What is the immediate management for a postpartum patient with embolic fluid embolism complicated by massive postpartum hemorrhage, severe hypotension, and Disseminated Intravascular Coagulation (DIC)?

Case Presentation: Amniotic Fluid Embolism with Massive Postpartum Hemorrhage

Patient Demographics and Presentation

A 28-year-old G2P1 at 39 weeks and 2 days gestation presented for labor induction. 1

• Initial cervical status: Unfavorable cervix (specific dilation not documented)
• Induction method: Oxytocin infusion with concurrent cervical ripening balloon placement
• Labor course: Balloon expelled after 10 hours, patient transferred to labor and delivery room
• Delivery: Successful vaginal delivery achieved

Immediate Postpartum Complications

Within minutes of delivery, the patient experienced sudden cardiovascular collapse characterized by the classic triad of amniotic fluid embolism: 1

• Severe hypotension with hemodynamic instability
• Acute hypoxia with respiratory distress
• Massive postpartum hemorrhage with rapid progression to disseminated intravascular coagulation (DIC)

Clinical Diagnosis

Amniotic fluid embolism was diagnosed clinically based on the sudden onset of cardiorespiratory collapse and coagulopathy in the immediate postpartum period, after excluding other causes. 1 The diagnosis remains clinical as no specific laboratory test can confirm or refute AFE. 1

Pathophysiology Illustrated

The patient's presentation followed the typical biphasic pattern of AFE: 1

1. Phase 1 - Acute cardiopulmonary collapse:

   • Disruption of maternal-fetal interface allowed amniotic fluid entry into maternal circulation 1
   • Pulmonary vasoconstrictors (endothelin) and mechanical obstruction caused acute right ventricular failure 1
   • Hemodynamic collapse resulted from right ventricular dysfunction and decreased left-sided cardiac output 1

2. Phase 2 - Hemorrhagic complications:

   • Amniotic fluid activated Factor VII and platelets, triggering DIC 1
   • Inflammatory cascade further activated clotting pathways 1
   • Massive hemorrhage ensued from combined uterine atony and consumptive coagulopathy 1

Immediate Management Implemented

The multidisciplinary team was immediately activated, including anesthesia, critical care, maternal-fetal medicine, and respiratory therapy. 1

Cardiopulmonary Resuscitation

• High-quality CPR with ACLS protocols was initiated for cardiovascular collapse 1
• Standard basic and advanced cardiac life support measures were employed 1

Hemodynamic Support

Vasopressors and inotropic agents were administered to maintain adequate perfusion while avoiding excessive fluid administration. 1

• Norepinephrine for blood pressure support (0.05-3.3 mcg/kg/min) 1
• Dobutamine or milrinone for inotropic support to address right ventricular failure 1
• Crystalloid fluids were minimized to prevent worsening pulmonary edema and right heart failure 1

Respiratory Management

• Immediate intubation and mechanical ventilation to ensure adequate oxygenation 1
• High FiO2 to address severe hypoxemia 1
• Ventilator settings adjusted to minimize right ventricular afterload 1

Massive Transfusion Protocol Activation

Standard massive transfusion protocol was initiated immediately with 1:1:1 ratio of packed red blood cells, fresh frozen plasma, and platelets. 1

• Early aggressive blood product replacement without waiting for laboratory results 1
• Target platelet count maintained above 50,000/mm³ 1
• Coagulation parameters (PT, aPTT, INR) normalized with FFP 1
• Cryoprecipitate was preferred over additional FFP to minimize volume overload risk 1

Antifibrinolytic Therapy

Tranexamic acid was administered to address hyperfibrinolysis associated with AFE-related coagulopathy. 1 Thromboelastography (TEG), when available, can guide the use of antifibrinolytics like tranexamic acid or epsilon aminocaproic acid. 1, 2

Management of Uterine Atony

Aggressive uterotonic therapy was employed: 1

• Oxytocin infusion (already running, increased dosage) 1, 3, 4
• Methylergonovine (Methergine) 0.2 mg IM for postpartum hemorrhage 1, 4
• Carboprost tromethamine (Hemabate) 250 mcg IM for refractory uterine atony 1, 3
• Consideration for uterine tamponade with intrauterine balloon if bleeding persisted 1

Surgical Interventions Considered

• Thorough inspection of cervix and vagina for lacerations contributing to hemorrhage 1
• Bilateral uterine artery ligation, B-Lynch compression suture, or hysterectomy as last resort measures 1
• Uterine artery embolization as alternative to hysterectomy for refractory bleeding 5

Laboratory Findings

Serial laboratory assessments revealed: 1

• Severe anemia (hemoglobin dropped from baseline ~120 g/L to <70 g/L)
• Prolonged PT and aPTT (PT >20 seconds, aPTT >60 seconds)
• Hypofibrinogenemia (fibrinogen <1.0 g/L)
• Elevated fibrin degradation products (FDP >640 mg/L)
• Thrombocytopenia (platelets <50,000/mm³)
• Evidence of consumptive coagulopathy consistent with DIC 1, 6, 7

Critical Care Course

The patient was transferred to the intensive care unit for ongoing management: 1

• Continued mechanical ventilation with lung-protective strategies
• Hemodynamic monitoring with arterial line and central venous access
• Serial assessment of coagulation status every 2-4 hours initially 1
• Transthoracic or transesophageal echocardiography to assess cardiac function 1
• Consideration for extracorporeal membrane oxygenation (ECMO) if refractory right ventricular failure 1

Outcome and Recovery

Despite the severity of presentation, with prompt recognition and aggressive multidisciplinary management, the patient survived this catastrophic event. 1 The case demonstrates that even with optimal management, AFE carries significant maternal morbidity and mortality risk. 1

Key Learning Points

This case illustrates several critical aspects of AFE management: 1

• Early recognition of the classic triad (hypoxia, hypotension, coagulopathy) is essential 1
• Immediate multidisciplinary team activation improves outcomes 1
• Avoidance of excessive crystalloid prevents worsening right heart failure 1
• Early massive transfusion protocol addresses consumptive coagulopathy 1
• Aggressive uterotonic therapy controls hemorrhage from uterine atony 1, 3, 4
• AFE can present with isolated DIC without preceding cardiorespiratory collapse in atypical cases 6, 7

Common Pitfalls to Avoid

• Delaying diagnosis by waiting for laboratory confirmation—AFE is a clinical diagnosis 1
• Excessive fluid resuscitation with crystalloids worsens pulmonary edema and right ventricular failure 1
• Delayed activation of massive transfusion protocol allows progression of coagulopathy 1
• Attributing hemorrhage solely to uterine atony without considering AFE as underlying cause 1
• Failure to involve critical care and cardiology early for management of right ventricular failure 1