Presentation on theme: "Amniotic Fluid Embolism Dr. Megha jain University College of Medical Sciences & GTB Hospital, Delhi"— Presentation transcript:
Amniotic Fluid Embolism Dr. Megha jain University College of Medical Sciences & GTB Hospital, Delhi www.anaesthesia.co.in email: firstname.lastname@example.org
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
Pathophysiology (contd….) Biochemical mediators Activation of factor X DIC (30min to 4 hr after phase 1) Hemorrhagic phase Massive hemorrhage & uterine atony Phase 2
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
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.
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 -
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
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
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
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.
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.
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
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