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Amniotic Fluid Embolism Dr. Megha jain University College of Medical Sciences & GTB Hospital, Delhi

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Presentation on theme: "Amniotic Fluid Embolism Dr. Megha jain University College of Medical Sciences & GTB Hospital, Delhi"— Presentation transcript:

1 Amniotic Fluid Embolism Dr. Megha jain University College of Medical Sciences & GTB Hospital, Delhi

2 Amniotic fluid embolism Occurs when amniotic fluid, fetal cells, hair or other debris enter maternal circulation. during labour during labour during caesarean section during caesarean section after normal vaginal delivery after normal vaginal delivery during II trimester termination of pregnancy during II trimester termination of pregnancy 1 in 8000 to 80,000 pregnancies. 1 in 8000 to 80,000 pregnancies. Definition Timing Incidence

3 Risk factors 1. Advanced maternal age 2. Multiparity 3. Meconium stained liquor 4. Placenta accreta 5. Polyhydramnios 6. Uterine rupture 7. Cervical laceration 8. Strong uterine contractions 9. Chorioamnionitis 10. Maternal atopy/ allergy

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5 Pathophysiology Debris in maternal circulation Biochemical mediators (endothelin,LT’s) Pulmonary artery spasm (pulm HTN)  RV pressure Hypoxia Myocardial damage LVF ARDS Phase 1

6 Pathophysiology (contd….) Biochemical mediators Activation of factor X DIC (30min to 4 hr after phase 1) Hemorrhagic phase Massive hemorrhage & uterine atony Phase 2

7 Immunological response to amniotic fluid exposure Maternal exposure to fetal tissue Majority patients – No effect Small no. of patients- Endogenous mediator release S/S depends on antigenic exposure And individual response SEVERE Hypoxia Cardiovascular collapse Coagulopathy Death LESS SEVERE : isolated finding Or prolonged presentation

8 Classical Triad ACUTE HYPOXIA ACUTE HYPOXIA HEMODYNAMIC COAGULOPATHY HEMODYNAMIC COAGULOPATHY COLLAPSE COLLAPSE

9 Signs and Symptoms Hypotension Hypotension Fetal distress Fetal distress Pulmonary edema or ARDS Pulmonary edema or ARDS Cardiopulmonary arrest Cardiopulmonary arrest Cyanosis Cyanosis Coagulopathy Coagulopathy Dyspnea Dyspnea Seizure Seizure Uterine atony Uterine atony Bronchospasm Bronchospasm Chest pain, dysrhythmias Chest pain, dysrhythmias

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11 Chest X ray in AFE

12 Is AFE an anaphylactoid reaction? Previous history of drug allergy or atopy Previous history of drug allergy or atopy Mediators assoc. with anaphylactoid reaction are released in AFE. Mediators assoc. with anaphylactoid reaction are released in AFE. AFE is not due to physical obstruction of pulmonary vasculature AFE is not due to physical obstruction of pulmonary vasculature Pre treatment with LT inhibitor prevents AFE collapse Pre treatment with LT inhibitor prevents AFE collapse Treatment with antihistaminic reduced degree of shock Treatment with antihistaminic reduced degree of shock Steroid - successfully used in mgmt. of AFE. Steroid - successfully used in mgmt. of AFE.

13 How to diagnose ? NON SPECIFIC 1.Complete blood count 2.FDP, Fibinogen 3.Coagulation profile 4.ABG 5.CXR 6.ECG 7.V/Q scan SPECIFIC 1.Zinc Coproporphyrin > 35 nmol/L in maternal plasma (a component of meconium) 2. Serum tryptase - 

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15 Lab tests in DIC Fibrinogen < 150mg/dl Fibrinogen < 150mg/dl Plt. Count < 50,000/mm lacs Plt. Count < 50,000/mm lacs Thrombin time> 100 sec sec Thrombin time> 100 sec sec PT > 100 sec sec PT > 100 sec sec PTTK > 100 sec sec PTTK > 100 sec sec FDP > 200 µg/ml 200 µg/ml < 16 µg/ml DICNormal values

16 Differential diagnosis 1. Cardiovascular – Myocardial infarction Primary arrhythmia Primary arrhythmia Hemorrhage(APH,PPH) Hemorrhage(APH,PPH) 2. Respiratory - Pulmonary embolism Air embolism Air embolism Aspiration pneumonitis Aspiration pneumonitis 3. CNS - Eclampsia 4. Regional - High/ Total spinal anesthesia LA toxicity anesthesia LA toxicity 5. Anaphylactoid reaction 6. Septic shock

17 Management 1. Restore CVS and pulmonary equilibrium 1.Maintain SBP > 90 mmHg 2.UO > 25 ml / hr 3.Arterial PO2 > 60 mmHg 2. Re establishing uterine tone 3. Correct coagulation parameters GOALS

18 Immediate measures # Intubate and ventilate with 100% oxygen # Initiate CPR if indicated # If undelivered, monitor fetus and deliver # Provide aggressive volume and pressor support pressor support may include- pressor support may include- *Dopamine: 2 – 5 µg/kg/min *Dopamine: 2 – 5 µg/kg/min *Dobutamine: 15 – 30 µg/kg/min *Dobutamine: 15 – 30 µg/kg/min *Noradrenaline: 0.1 – 0.4 µg/kg/min *Noradrenaline: 0.1 – 0.4 µg/kg/min *Adrenaline: 0.15 – 0.30 µg/kg/min *Adrenaline: 0.15 – 0.30 µg/kg/min # Restrict fluid to maintainence levels ( ARDS follows in 70%) Convert regional to GA immediately

19 Restore uterine tone Uterine massage Uterine packing Oxytocin PG analouges – PG F2 alpha Improve CO & Uterine perfusion Displacement of the patient’s uterus towards left – improves venous return and uterine blood flow.

20 Manage coagulopathy DIC – depletion of fibrinogen, platelets, coagulation factors Invg- PT/ PTTK, platelet count Treatment 1. FFP 2. cryoprecipitate – fibrinogen <100 mg/dl 3. platelet transfusion – at < 50,000 / mm3 or if spontaneous bleeding is present.

21 Management in ICU Monitor – ECG, PO2, PCO2, urine output Arterial catheterization – for repeated ABGs CV catheterisation – diagnose RV overload guide fluid therapy guide fluid therapy Pulmonary artery catheterisation and PCWP- measure LV function and compliance

22 Prognosis 60% die within 1 hr of embolism Of survivors, 75% have long term neurological deficits 50% develop DIC (persistent bleeding) 10-15% develop GTCS Mortality – 1. sudden cardiac arrest 2. hemorrhage ( coagulopathy) 2. hemorrhage ( coagulopathy) 3. ARDS and multiple organ failure 3. ARDS and multiple organ failure (if in utero at the time of event) (if in utero at the time of event) 70% survive, 50% have neurological deficit. Maternal Fetal

23 Thank You


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