1. Amniotic fluid embolism Dr. S. Parthasarathy MD., DA., DNB, MD (Acu), Dip. Diab.DCA, Dip. Software statistics, Phd Mahatma Gandhi Medical college and research institute, puducherry, India

2. What is it ?? Amniotic fluid embolism (AFE) is a catastrophic obstetric emergency sudden, profound, and unexpected maternal collapse hypotension, hypoxaemia, and disseminated intravascular coagulation (DIC). Altered mental status ??

3. Precipitating factors labor, cesarean delivery, or dilation and evacuation or within 30 minutes postpartum with no other explanation for the clinical findings. Rarely after abdominal trauma in pregnant

4. History The entry of the amniotic fluid was first described by Ricardo Meyer in 1926 In 1941, Steiner and Luschbaugh described histopathologic findings in the pulmonary vasculature in 8 multiparous women dying of sudden shock during labor. Findings included mucin, amorphous eosinophilic material, and in some cases squamous cells..

5. Incidence Unknown 1 in 8000 deliveries to 1 in 80000 deliveries 1980 s - mortality – 80 % 2002 --- - mortality- 25 % 75 % autopsy evidence Neonatal mortality – 70 %

6. A TRIUMPH- pneumonic advanced maternal age; ?? multiparity; meconium stained liquor; intrauterine fetal death; Poly hydramnios; frequent or tetanic uterine contractions; maternal history of allergy or atopy; microsomia; uterine rupture; and placenta accreta Infection.

7. The process Amniotic fluid enters maternal circulation ruptured membranes ruptured uterine or cervical vessels down a pressure gradient from the uterus to veins. Portals placenta, endocervical, -- tears

8. What happens Physical Immunological

9. Physical theory Pulmonary obstruction, pulmonary vasospasm Hypoxemia Cardiac arrest

10. Clarke theory Phase 1 - pulmonary artery vasospasm followed by pulmonary hypertension. Hypoxemia – myocardial dysfunction Release by amniotic fluid

11. Phase 2 Left ventricular failure and pulmonary edema occurs. Biochemical mediators trigger DIC leading to massive haemorrhage and uterine atony.

12. One more theory A more recent hypothesis is that amniotic fluid contains a direct myocardial depressant

13. Clinical features Acute maternal collapse 5 minutes to 48 hours

14. Premonitory symptoms ?? Breathlessness Chest pain Lightheadedness Distress or panic “Pins and needles” in the fingers Nausea and vomiting Feeling cold

16. To be simple 1) Respiratory distress (2) Cyanosis (3) Cardiovascular collapse cardiogenic shock (4) Hemorrhage (5) Coma. Breathing, bleeding and three C s

17. Pathophysiology of DIC procoagulant is sloughed fetal skin and respiratory, gastrointestinal, and genitourinary epithelia. Tissue factor is responsible for activating the extrinsic pathway by binding with factor VII. This complex in turn triggers clotting by activating factor X. DIC

20. Clinical scenario A sudden drop in O 2 saturation can be the initial indication of AFE during LSCS. More than 1/2 of patients die within the first hour. Of the survivors 50 % will develop DIC which may manifest as persistent bleeding from incision or venipuncture sites. The coagulopathy typically occurs 0.5 to 4 hours after phase 1 10 % have seizures Mortality – 25 to 60 %

21. Diagnosis ABG – hypoxemia CXR may be normal or show effusions, enlarged heart, or pulmonary edema. ECG may show a right strain pattern with ST-T changes and tachycardia. Fetal squamous cells in PA catheter The Sialyl Tn antigen test TKAH 2 antibody test Antibody to fetal mucin

22. SERUM TRYTASE LEVEL MAST CELL DEGRANULATION AND ANAPHYLACTOID FEATURES

23. Diagnosis Measurement of the maternal plasma concentration of zinc coproporphyrin, a component of meconium, also has been proposed as a sensitive test for the diagnosis of amniotic fluid embolism Coagulopathy screening

24. TEE First 30 minute -- Transesophageal 4-chamber images showed severe pulmonary hypertension, acute right ventricular failure with a leftward deviation of the inter atrial and inter ventricular septum, and severe tricuspid regurgitation.

25. Differential diagnosis Anaphylaxis (Collapse) Pulmonary embolus (Collapse) Aspiration (Hypoxaemia) Pre-eclampsia or eclampsia (Fits, Coagulopathy) Haemorrhage (APH ; PPH) Septic shock Drug toxicity (MgSO 4, total spinal, LA toxicity) Aortic dissection

26. Diagnosis of exclusion and suspicion Usually at autopsy

27. Management

28. Principles Oxygenation Cardiac output maintenance Coagulopathy correction Uterine tone and delivery of the baby

29. Oxygenation Maintaining oxygenation may necessitate intubation and ventilation. CPAP or PEEP may be indicated.

30. Haemodynamic stability Rapid infusion of crystalloids, colloids, Inotropes PAWP catheter ??? COAGULOPATHY

31. Coagulopathy Plasma, cryoprecipitate, and platelets are frequently required. Recombinant factor VII has been used to treat uncontrollable massive obstetric haemorrhage if haemorrhage becomes difficult to control. Hematologists consultation

32. Cryoprecipitate is useful it can replenish clotting factors cryoprecipitate contains fibronectin it could facilitate the removal of cellular and particulate matter, such as amniotic fluid debris, from the blood via the monocyte /macrophage system

33. Uterine tone Oxytocin Methergin PGs Bimanual massage

34. Baby delivery The baby should be delivered as quickly as possible. If the mother is undergoing CPR, surgical delivery should be performed within 5 min for improved maternal outcome.

35. Possible treatment on survival Steroids, prostacyclin, nitric oxide as well as plasma exchange, haemo filtration, and cardiopulmonary bypass

36. All these remain true ?? Catastrophic Unpredictable Unpreventable ? Untreatable

37. SUMMARY Definition Risk factors -- a triumph Pathophysiology Clinical features Diagnosis Treatment

38. The term AFE now appears to be a misnomer. Proposed new names include “sudden obstetric collapse syndrome” and “anaphylactoid syndrome of pregnancy”.

39. Thank you