Amniotic fluid embolism (AFE) is a life-threatening obstetric emergency that occurs when amniotic fluid, fetal cells, hair or debris enters the mother's bloodstream during labor and delivery. It can cause sudden collapse, hypoxemia and disseminated intravascular coagulation (DIC). Treatment is supportive and aims to maintain oxygenation and hemodynamic stability through oxygen supplementation, IV fluids, vasopressors and blood products. Even with aggressive management, AFE carries a high risk of developing acute respiratory distress syndrome, heart failure and death.

1. AMNIOTIC FLUID EMBOLISM
DR PRITI PATIL,
FORTIS HOSPITAL,MULUND.

2. AMNIOTIC FLUID EMBOLISM
• Amniotic fluid embolism (AFE) is a life-threatening obstetric emergency.
• It happens due to sudden gush of amniotic fluid ,fetal cells , hair and amniotic
debry entering the maternal circulation.
• Signs and Symptoms:
1. Sudden collapse due to profound hypotension.
2. Hypoxemia
3. DIC (Disemminated intravascular coagulation)

3. Differential Diagnosis
Obstetric Causes
• Acute hemorrhage
• Amniotic fluid embolism
• Placental abruption
• Uterine rupture
• Uterine atony
• Eclampsia
• Peripartum cardiomyopathy
Anesthetic Causes
• High spinal anesthesia
• Aspiration
• Local anesthetic toxicity
Non obstetric Causes
• Pulmonary embolism
• Air embolism
• Anaphylaxis
• Sepsis/septic shock
• Intracerebral bleed
• Drug toxicity
• Acute myocardial infarction

4. Factors that may be associated with AFE
• Advanced maternal age
• Multiparity
• Meconium stained liquor
• Obstructed labor
• Intrauterine fetal death
• Polyhydramnios
• Tetanic uterine contractions
• Maternal history of allergy or atopy
• Uterine rupture
• Placenta accreta
• Trauma
• Diabetes mellitus
• Operative delivery including cesarean section.

5. • It is uncommonly known as Anaphylactoid Syndrome of Pregnancy.
• Exposure of maternal circulation to the amniotic fluid , fetal cells/debry may lead to
hypoxemia, pulmonary vasospasm, cardiac failure or even death.
• Which may result in activation of the complement cascade stimulating endogenous
immunomediators, producing a reaction similar to anaphylaxis.
• Amniotic fluid also contains procoagulant tissue factor.
• It is described as a Biphasic Response
 PhaseI – The biochemicals released after the entry of the amniotic material has
entered causes severe pulmonary artery vasospasm → pulmonary hypertension→
increased right ventricular pressures→ right ventricular dysfunction.
(Lasts for 30 mins)
 Phase II- Left ventricular failure and pulmonary edema.Biochemical mediators
lead to DIC which leads to massive hemorrhage and DIC.

6. Symptoms Signs
Dyspnea Hypotension
Cough Fetal Distress
Headache Pulmonary edema/ARDS
Chest Pain Cyanosis
Coagulopathy
Seizures
Bronchospasm
Cardiopulmonary arrest
Uterine Atony
Clinical Features

7. Treatment
• Amniotic fluid embolism is a diagnosis of exclusion.
• Management is symptomatic and supportive.
• Targets- Maintaining oxygenation ,hemodynamic support and
correction of coagulopathy
• Immediate Resuscitation- ABC
 Airway and breathing
• Administer 100% oxygen via a non-rebreathing reservoir face
mask
• Prompt assessment, with control of the airway and ventilation
of the lungs with tracheal intubation may be essential.
 Circulation
• 2 large bore iv lines, send blood for coagulation profile, CBC,
crossmatch, arrange 6units blood.
• Left lateral tilt/Manual uterine displacement.
• Hemodynamic support would include preload optimization and
vasopressors.

8. • Fluid resuscitation with crystalloid/colloid to optimize filling.
• Infusion of an inotrope may be required to maintain a mean arterial blood pressure
and achieve an adequate urine output.
• An arterial line for continuous blood pressure monitoring is essential, and the use
of a non-invasive cardiac output monitor may be helpful.
• Continuously monitor the fetus and early consideration should be given to delivery
of baby.
 Uterine tone –Pharmacologic agents such as oxytocin, ergometrine and
prostaglandins carboprost and misoprost.
 Coagulation:
• Use of plasma, cryoprecipitate, and platelets to be guided by clinical condition of
the patient and laboratory investigations.
• Recombinant factor VII may be used, but one should be careful as this can cause
thrombotic complications
 Antifibrinolytics, like e-aminocaproic acid and tranexamic acid, might be helpful
but evidence is lacking.

9. Investigations
• Coagulation profile: AFE is associated with DIC in >80% cases
• Electrocardiogram shows tachycardia, ST segment and T-wave changes,
and findings consistent with right ventricle strain
• Arterial blood gases: changes consistent with hypoxia
• Chest X-ray: consistent with pulmonary edema
• Echocardiogram
• Serum tryptase

10. Management
• Intensive care monitoring
• One should be aware that there is high-risk at developing: ARDS, heart failure,
DIC
• Supportive treatment: Ventilation, inotropic support, Hematological support
• Steroids may be useful
Potential Interventions for Severe Life Threatening Cases of AFE
• Inhaled nitric oxide for pulmonary hypertension leading to right-sided heart
failure
• ECMO for severe hypoxia and left heart failure.

11. Thank You