterine displacement maintained throughout
   • IV/IO access above the diaphragm (femoral access less effective due to IVC compression)
4. Defibrillation — Use standard energy levels; safe in pregnancy; remove fetal monitors
5. Medications — Standard ACLS doses of epinephrine, amiodarone (no dose adjustment)
   • Avoid vasopressin (uterotonic effect, though not absolutely contraindicated)
   • Magnesium toxicity → calcium gluconate/chloride antidote
6. Perimortem Cesarean Delivery (PMCD)
   • Begin at 4 minutes of cardiac arrest if no ROSC
   • Deliver by 5 minutes ("4-and-5 rule")
   • Improves maternal venous return by relieving aortocaval compression
   • Perform at the site of arrest — do NOT transport to OR
   • Gestational age ≥20 weeks (uterus at umbilicus level)
   • No need for anesthesia or sterile prep in active arrest

AFE-Specific Resuscitation Targets

• Vasopressors: Norepinephrine preferred; phenylephrine for vasodilation without bradycardia
• RV failure: Avoid excessive fluids (worsen RV dilation); consider inhaled NO, prostacyclins, or sildenafil for pulmonary hypertension
• ECMO (VA-ECMO): Increasingly used for refractory AFE cardiac arrest — consider early activation if available
• Atropine/glucagon if bradycardia from anaphylactoid response

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Management of AFE

Immediate (Minutes)

• A — Secure airway immediately; RSI, mechanical ventilation
• B — 100% FiO₂; target SpO₂ >95%
• C — Large-bore IV ×2, arterial line, central access; resuscitate with vasopressors (norepinephrine first-line)
• Call for help — OB, ICU, anesthesia, hematology, blood bank

Hemodynamic Support

Coagulopathy (DIC) — Critical Component

• Activate massive transfusion protocol (MTP)
• Targets: Fibrinogen >2 g/L (give cryoprecipitate or fibrinogen concentrate early — fibrinogen is the rate-limiting factor)
• Tranexamic acid (TXA) 1g IV stat (per WHO/WOMAN trial — reduces hemorrhagic death)
• pRBC : FFP : Platelets = 1:1:1 ratio
• Thromboelastography (TEG/ROTEM) to guide component therapy
• Recombinant FVIIa (rFVIIa) as rescue therapy for refractory hemorrhage (Management of Severe Peri-Operative Bleeding, p. 49)
• PCC (prothrombin complex concentrate) may reduce FFP requirement

Uterine Atony

• Oxytocin, ergometrine, carboprost, misoprostol
• Intrauterine balloon tamponade (Bakri balloon)
• B-Lynch suture / uterine compression sutures
• Uterine artery embolization (if stable enough)
• Hysterectomy as last resort (peripartum hysterectomy)

Adjuncts (Evidence Emerging)

• Ondansetron + atropine + ketorolac — "A-OK" protocol (anecdotal reports)
• Hydrocortisone (immune modulation)
• Plasma exchange — case reports of benefit

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Cardiovascular Involvement & Shunts in AFE

Cardiovascular Pathophysiology in AFE

• Amniotic fluid triggers pulmonary vasoconstriction → acute pulmonary hypertension
• RV pressure overloads → RV dilation → D-septum shift → interventricular septal deviation (impairs LV filling)
• Mechanism: endothelin, thromboxane A₂, leukotrienes released from fetal material
• TEE/TTE: dilated RV, flattened/D-shaped septum, TR, elevated RVSP

• Myocardial depression (direct inflammatory mediator toxicity)
• LV dysfunction may outlast the initial insult
• Pulmonary edema from elevated LVEDP

Cardiac Shunts in AFE

• Prevalence: ~25–30% of general population
• In AFE: acute RV pressure elevation exceeds LA pressure → right-to-left shunt through PFO → paradoxical embolism of amniotic debris/thrombus directly into systemic circulation
• Clinical consequences:
  • Worsening hypoxemia refractory to high FiO₂ (hallmark of right-to-left shunt)
  • Systemic embolism — stroke, coronary artery embolism → MI
  • Consider TEE to identify PFO when unexplained refractory hypoxia is present

• Pre-existing ASD — similar R→L shunting during RV pressure crisis
• VSD — can cause bidirectional shunting under elevated pulmonary pressures
• Eisenmenger syndrome (pre-existing) — AFE in a patient with Eisenmenger is catastrophic (near-100% mortality); fixed pulmonary hypertension + systemic vasodilation = irreversible circulatory collapse

Echo Findings in AFE

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Post-Operative / Post-Arrest Considerations

ICU Monitoring

• Arterial line, CVC, urinary catheter mandatory
• Consider PAC (pulmonary artery catheter) or serial echo to guide hemodynamics
• Continuous ECG monitoring

Respiratory

• Protective lung ventilation: Vt 6 mL/kg IBW, PEEP 5–8 cmH₂O, plateau pressure <30 cmH₂O
• Target SpO₂ ≥95%; wean FiO₂ as tolerated
• Prone positioning if ARDS develops (PaO₂/FiO₂ <150)

Cardiovascular

• Serial echocardiography to track RV and LV recovery
• Wean vasopressors/inotropes guided by echo + hemodynamics
• If PFO confirmed with significant shunting → consider percutaneous closure (after stabilization)
• Monitor for arrhythmias (atrial flutter/fibrillation common after RV stress)

Hematological

• Serial CBC, fibrinogen, PT/aPTT, TEG/ROTEM q4–6h until coagulopathy resolves
• Fibrinogen target >2 g/L; platelets >50 ×10⁹/L (>100 if surgical)
• Watch for HIT if heparin used during ECMO
• Transition to therapeutic anticoagulation once coagulopathy resolved (if mechanical valve, VTE, or ECMO circuit)

Neurological

• Post-cardiac arrest care if ROSC achieved:
  • Targeted temperature management (TTM): 32–36°C for 24h (individualize — some data in obstetric arrest is limited)
  • Continuous EEG if unconscious to detect subclinical seizures
  • MRI brain when stable to assess anoxic injury
• Assess for stroke (paradoxical embolism via PFO)

Renal

• Acute tubular necrosis from hypoperfusion is common
• Monitor creatinine, urine output hourly
• Early nephrology input; RRT if needed

Obstetric/Surgical

• If uterus preserved: monitor for secondary PPH, uterine atony, infection
• If hysterectomy performed: wound care, VTE prophylaxis once coagulopathy resolved
• DVT/PE prophylaxis: mechanical compression immediately; LMWH when hemostasis assured (typically 12–24h post-op if no ongoing coagulopathy)

Psychological

• AFE survivors face PTSD, grief (neonatal loss, hysterectomy, near-death)
• Multidisciplinary support: psychology, social work, chaplaincy
• Perinatal bereavement support if fetal/neonatal loss
• Inform patient about the AFE Foundation registry

Prognosis

• Mortality: historically 60–80%; modern series 20–40% with aggressive management
• Neurological impairment in survivors: ~85% if cardiac arrest occurred
• Recurrence in subsequent pregnancies: not documented (thought to be a one-time immune event)

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Key Take-Home Points:

• AFE = diagnosis of exclusion; DIC + cardiovascular collapse in peripartum period
• PMCD at 4 min of arrest, deliver by 5 min — do not delay, do not transport
• RV failure is the initial killer; LV failure and DIC follow
• PFO is the critical shunt — R→L flow under elevated RV pressure causes paradoxical embolism and refractory hypoxemia
• Fibrinogen is the rate-limiting coagulation factor — replace early and aggressively
• VA-ECMO is a rescue option for refractory AFE arrest